RU2202370C1 - Neuropsychotropic medicinal agent - Google Patents

Abstract

FIELD: medicine, pharmacy. SUBSTANCE: invention relates to medicinal agent comprising activated form of super small doses of monoclonal or polyclonal immune antibodies raised to exogenous or endogenous substance exhibiting neuropsychotropic effect. Activated form of medicinal agent is prepared by multiple successive dilution and external impact being by homeopathic technology mainly. Invention provides the development of effective antibody-base neuropsychotropic agent without negative adverse effect. Invention can be used for preparing neuropsychotropic medicinal preparations. EFFECT: valuable properties of agent. 135 cl, 395 ex

Description

 The invention relates to medicine and can be used to obtain drugs.

 The use of antibodies for the treatment of pathological syndromes is known from the prior art (SU 1131508 A, A 61 K 39/00, 1984; SU 1730144 A1, C 12 N 7/00, 1992).

 Closest to the invention can be considered the use as a neurotropic drug - antibody-antiserum to brain-specific proteins for the treatment of certain demyelinating diseases of the central nervous system (see M.B. Stark. Brain-specific proteins / antigens / and neuron functions. M .: Medicine, 1985, p. 234-236, 224-225).

 However, such drugs are characterized by narrow specificity and, as a rule, insufficient activity; in addition, their use may be associated with undesirable side effects associated, in particular, with the introduction of significant doses of a foreign protein into the body. At the same time, antibodies to brain-specific proteins or other neurotropic substances block this protein or cause immunological reactions aimed in some cases at the destruction of the cell carrying this protein, which limits the scope of their therapeutic use.

 The invention is aimed at creating an effective neuropsychotropic agent based on antibodies that does not have a negative side effect.

 The solution to this problem is provided by the fact that the drug contains ultra-low doses of monoclonal, polyclonal, immune or natural antibodies in an activated form, to an exogenous or endogenous substance that has a neuropsychotropic effect; while the activated form of antibodies is obtained by repeated serial dilution and external exposure, mainly by homeopathic technology.

 In addition, when obtaining antibodies to a substance of a polypeptide structure that has a neuropsychotropic effect, it is possible to use a fragment of the polypeptide structure of a molecule with a size of at least three amino acid residues.

In this case, use:
antibodies to acetylcholinesterase inhibitors;
antibodies to M1 agonists of the acetylcholine receptor subtype;
antibodies to antagonists of M1 acetylcholine receptor subtype;
antibodies to antagonists of M2 acetylcholine receptor subtype;
antibodies to antagonists of M3 acetylcholine receptor subtype;
antibodies to antagonists of M4 acetylcholine receptor subtype;
antibodies to nicotinic receptor agonists;
antibodies to substances that increase the concentration of acetylcholine in the synaptic cleft;
antibodies to endogenous glutamate receptor ligands;
antibodies to competitive antagonists of NMDA receptors;
antibodies to non-competitive NMDA receptor antagonists;
antibodies to NMDA receptor channel blockers;
antibodies to antagonists of the glycine site of the glutamate receptor;
antibodies to glutamate receptor glycine agonists;
antibodies to antagonists of the polyamine portion of the NMDA receptor complex and NMDAR2B selective antagonists;
antibodies to agonists, antagonists, and positive modulators of AMPA receptors;
antibodies to substances that enhance the function of GABA _A -ergic system;
antibodies to GABA _A receptor agonists;
antibodies to GABA deactivation inhibitors;
antibodies to substances that increase the content of GABA; antibodies to benzodiazepine receptor agonists;
antibodies to complete benzodiazepine receptor agonists;
antibodies to partial agonists of benzodiazepine receptors;
antibodies to reverse (inverse) benzodiazepine receptor agonists;
antibodies to benzodiazepine receptor antagonists;
antibodies to substances that weaken the function of GABA _A -ergic system;
antibodies to GABA _A receptor antagonists;
antibodies to GABA _A receptor chlorine channel blockers;
antibodies to GABA synthesis inhibitors;
antibodies to substances that enhance the function of GABA _B- ergic system;
antibodies to GABA _B receptor agonists;
antibodies to substances that weaken the function of GABA _B- ergic system;
antibodies to GABA _B receptor blockers;
antibodies to dopamine receptor antagonists;
antibodies to dopamine receptor antagonists of type D ₂ ;
antibodies to dopamine receptor antagonists of type D ₃ ;
antibodies to dopamine receptor antagonists of type D ₂ -D ₄ ;
antibodies to dopamine receptor antagonists of type D ₁ and D ₅ ;
antibodies to dopamine receptor agonists;
antibodies to dopamine receptor agonists of type D ₂ -D ₄ ;
antibodies to dopamine receptor agonists of type D ₂ -D ₃ ;
antibodies to dopamine receptor agonists of type D ₃ -D ₄ ;
antibodies to dopamine receptor agonists of type D ₁ -D ₅ ;
antibodies to dopamine precursors;
antibodies to serotonergic receptor agonists;
antibodies to serotonin receptor agonists of type 5-HT _1a ;
antibodies to serotonin receptor agonists of type 5HT _1b ;
antibodies to serotonin receptor agonists of type 5HT _1d :
antibodies to serotonin receptor agonists of type 5HT _2a ;
antibodies to serotonin receptor agonists of type 5HT _2c ;
antibodies to serotonin receptor agonists of type 5HT ₃ ;
antibodies to serotonergic receptor antagonists;
antibodies to serotonin receptor antagonists of type 5HT _1a ;
antibodies to serotonin receptor antagonists of type 5HT _1b ;
antibodies to serotonin receptor antagonists of type 5HT _1d ;
antibodies to serotonin receptor antagonists of type 5HT _2a ;
antibodies to serotonin receptor antagonists of type 5HT _2b ;
antibodies to serotonin receptor agonists of type 5HT _2c ;
antibodies to serotonin receptor agonists of type 5HT ₃ ;
antibodies to adrenergic receptor agonists;
antibodies to α ₁ -adrenergic receptor agonists;
antibodies to α ₂ -adrenergic receptor agonists;
antibodies to β-adrenergic receptor agonists;
antibodies to adrenergic receptor antagonists;
antibodies to α ₁ -adrenergic receptor antagonists;
antibodies to antagonists of α ₂ -adrenergic receptors;
antibodies to β ₁ -adrenergic receptor antagonists;
antibodies to β ₂ -adrenergic receptor antagonists;
antibodies to β ₃ -adrenergic receptor antagonists;
antibodies to β ₄ -adrenergic receptor antagonists;
antibodies to adenosine substances (P ₁ purinergic);
antibodies to A ₁ adenosine receptor agonists;
antibodies to A ₁ adenosine receptor antagonists;
antibodies to A _2A adenosine receptor agonists;
antibodies to A _2A adenosine receptor antagonists;
antibodies to A _2B adenosine receptor agonists;
antibodies to A _2B adenosine receptor antagonists;
antibodies to A ₃ adenosine receptor agonists;
antibodies to antagonists of A ₃ adenosine receptors;
antibodies to P ₂ purinergic receptors;
antibodies to P _2X purinoreceptor agonists;
antibodies to P _2X purinoreceptor antagonists;
antibodies to P _2Y purinoreceptor agonists;
antibodies to P _2Y purinoreceptor antagonists;
antibodies to P _2U purinoreceptor agonists;
antibodies to P _2T purinoreceptor agonists;
antibodies to P _2T purinoreceptor antagonists;
antibodies to P _2Z purinoreceptor agonists;
antibodies to histamine receptor agonists;
antibodies to histamine H ₁ receptor agonists;
antibodies to histamine H ₂ receptor agonists;
antibodies to histamine H ₃ receptor agonists;
antibodies to histamine receptor antagonists;
antibodies to histamine H ₁ receptor antagonists;
antibodies to histamine H ₂ receptor antagonists;
antibodies to histamine H ₃ receptor antagonists;
antibodies to histamine release inhibitors;
antibodies to activators of diamine oxidase - an enzyme of histamine deactivation;
antibodies to dopamine reuptake inhibitors;
antibodies to norepinephrine reuptake inhibitors;
antibodies to serotonin reuptake inhibitors;
antibodies to GABA reuptake inhibitors;
antibodies to substances that affect the function of calcium channels;
antibodies to substances that affect the function of calcium channels of the L-type;
antibodies to L-type calcium channel agonists;
antibodies to calcium blockers;
antibodies to L-type calcium channel antagonists;
antibodies to N-type calcium channel antagonists;
antibodies to P-type calcium channel antagonists;
antibodies to Q-type calcium channel antagonists;
antibodies to hypothalamic liberins and statins;
antibodies to liberins;
antibodies to statins;
antibodies to opioid peptides;
antibodies to enkephalin opioids;
antibodies to melanocortins;
antibodies to corticotropins;
antibodies to melanotropins;
antibodies to vasopressin-tocins;
antibodies to vasopressins;
antibodies to tocins;
antibodies to pancreatic peptides;
antibodies to peptides similar to gastrin;
antibodies to tachykinins;
antibodies to neurotensins;
antibodies to bombesins;
antibodies to kinins;
antibodies to angiotensins;
antibodies to endosepins;
antibodies to galanin;
antibodies to the peptide inducer of slow wave sleep (DSIP);
antibodies to prolyl endopeptidase inhibitors;
antibodies to substances with an antioxidant mechanism of action.

 It is preferable to use a mixture of various, mainly hundred, homeopathic dilutions of the drug.

 It has been experimentally confirmed that when activated (potentiated) forms of antibodies to a substance having a neuropsychotropic effect are introduced into the body, it is not suppression, but a modification of the activity and / or functional state of the latter that determines the therapeutic effectiveness of the claimed solution.

 Obtained in accordance with the invention, the drug is a new pharmacological preparation, which is characterized by the presence of specific pharmacological activity, the absence of side effects, environmental cleanliness and low cost.

 The drug is prepared as follows.

 For the treatment of a specific disease or pathological syndrome, including neuropsychopathological disorders, exogenous or endogenous substance that exerts a neuropsychotropic effect and is able to influence physiological mechanisms, the violation of which leads to the formation of a pathological syndrome, is detected by experimental clinical methods.

 The identified substance, if necessary in the form of a conjugate with a macromolecular carrier, is used as an immunogen to immunize laboratory animals to obtain immune antibodies or in hybridoma technology to obtain monoclonal antibodies. The resulting antibodies are purified by affinity chromatography.

 The method of obtaining immune and monoclonal antibodies is described, for example, in the book: Immunological methods / ed. G. Fremel, Moscow: Medicine, 1987, p. 9-33.

 The isolated antibodies are sequentially diluted repeatedly and subjected to external influences to obtain ultra-low or low doses, for example, according to the homeopathic potentiation technology (see Homeopathic medicines. Description and Production Manual, V. Schwabe, Moscow, 1967, p. 12-38). In this case, a uniform decrease in concentration is made by successive dilution of 1 volume part of the starting substance (antibodies) in 9 volume parts (for decimal dilution D) or in 99 volume parts (for hundred dilution C) of a neutral solvent with multiple vertical shaking of each dilution obtained and using mainly separate containers for each subsequent dilution - until the required dose (potency) is obtained.

 External processing in the process of reducing the concentration can also be carried out by ultrasound, electromagnetic or other physical effects.

 A drug prepared in this way is used, mainly in dosage forms and dilutions accepted in homeopathic practice, in the form of alcohol or aqueous solutions or tablets (granules), obtained by soaking the filler in the dosage form by saturation with a potentized solution or by directly introducing the latter into a liquid dosage form .

 Examples.

Antibodies to substances that affect the balance of neurotransmitters in the nervous system
Antibodies to Cholinergic Substances
Antibodies to acetylcholinesterase inhibitors
Example 1. Patient K., aged 68 years old, complained of memory impairment for current events, decreased attention. A solution of antibodies to physostigmine (a mixture of homeopathic dilutions C12 + C30 + C200) is proposed - 1 tablet 2 times a day for a month. The patient has improved memory, attention, improved learning processes for new skills. Side effects were not observed.

 Example 2. Patient A., aged 6 years old, with a diagnosis of motor disorders with spastic form of childhood paralysis. Course treatment (30 days) with antibodies to galantamine (a mixture of homeopathic dilutions C12 + C30 + C200) - 1 tablet 2 times a day led to a significant improvement in the patient's condition. The patient improved neuromuscular conduction, increased contractility of muscles, improved mnemonic functions, and learning ability. Side effects were not observed.

 Example 3. Antibodies to rivastigmine cause selective inhibition of brain acetylcholinesterase compared to peripheral forms of cholinesterase. It was shown that the introduction of antibodies to rivastigmine (a mixture of homeopathic dilutions C12 + C30 + C200) - 1 ml of an aqueous solution of per os 2 times a day to sexually mature rats for 7 days improves the fixation of the memorial trail during the development of the reflex in the U-shaped complex maze . Under the influence of the drug, an improvement in orientation and acceleration of the reflex is observed.

 Example 4. Patient O., aged 58 years old, complained of periodically occurring memory impairments for current events, impaired attention, impaired motor reactions, myasthenia gravis. It is proposed to take a solution of antibodies to amiridine (a mixture of homeopathic dilutions C12 + C30 + C200) - 1 tablet 2 times a day for two months. The patient has improved memory, attention, improved learning processes for new skills, decreased motor impairment. Side effects were not observed.

 Example 5. In experiments on rats, it was shown that antibodies to tacrine (a mixture of homeopathic dilutions C12 + C30 + C200) when administered orally in an aqueous solution had a pronounced antiamnestic effect. The substance, when administered once, eliminated amnesia caused by the maximum electroconvulsive seizure immediately after learning the conditioned reflex of passive avoidance in the dark-light chamber test. Under the influence of antibodies to tacrine, the latent time of entry into the dangerous dark chamber increased by 70% and the time spent in the dark chamber decreased (by 55%).

 Example 6. It is shown that antibodies to metrifonate retain its properties as prodrugs. Pharmacokinetic methods have shown that the active substance is slowly released into the bloodstream and as a result, a mild and prolonged acetylcholinesterase inhibitory effect is achieved. In experiments on rats, it was shown that antibodies to metrifonate (a mixture of homeopathic dilutions C12 + C30 + C200) when administered 1 ml of an aqueous solution with a single injection eliminated amnesia caused by the maximum electroconvulsive seizure immediately after learning the conditioned reflex of passive avoidance in the dark test bright camera. Under the influence of antibodies to metrifonate, the latent time of entry into the dangerous dark chamber increased by 60% and the time spent in the dark chamber decreased (by 45%). The results obtained indicate the presence of anti-anamnestic effects in antibodies to metrifonate.

 Example 7. Antibodies to donepezil (arisept) were studied in experiments on old rats aged 18 months, in which there was a deterioration in the formation of a memorial trace. A three-month administration of a substance (a mixture of homeopathic dilutions C12 + C30 + C200) of 1 ml of an aqueous solution per os daily caused a significant relief in the development of a conditioned reflex of active avoidance in the shuttle-box chamber, which was manifested in a faster reflex with shorter latent periods.

 Example 8. Antibodies to Huperzine and new substances TAK-147, DMP-543, T-82, Penserin were studied in experiments on adult rats with impaired memory for pain shock irritation. It was shown that antibodies to these substances (a mixture of homeopathic dilutions C12 + C30 + C200), when administered 1 ml per os aqueous solution daily, had a pronounced and statistically significant antiamnestic effect. With a single administration of the antibody, the amnesia caused by the maximum electroconvulsive seizure immediately after learning the conditioned reflex of passive avoidance in the dark-light chamber test was eliminated. Under the influence of antibodies, the latent time of entry into a dangerous dark chamber increased and the time spent there was reduced compared with the control.

Muscarinic Receptor Ligands Antibodies
Antibodies to agonists of M ₁ acetylcholine receptor subtype
Example 9. In experiments on rats, it was found that a single administration of antibodies to arecoline intragastrically and intraperitoneally (a mixture of homeopathic dilutions C12 + C30 + C200) of 0.5 ml of an aqueous solution significantly facilitates the learning process of the conditioned reflex of active avoidance in the shuttle box installation, where A sound signal was used as a conditioned stimulus, and an electric current to the floor was used as an unconditioned stimulus. Under the influence of a substance, a decrease in the number of combinations necessary to achieve the learning criterion is observed.

 Example 10. In experiments on mice, the use of antibodies to the M1 agonist of the acetylcholine receptor xanthomelin (a mixture of homeopathic dilutions C12 + C30 + C200) of 1 ml of an aqueous solution of per os leads to an acceleration of the production of the reflex of food reinforcement in the T-shaped labyrinth, where the sound served as a conditioned signal opening the door of the starting compartment. Under the influence of a substance, the number of runs to the finish compartment decreased, and the running time was reduced (1.6 times), which indicates a positive effect of the substance on memory.

 Example 11. Antibodies to sabcomelin and tsevimelin (a mixture of homeopathic dilutions C12 + C30 + C200), administered orally in an aqueous solution to outbred rats 30 minutes before the development of a conditioned reflex of active avoidance in a shuttle box installation with a light conditioned stimulus, statistically significantly improved production rate reflex, reducing the number of workouts (1.8 times for antibodies to sabcomelin and 1.5 times for antibodies to cevimeline), necessary to achieve the criterion for the development of reflex.

 Example 12. Under the influence of antibodies to milamelin, substances UM-795 or AF151 (a mixture of homeopathic dilutions C12 + C30 + C200) with the introduction of 1 ml of an aqueous solution of per os in animals, the process of reproducing a memorable trace is improved. Previously, a stable reflex of passive avoidance of the conditioned reflex in a dark-bright chamber was developed in rats, and then it was extinguished. The introduction of drugs before reproduction of the reflex improved its extraction from memory.

 Despite the extinction of the reflex, the latent period of the reflex was reduced in treated animals by 30%.

 Additional examples.

Antibodies to antagonists of M ₁ acetylcholine receptor subtype
Example 13. Antibodies to atropine, a blocker of M- and to a lesser extent N-cholinergic receptors, in an experiment in mice in high doses, caused activation of animal behavior, mental and motor excitement, anxiety state upon single oral administration of 0.1 ml of antibody solution in homeopathic dilution C200. In electroencephalographic studies in experiments on rats, the ability of antibodies to atropine in homeopathic dilutions of C200 to cause activation of the cerebral cortex biopotentials after oral administration of 0.2 ml of the solution was revealed.

 Example 14. Antibodies to scopolamine in studies on rats cause a decrease in motor activity in the open field test. The introduction of a solution of antibodies in homeopathic dilution of C200 before training or immediately after it violates the development of a conditioned reflex of passive avoidance in rats in the dark-light chamber test. Animals forget the trained and do not fulfill the tasks. Rats with a short latency period enter the dark, dangerous compartment of the chamber, despite receiving earlier pain irritation.

 Example 15. Antibodies to pirenzepine. In vitro experiments using electrophysiological methods have shown that antibodies to pirenzepine (an M1 receptor antagonist) in homeopathic dilution of C200, when introduced into the incubation medium, negatively affect the depolarization caused in the upper cervical ganglia of the rat by acetylcholine. A solution of antibodies in homeopathic dilution of C200 with a single oral administration of 0.1 ml to rats causes a similar effect in the body, that is, it eliminates the depolarization caused by acetylcholine in these formations.

Example 16. In in vitro experiments using radioligand methods, tritium-labeled ligands, for example [ ³ H] -pirenzepine, bind in the body to receptors in the case of pirenzepine - receptors of type M ₁ . The amount of bound ligand can be determined by counting the radioactivity of tissue samples. When a solution of antibodies to pirenzepine was added to the medium in a homeopathic dilution of C200, it was shown that they interfere with the binding of the labeled ligand. This leads to a change in the radioactivity of the tissue, which can be detected during its determination. In addition, it was shown that in vitro experiments with cholinergic receptors of type M ₁ bind the labeled ligand [ ³ H] -quinuclidinyl benzylate. Antibodies to pirenzepine in homeopathic dilution of C200 displace it from the receptors, reducing the radioactivity of the tissue sample.

Example 17. Antibodies to MT7 toxin obtained from the green mamba venom, in vitro experiments have shown that antibodies to MT7 toxin are a selective antagonist of M ₁ receptors. Antibodies to MT7 toxin in homeopathic dilution of C200 eliminate the contraction of segments of the venous vessels (v. Saphenous) of the dog caused by acetylcholine.

Example 18. It was shown in experiments in vitro using radioligand methods that antibodies to MT7 toxin in homeopathic dilution of C 100 displace tritium-labeled ligands, preventing them from binding to receptors, in particular, they displace [ ³ H] -pirenzepine, significantly reducing radioactivity tags. Antibodies to MT7 toxin in experiments in vitro also displace another labeled ligand - [ ³ H] -quinuclidinyl benzylate in C200 homeopathic dilution.

Antibodies to antagonists of M ₂ acetylcholine receptor subtype
Example 19. Antibodies to tripitramine. Tripitramine, being a selective antagonist of acetylcholine receptors of type M ₂ , displaces labeled ligands. So, in experiments in vitro using radioligand methods, it prevents the binding of receptors labeled with tritium [ ³ H] -quinuclidinyl benzylate, reducing the radioactivity of the label. Antibodies to tripitramine have a similar effect in homeopathic dilution of C200, preventing the binding of tritium-labeled ligand to receptors and reducing the radioactivity of the label.

Antibodies to antagonists of M ₃ acetylcholine receptor subtype
Example 20. Antibodies to darifenacin, a selective antagonist of acetylcholine receptors of type M ₃ . Antibodies to darifenacin in in vitro experiments using radioligand methods have shown the ability to displace labeled ligands from the receptor. Antibodies to darifenacin displace tritium-labeled [ ³ H] -darifenacin in C200 homeopathic dilution, reducing label radioactivity. In addition, antibodies to darifenacin are displaced from the receptor by another labeled ligand of [ ³ H] -quinuclidinyl benzylate in homeopathic dilution of C200. They also inhibit the binding of acetylcholine receptors to [ ³ H] -quinuclidinyl benzylate, reducing the radioactivity of the drug.

Antibodies to antagonists of M ₄ acetylcholine receptor subtype
Example 21. Antibodies to PD102807. In vitro experiments using radioligand methods have shown that antibodies to PD102807 displace labeled ligands from the receptor. Under the influence of antibodies in homeopathic dilution of C 100, displacement of tritium-labeled [ ³ H] -quinuclidinyl benzylate is observed.

Example 22. Antibodies to toxin MT3 - a selective antagonist of type M ₄ receptors. In vitro experiments using radioligand methods, it was found that antibodies to MT3 toxin displace labeled ligands from the acetylcholine receptor. In particular, anti-C200 antibodies in homeopathic dilution displace tritium-labeled [ ³ H] -quinuclidinyl benzylate, decreasing label radioactivity.

Antibodies to nicotinic receptor ligands
Antibodies to nicotinic receptor agonists
Example 23. Antibodies to anabazine facilitate the process of learning the conditioned reflex of active avoidance in a shuttle box installation, where a sound signal was used as a conditioned stimulus, and an electric current supplied to the electrode floor was used as an unconditioned stimulus. The improvement in learning under the influence of a single oral administration of 0.1 ml of a solution of antibodies in homeopathic dilution of C200 was expressed in a significant decrease in the number of combinations (by 42%) required to achieve the learning criterion and in reducing the latent time of the conditioned reflex - diving in response to an audio signal ( 30%).

 Example 24. Antibodies to RJR-2557 or SIB-1553A facilitate the development of a conditioned reflex of active avoidance by installing jumping onto a vertical rod in response to a conditioned stimulus — a sound signal and an unconditioned stimulus — an electric current supplied to the electrode floor. 7-day oral administration of 0.2 ml of a solution of antibodies in homeopathic dilution of C200 led to improved learning, which was expressed in a significant decrease (by 55%) in the number of combinations required to achieve the learning criteria and in reducing the latent time of the conditioned reflex - jumping to the vertical rod in response to an audio signal.

 Example 25. Antibodies to nefiracetam. Electrophysiological studies have shown that antibodies to nephiracetam in homeopathic dilution of C200 when 1% is added to the incubation medium facilitates the hippocampal neurotransmission of the LTP type (prolonged potentiation), which is realized through the effect on nicotinic AChR. It has been shown that the modulation of currents through nicotinic receptors by a substance occurs through 2 different signaling transdictory mechanisms: depression is caused by activation of a G-protein-regulated, cAMP-dependent protein kinase - RCA followed by phosphorylation of AChP, and a prolonged increase in ACh currents is caused by activation of calcium-dependent protein kinase C.

 Example 26. Antibodies to nefiracetam have a pronounced antiamnestic effect. A solution of antibodies in homeopathic dilution of C200 with a single injection of 0.1 ml eliminated the amnesia caused in experiments on rats by conducting the maximum electroconvulsive seizure immediately after learning the conditioned reflex of passive avoidance in the dark-light chamber test. Under the influence of antibodies, the latent time of entry into the dangerous dark chamber was increased (by 75%) and the time spent there was decreased (by 55%) compared with the control.

 Antibodies to substances that increase the amount of acetylcholine (by increasing the pool of precursors, increasing the release of acetylcholine, enhancing the synthesis of acetylcholine, enhancing choline reuptake).

 Example 27. Antibodies to substances that increase the pool of acetylcholine precursor - choline were studied using antibodies to choline, lecithin, phosphotidylcholine, gliatilin as an example. In experiments on young rats with a learning disability (under-education), the ability of antibodies to the substances indicated above to improve the ability of animals to develop a reflex in a T-shaped labyrinth with positive reinforcement (a drinker with water) was studied. Substances were administered intraperitoneally in 0.1 ml for 14 days as a solution in homeopathic dilution C200. An improvement has been established after the introduction of antibodies in the learning process and the resulting fulfillment of the conditioned reflex with the correct finding of positive reinforcement.

 Example 28. Antibodies to linopidine and T-588 - substances that cause increased release of Atsh. In experiments on young rats with a learning disability (under-education), the ability of antibodies to the substances indicated above to improve the ability of animals to develop a reflex in a T-shaped labyrinth with positive reinforcement (a drinker with water) was studied. Antibodies to linopidine were administered intraperitoneally for 14 days, 0.1 ml daily as an aqueous solution in homeopathic ultra-high dilution C200. The improvement of the reflex production process after administration of antibodies to linopidine was established, which was expressed in a faster finding of the drinker with water and a smaller (by 24%) number of errors made.

 Example 29. Antibodies to acetyl-L-carnitine and L-carnitine cause increased synthesis of acetylcholine. In vitro studies have shown the ability of antibodies to acetyl-L-carnitine in homeopathic dilution of C200 to increase acetylcholine synthesis by transferring the acetyl group from acetylcarnitine to acetylcholine in the presence of coenzyme A and the participation of synaptosomal choline acetyltransferase. In electrophysiological experiments with microionophoretic addition of a solution of antibodies to acetyl-L-carnitine in a homeopathic dilution of C200 to brain neurons, the ability of antibodies to enhance the neuronal response to acetylcholine was shown.

 Example 30. Antibodies to the ISS-231 - choline reuptake amplifier. In vitro experiments by neurochemical methods have shown the ability of antibodies to the new compound MKS-231 in homeopathic dilution of C 100 to enhance the uptake by presynaptic terminals of endogenous choline formed by the enzymatic decomposition of acetylcholine by acetyl cholinesterase. Thus, antibodies to MKS-231 are an activator of the high affinity choline uptake system, a key link in acetylcholine resynthesis.

Glutamatergic antibodies
Antibodies to endogenous glutamate receptor ligands
Example 31. Antibodies to glutamate, aspartate, glycine, D-serine, polyamines. In experiments using radioligand and neurochemical methods, it was shown that antibodies to the designated substances - endogenous ligands of the glutamate receptor in homeopathic ultra-high dilution C200 are allosteric modulators of the glutamate receptor.

Antibodies to Competitive Antagonists of NMDA Receptors
Example 32. Antibodies to selfotel. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that the oral administration of 0.1 ml of a solution of antibodies to selffotel in homeopathic dilution of C200 reduces the infarction zone and reduces damage to hippocampal cells by 30%.

 Example 33. Antibodies to D-CPP. In experiments on rats, a brain injury was simulated by mechanical compression of the frontal zone of the cortex, which caused cerebral edema and impaired central functions, in particular, impaired development of conditioned reflexes of active avoidance in a two-chamber shuttle-box installation, where a light signal was used as a conditional signal. The introduction of animals of antibodies to D-CPP in homeopathic ultra-high dilutions of C200 0.2 ml orally after a brain injury caused a decrease in the zone of cerebral edema and improved the learning process of animals in the defensive reflex, which was reflected in a decrease in the latency period of the reflex and in the decrease in the number of trainings (by 45%) needed to develop a reflex.

 Example 34. Antibodies to MDL-100453. The studies were carried out in experiments on mice that caused a convulsive seizure by subcutaneous administration of pentelentetrazole. Oral administration of 0.1 ml of a solution of antibodies to MDL-100453 in homeopathic dilution of C200 to animals before administration of a convulsive drug prevented the development of a convulsive seizure, significantly reduced the duration and severity of clonic and tonic-clonic seizures, and increased the latent time of their onset.

 Example 35. Antibodies to CGP-37849. The studies were carried out in experiments on mice that caused a convulsive seizure by subcutaneous administration of pentelentetrazole. Oral administration of 0.1 ml of a solution of antibodies to CGP-37849 in homeopathic ultra-high dilution of C200 to animals before the administration of the convulsive drug prevented the development of a convulsive seizure, significantly reduced the duration and severity of clonic and tonic-clonic seizures and increased the latent time of their onset.

 Example 36. Antibodies to CGS-19755. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that the oral administration of 0.2 ml of a solution of antibodies to CGS-19755 in homeopathic dilution C 100 reduces the infarction zone, improves the general condition of the animals, their neurological status.

 Example 37. Antibodies to SDZ-EAA-494. The studies were carried out in experiments on mice in which a convulsive seizure was caused by conducting a maximum electroconvulsive seizure through corneal electrodes. The administration of anti-SDZ-EAA-494 antibodies to animals prior to the maximum electric shock of 0.1 ml orally in homeopathic dilution of C200 prevented the development of a convulsive seizure, significantly reduced the duration and severity of tonic-clonic seizures and increased the latent time of their onset (by 25%), decreased (38%) percentage of death of animals.

 Example 38. Antibodies to LY-235959. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 75% hippocampal cell death. Oral administration of 0.2 ml of a solution of antibodies to LY-235959 in homeopathic dilution of C200 5 minutes before vascular constriction led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 40%.

Antibodies to non-competitive NMDA receptor antagonists
Example 39. Antibodies to disocilpin (MK-801). The experiments were carried out in experiments on outbred white rats under the conditions of passive avoidance technique in a dark-light chamber, when animals received painful training stimulation through the electrode floor in a dark chamber. Administration to rats intraperitoneally of 0.1 ml of a solution of antibodies to disocilpin in homeopathic dilution of C200 before the start of training caused amnesia, which was manifested in the fact that the animals, despite the received pain irritation, entered the dark dangerous compartment with a short latent period and spent there more (on 58%) of the time.

 Example 40. Antibodies to phencyclidine. The experiments were carried out in experiments on outbred white rats under the conditions of passive avoidance technique in a dark-light chamber, when animals received painful training irritation through the electrode floor in a dark chamber. Administration to rats prior to the start of oral administration of 0.1 ml of a solution of antibodies to phencyclidine in homeopathic dilution of C 100 caused amnesia, and the animals, despite the received pain irritation, entered the dark dangerous compartment with a short latent period and spent a longer period there (by 34%) ) time in comparison with control animals.

 Example 41. Antibodies to ketamine. The experiments were carried out in experiments on outbred white rats under the conditions of passive avoidance technique in a dark-light chamber, when animals received painful training irritation through the electrode floor in a dark chamber. Administration of 0.1 ml of oral antibodies to ketamine in rats with homeopathic dilution of C200 caused amnesia before rats started training, and the animals, despite the pain irritation, entered the dark dangerous compartment with a short latent period and spent there a longer period (32%) of time comparison with control animals.

 Example 42. Antibodies to memantine. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that intraperitoneal administration of 0.1 ml of a solution of antibodies to memantine in homeopathic ultra-high dilution C200 before the experiment reduces the infarction zone, improves the general condition of the animals, their neurological status.

 Example 43. Antibodies to remacemid. The studies were carried out in experiments on mice in which a convulsive seizure was caused by conducting a maximum electroconvulsive seizure through corneal electrodes. Oral administration to animals of 0.1 ml of a solution of antibodies to remacemide in homeopathic ultra-high dilution C 100 until the maximum electroshock prevented the development of a convulsive seizure, significantly reduced the duration and severity of tonic-clonic seizures and increased (by 1.4 times) the latent time of their onset, reduced (40%) death of animals.

 Example 44. Antibodies to dextromethorphan. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 80% hippocampal cell death. The intraperitoneal administration of 0.1 ml of a solution of antibodies to dextromethorphan in homeopathic ultra-high dilution of C200 before the experiment led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 50%.

 Example 45. Antibodies to CNS-1102. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that the oral administration of 0.1 ml of a solution of antibodies to CNS-1102 in homeopathic ultra-high dilution of C200 before clamping the artery reduces the infarction zone, improves the general condition of the animals, their neurological status.

 Example 46. Antibodies to CNS-1505. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 75% hippocampal cell death. The introduction of 0.1 ml of an oral solution of antibodies to CNS-1505 in homeopathic dilution of C200 led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 30%.

Antibodies to NMDA receptor channel blockers
Example 47. Antibodies to amantadine. The experiments were carried out in experiments on outbred white rats, which were injected with haloperidol and then within 4 hours the severity of extrapyramidal disorders, expressed in catalepsy, determined in points by the Morpurgo method, was determined. Oral administration of 0.1 ml of a solution of antibodies to amantadine to animals in homeopathic dilution of C200 simultaneously with haloperidol had an antiparkinsonian effect, reducing the severity of catalepsy. This effect was expressed in a decrease (by 40%) in the total number of points for evaluating extrapyramidal disorders.

 Example 48. Antibodies to budipine. The experiments were carried out in experiments on outbred white rats, which were injected with haloperidol and then within 4 hours the severity of extrapyramidal disorders, expressed in catalepsy, determined by the Morpurgo method, was determined. Administration to animals together with haloperidol orally 0.1 ml of a solution of antibodies to budipine in homeopathic ultra-high dilution of C200 had an antiparkinsonian effect, reducing the severity of catalepsy. This effect was expressed in a decrease (by 20%) in the total number of points for evaluating extrapyramidal disorders.

 Example 49. Antibodies to cerestat. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 70% hippocampal cell death. Oral administration of 0.1 ml of a solution of antibodies to cerestat in homeopathic dilution of C200 led to a neuroprotective effect, which was manifested in the restoration of hippocampal cells by 35% and improved neurological deficits and the general condition of the animals.

 Example 50. Antibodies to ARR-15896AR. The studies were carried out in experiments on mice in which a convulsive seizure was caused by conducting a maximum electroconvulsive seizure through corneal electrodes. Oral administration to animals of 0.1 ml of a solution of antibodies to ARR-15896AR in homeopathic dilution of C200 before maximum electroshock prevented the development of a convulsive seizure, significantly reduced the duration and severity of tonic-clonic seizures. An increase in the latent time of onset of seizures was observed and decreased by 30 percent death of animals.

 Example 51. Antibodies to ADCI. The studies were carried out in experiments on mice that caused a convulsive seizure by subcutaneous administration of pentelentetrazole. Oral administration of 0.1 ml of a solution of antibodies to ADCI in homeopathic dilution of C200 to animals prior to the administration of a convulsive drug prevented the development of a convulsive seizure, significantly reduced the duration and severity of clonic and tonic-clonic seizures, and increased the latent time of their onset.

 Example 52. Antibodies to WIN-63480. The experiments were carried out in experiments on outbred white rats. The animals were trained in the development of a conditioned reflex of active avoidance in a two-section shuttle-box chamber. A 7-day oral administration of 0.1 ml of a solution of anti-WIN-63480 antibodies to animals in a homeopathic dilution of C200 orally improved the reflex production process, reduced the latent periods of the reflex and the number of training sessions (by 30%) necessary to achieve the criterion for reflex production.

Antibodies to antagonists of the glycine region of the glutamate receptor
Example 53. Antibodies to D-cycloserine. The experiments were carried out in experiments on outbred white rats. The animals were trained in the development of a conditioned reflex of active avoidance in a two-section shuttle-box chamber. A 7-day oral administration of 0.1 ml of a solution of anti-D-cycloserine antibodies to animals in a homeopathic dilution of C 100 improved the reflex production process, reduced the latent periods of the reflex and the number of training sessions (by 25%) necessary to achieve the criterion for reflex production.

 Example 54. Antibodies to ACEA-1021 (lycostinel). Studies were performed on white outbred rats. We used the method of painful stimulation of the animal’s tail by thermal stimulation (lowering the tail into hot water). Administration to animals of 0.2 ml of an oral solution of anti-lycostinel antibodies in homeopathic dilution of C200 had an analgesic effect, as evidenced by a statistically significant increase (by 54%) in the thresholds of pain response.

 Example 55. Antibodies to felbamate. The studies were carried out in experiments on mice that caused a convulsive seizure by subcutaneous administration of pentelentetrazole. Oral administration of 0.1 ml of a solution of antibodies to felbamate in ultra-high dilution homeopathic C200 to animals prior to the administration of a convulsive drug prevented the development of a convulsive seizure, significantly reduced the duration and severity of clonic and tonic-clonic seizures and increased the latent time of their onset.

 Example 56. Antibodies to ZD-9379. Studies were performed on white outbred rats. We used the method of painful stimulation of the animal’s tail by thermal stimulation (lowering the tail into hot water). Oral administration of 0.1 ml of a solution of antibodies to ZD-9379 in homeopathic dilution of C200 orally to the animals had an analgesic effect, as evidenced by an increase (1.4 times) in the thresholds of pain response.

 Example 57. Antibodies to L-701252. The studies were carried out in experiments on mice in which a convulsive seizure was caused by conducting a maximum electroconvulsive seizure through corneal electrodes. Oral administration of 0.1 ml of a solution of antibodies to L-701252 in homeopathic dilution of С100 to animals prior to the maximum electroshock prevented the development of a convulsive seizure, significantly reduced the duration and severity of tonic-clonic seizures and increased the latent time of their onset, and reduced the percentage of death of animals.

 Example 58. Antibodies to L-687414. The studies were carried out in experiments on mice that caused a convulsive seizure by subcutaneous administration of pentelentetrazole. Oral administration of 0.1 ml of a solution of antibodies to L-687414 in homeopathic dilution of C200 to animals prior to the administration of a convulsive drug prevented the development of a convulsive seizure, significantly reduced the duration and severity of clonic and tonic-clonic seizures and increased the latent time of their onset.

 Example 59. Antibodies to L-704324. Studies were performed on white outbred rats. We used the method of painful stimulation of the animal’s tail by thermal stimulation (lowering the tail into hot water). Oral administration of 0.1 ml of a solution of antibodies to L-704324 in a homeopathic dilution of C200 orally had an analgesic effect, as evidenced by an increase in the thresholds for pain response.

 Example 60. Antibodies to M-244249. In an experiment on outbred white rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that the administration of 0.1 ml of a solution of antibodies to M-244249 in homeopathic dilution of C200 orally reduces the infarction zone before treatment, improves the general condition of the animals, their neurological status .

 Example 61. Antibodies to MDL-1000748. The studies were carried out in experiments on mice in which a convulsive seizure was caused by conducting a maximum electroconvulsive seizure. Oral administration of 0.2 ml of a solution of antibodies to MDL-1000748 in homeopathic dilution of C200 to animals prior to maximum electroshock prevented the development of a convulsive seizure, significantly reduced the duration and severity of tonic-clonic seizures, increased the latent time of their onset, and reduced the death of animals by 32 percent.

 Example 62. Antibodies to indole-3-pyruvate. The studies were carried out in experiments on rats using the methodology of the conflict situation, which was created by the collision of drinking and defensive reflexes. Under these conditions, animals are afraid and refuse to take water from a drinking bowl, because at the same time receive pain irritation. Oral administration of 0.2 ml of a solution of antibodies to indole-3-pyruvate in homeopathic dilution of C200 eliminates the fear in animals, which is expressed in an increase (1.3 times) in the number of punishable water intake (water intake, despite receiving pain irritation) , which indicates an anxiolytic effect.

 Example 63. Antibodies to ACRS. The studies were carried out in experiments on mice that caused a convulsive seizure by subcutaneous administration of pentelentetrazole. Oral administration of 0.2 ml of a solution of antibodies to ACRS in homeopathic dilution of C100 to animals prior to the administration of a convulsive drug prevented the development of a convulsive seizure, significantly reduced the duration and severity of clonic and tonic-clonic seizures, and increased the latent time of their onset.

Antibodies to the glutamate receptor glycine agonists
Example 64. Antibodies to milacemide. In experiments on rats, it was shown that antibodies to milacemide when administered orally had a pronounced antiamnestic effect. A single oral administration of 0.2 ml of antibody solution in homeopathic dilution of C200 eliminated amnesia caused by the maximum electroconvulsive seizure immediately after learning the conditioned reflex of passive avoidance in the dark-light chamber test. In animals, the latent time of entry into the dark chamber increased and the time spent in the dark chamber decreased.

 Example 65. Antibodies to capaxa. In experiments on rats, it was shown that antibodies to capax when administered 0.2 ml of a solution of antibodies in homeopathic dilution of C200 had a pronounced antiamnestic effect. The substance, when administered once, eliminated amnesia caused by the maximum electroconvulsive seizure immediately after learning the conditioned reflex of passive avoidance in the dark-light chamber test. In animals, the latent time of entry into the dark chamber increased (1.4 times) and the time spent in the dark chamber decreased compared to the control indices.

Antibodies to the polyamine site antagonists of the NMDA receptor complex and NMDAR2B selective antagonists
Example 66. Antibodies to Eliprodil. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 80% hippocampal cell death. Oral administration of 0.2 ml of a solution of antibodies to eliprodil in homeopathic dilution of C 100 led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 65%.

 Example 67. Antibodies to ifenprodil. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 80% hippocampal cell death. Oral administration of 0.1 ml of a solution of antibodies to ifenprodil in homeopathic ultra-high dilution of C200 led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 45%.

 Example 68. Antibodies to CP-101,606. In an experiment on outbred white rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that the administration of 0.1 ml of a solution of antibodies to CP-101,606 in homeopathic dilution of C200 orally reduces the infarction zone, improves the general condition of the animals, their neurological status.

 Example 69. Antibodies to Ro-256981. In an experiment on outbred white rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was established that the administration of 0.1 ml of a solution of antibodies to Ro-256981 in homeopathic dilution of C100 orally reduces the infarction zone, improves the general condition of the animals, their neurological status.

 Example 70. Antibodies to SL-820715. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 80% hippocampal cell death. Oral administration of 0.2 ml of a solution of antibodies to SL-820715 in homeopathic dilution of C200 led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 50%.

Antibodies to agonists, antagonists and positive modulators of AMPA receptors
Example 71. Anti-quisqualate antibodies. In hi vitro experiments using radioligant research methods, it was shown that anti-quisqualate antibodies have the properties of a non-competitive antagonist, AMPA blocker of the glutamate channel subtype in homeopathic dilution C100
Example 72. Antibodies to spermine. In vitro experiments using radioligand research methods showed that spermine antibodies possess the properties of a non-competitive antagonist, AMPA blocker of the glutamate channel subtype in homeopathic dilution of C200.

 Example 73. Antibodies to ampakines (ampalex). A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 85% hippocampal cell death. Oral administration of 0.2 ml of a solution of antibodies to ampalex in homeopathic dilution of C200 led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 60%.

 Example 74. Antibodies to AN-1792. In experiments in rats in vivo and in vitro in morphohistochemical studies, it was shown that a 10-day oral administration of 0.1 ml of a solution of antibodies to AN-1792 in homeopathic dilution of C200 stops the development of amyloid plaques in the brain tissue and reduces their size.

 Example 75. Antibodies to ZK200775. In experiments on rats, a brain injury was simulated by mechanical compression of the frontal zone of the cortex, which caused cerebral edema and impaired central functions, in particular, impaired development of conditioned reflexes of active avoidance in a two-chamber shuttle-box installation, where a light signal was used as a conditional signal. Oral administration to animals of 0.1 ml of a solution of antibodies to ZK200775 in homeopathic dilution of C200 after a brain injury caused a decrease in the area of cerebral edema and improved the learning process of animals in the defensive reflex, which was reflected in a decrease in the latency period of the reflex and in the reduction in the number of trainings necessary to develop the reflex .

 Example 76. Antibodies to LY-300164. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that the introduction of antibodies to LY-300164 The preparation of antibodies in homeopathic ultra-high dilution C200 reduces the infarction zone, improves the general condition of animals, their neurological status.

 Example 77. Antibodies to YM-872. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that the introduction of antibodies to YM-872 The preparation of antibodies in homeopathic ultra-high dilution C200 reduces the infarction zone, improves the general condition of animals, their neurological status.

 Example 78. Antibodies to LY293558. Studies were performed on white outbred rats. We used the method of painful stimulation of the animal’s tail by thermal stimulation (lowering the tail into hot water). The introduction of animals antibodies to LY293558 The preparation of antibodies in homeopathic ultra-high dilution of C200 had an analgesic effect, as evidenced by an increase (by 45%) in the thresholds of pain response.

 Example 79. Antibodies to GYKI-52466. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that the introduction of antibodies to GYKI-52466 The preparation of antibodies in homeopathic ultra-high dilution C200 reduces the infarction zone, improves the general condition of animals, their neurological status.

 Example 80. Antibodies to NBQX. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 75% hippocampal cell death. Introduction of antibodies The preparation of antibodies in homeopathic ultra-high dilution of C200 to ampalex led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 50%.

 Example 81. Antibodies to SYM-2206. The studies were carried out in experiments on mice that caused a convulsive seizure by subcutaneous administration of pentelentetrazole. Introduction of anti-SYM-2206 antibodies to animals The preparation of antibodies in the homeopathic ultra-high dilution C200 before the administration of the convulsive preparation prevented the development of a convulsive seizure, significantly reduced the duration and severity of clonic and tonic-clonic seizures, and increased the latent time of their onset by 30% compared to the control data.

 Example 82. Antibodies to SYM-2081. Studies were performed on white outbred rats. We used the method of painful stimulation of the animal’s tail by thermal stimulation (lowering the tail into hot water). Introduction to animals of antibodies to SYM-2081 The preparation of antibodies in homeopathic ultra-high dilution of C200 exerted an analgesic effect, as evidenced by an increase (1.4 times) in thresholds of pain response compared to control animals.

 Example 83. Antibodies to S-18986-1. In studies on old rats (24 months), there was a violation of the processes of learning and reproduction of information, neurological deficits were detected. The use of antibodies to S-18986-1 The preparation of antibodies in homeopathic ultra-high dilution of C200 caused an improvement in memory, learning processes and restored neurological deficits. In studies on rats, it was found that under the influence of the substance, the training of animals in the T-shaped labyrinth improved, which was expressed in a decrease in the latent periods of the reflex (by 20%) and the number of erroneous runs into the non-reinforced labyrinth sleeve during the reflex.

 Example 84. Antibodies to IDRA-21. In studies on old rats (24 months), there was a violation of the processes of learning and reproduction of information, neurological deficits were detected. The use of antibodies to IDRA-21 The preparation of antibodies in homeopathic ultra-high dilution of C200 caused an improvement in memory, learning processes and restored neurological deficits. In studies on rats, it was found that under the influence of the substance, the training of animals in the T-shaped labyrinth improved, which was expressed in a decrease in the latent periods of the reflex (by 32%) and the number of erroneous runs into the non-reinforced labyrinth sleeve during the reflex.

 Example 85. Antibodies to Aniracetam. In vitro experiments using electrophysiological methods and radioligant studies have shown the ability of aniracetam antibodies. The preparation of antibodies in homeopathic ultra-high dilution C200 induce positive modulation of the AMPA subtype of the glutamate receptor, enhance the excitatory postsynaptic potential generated by the AMPA, decrease the desensitization of the AMPA receptor, and slow down the deactivation of the AMPA receptor.

 In experiments on rats, the antiamnestic effect of aniracetam antibodies was shown. Substance with a single administration The antibody preparation in homeopathic ultra-high dilution C200 eliminated the amnesia caused by the maximum electroconvulsive seizure immediately after learning the conditioned reflex of passive avoidance in the dark-light chamber test. Under the influence of substances, the latent time of entry into the dangerous dark chamber increased (by 40%) and the time spent in the dark chamber decreased (by 30%).

GABAergic Antibodies
Antibodies to substances that enhance the function of GABA _A -ergic system
Antibodies to GABA _A receptor agonists
Example 86. Antibodies to the GABA _A receptor agonist muscimol. The experiments were carried out on outbred white male rats in which postsynaptic potentials in the cerebral cortex were studied by electrophysiological methods using intracellular microelectrodes. It has been established that antibodies to muscimol Antibody preparation in homeopathic ultra-high dilution of C200 cause an increase in the amplitude and duration of postsynaptic inhibitory potentials that occur in the cerebral cortex upon stimulation.

Example 87. Antibodies to the GABA _A receptor agonist isoguvacin. The experiments were performed on outbred white male rats, in which the postsynaltic potentials in the hippocampus were studied using electrophysiological methods using intracellular microelectrodes. Antibodies to isoguvacin The preparation of antibodies in homeopathic ultra-high dilution of C200 was found to increase the postsynaptic inhibition that occurs in the rat hippocampus upon stimulation of the septum.

Antibodies to GABA Deactivation Inhibitors
Example 88. Antibodies to a GABA deactivation inhibitor sodium valproate (depakine). The experiments were performed on outbred white male rats, in which, using the electrophysiological method, we studied the recovery cycles of the primary response that occurs in the sensorimotor cortex during peripheral stimulation. Antibodies to sodium valproate antibodies The preparation of antibodies in homeopathic ultra-high dilution of C200 enhances the depression phase of the test response in the recovery cycles of the primary response that occurs in the sensorimotor cortex during peripheral stimulation.

 Example 89. Antibodies to the inhibitor of GABA deactivation valproic acid. The experiments were performed on outbred white male rats, in which, using the electrophysiological method, we studied the recovery cycles of the primary response that occurs in the sensorimotor cortex during peripheral stimulation. Antibodies to valproic acid Antibodies in homeopathic ultra-high dilutions of C200 enhance the depression of the test response in the recovery cycles of the primary response that occurs in the sensorimotor cortex during peripheral stimulation.

Antibodies to substances that increase the content of GABA
Example 90. Antibodies to aminalon (γ-aminobutyric acid). Patient I., 55 years old, complained of impaired memory, attention, dizziness, and headache. After a course of treatment with antibodies to aminalon, the preparation of antibodies in homeopathic ultra-high dilution C200 described symptoms disappeared. It is recommended to continue treatment with a preventive purpose.

 Example 91. Antibodies to picamilon (nicotinoyl GABA). Patient K., 61 years old, complained of impaired memory, attention, dizziness, headache, general fatigue, chest pain. After a course of treatment with antibodies to picamilon The preparation of antibodies in homeopathic ultra-high dilution C200 described symptoms disappeared. It is recommended to continue treatment with a preventive purpose.

Antibodies to benzodiazepine receptor agonists
Antibodies to complete benzodiazepine receptor agonists
Example 92. Antibodies to the complete benzodiazepine receptor agonist diazepam. The experiments were carried out on outbred white male rats using the technique of a conflict situation in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. It was found that the administration of anti-diazepam antibodies to rats The preparation of antibodies in homeopathic ultra-high dilution C200 increases (by 75%) the number of water taken from the drinker, despite the receipt of pain irritation (punishable by the rat taking water), which indicates the anxiolytic effect of antibodies to the substance.

 Example 93. Antibodies to the complete benzodiazepine receptor agonist phenazepam. The experiments were carried out on outbred white male rats using the technique of a conflict situation in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. It was found that the administration of anti-phenazepam antibodies to rats The preparation of antibodies in homeopathic ultra-high dilution C200 increases (by 97%) the number of water taken from the drinker, despite the receipt of pain irritation (punishable by the rat taking water), which indicates the anxiolytic effect of antibodies to the substance.

 Example 94. Antibodies to the complete agonist of benzodiazepine clonazepam. The experiments were carried out on outbred white male mice, which were convulsed as a result of subcutaneous administration of corazole at a dose of 80 mg / kg. It was found that antibodies to clonazepam The preparation of antibodies in homeopathic ultra-high dilution of C200 significantly weaken the convulsive effect of corazole, increasing the latent period of the onset of seizures and reducing the duration of clonic seizures.

 Example 95. Antibodies to the benzodiazepine receptor agonist alprazolam. The experiments were performed on outbred white male rats under the conditions of the forced swimming technique in a vessel with freely rotating wheels, according to which rats placed in water unsuccessfully try to get out of it by rotating the wheels. It was found that the Antibody preparation in homeopathic ultra-high dilution of C200 antibodies to alprazolam increase the number of wheel revolutions and increase the correlation between the number of revolutions during the first and second 5 min of observation, showing antidepressant properties.

Antibodies to Partial Agonists of Benzodiazepine Receptors
Example 96. Antibodies to a partial agonist of benzodiazepine receptors bretazenil. The experiments were conducted under conditions of free behavior on outbred white male rats with electrodes implanted in the cerebral cortex. Convulsive discharges in an electroencephalogram were induced in rats using corazole administered at a dose of 35-40 mg / kg. It was found that the preparation of antibodies in homeopathic ultra-high dilution of C200 antibodies to bretazenil reduces the severity of convulsive manifestations in the rat electroencephalogram.

 Example 97. Antibodies to ambocarb (carbocetam). The experiments were carried out on outbred white male rats under the conditions of the technique for developing a conditioned passive avoidance reflex. To induce amnesia, the introduction of the scopolamine m-cholinergic receptor blocker before reflex production was used. It was established that antibodies to ambocarb have an antiamnestic effect. The rats of the control group remember that the usually preferred dark compartment of the chamber becomes dangerous, and do not go into it during testing, as evidenced by the long latent period of the first entry into the dark chamber and the short time spent in it. Animals treated with scopolamine on the first day of the experiment, on the contrary, enter the dark compartment with a short latent period and spend a long time in it. This indicates the formation of amnesia under the influence of scopolamine. Rats that received antibodies to ambocarb along with scopolamine The antibody preparation in homeopathic ultra-high dilution C200, like the control animals of the first group, remembered the punishment received the day before in a dark chamber. Therefore, they entered it with a long latent period and spent little time in it. This indicates activation under the influence of antibodies to ambocarb of memory consolidation impaired by scopolamine.

 Example 98. Antibodies to MDL-26479. The experiments were carried out on outbred white male rats under the conditions of the technique for developing a conditioned passive avoidance reflex. To induce amnesia, the introduction of the scopolamine m-cholinergic receptor blocker before reflex production was used. It was found that antibodies to MDL-26479 have an antiamnestic effect. The rats of the control group remember that the usually preferred dark compartment of the chamber becomes dangerous, and do not go into it during testing, as evidenced by the long latent period of the first entry into the dark chamber and the short time spent in it. Animals treated with scopolamine on the first day of the experiment, on the contrary, enter the dark compartment with a short latent period and spend a long time in it. This indicates the formation of amnesia under the influence of scopolamine. Rats that received anti-MDL-26479 antibodies along with scopolamine The antibody preparation in homeopathic ultra-high dilution C200, like control animals of the first group, remembered the punishment received the day before in a dark chamber. Therefore, they entered it with a long latent period and spent little time in it. This indicates activation under the influence of antibodies to MDL-26479 of memory consolidation impaired by scopolamine.

Antibodies to reverse (inverse) benzodiazepine receptor agonists
Example 99. Antibodies to the partial inverse agonist of benzodiazepine receptors RO 15-4513. The experiments were carried out under conditions of free behavior on outbred white male mice, which developed an operant skill, which was subsequently destroyed by ethanol. It was found that antibodies to RO 15-4513 The preparation of antibodies in homeopathic ultra-high dilution C200 stop the negative effect of ethanol in relation to operant behavior.

 Example 100. Antibodies to the inverse agonist of benzodiazepine receptors FG-7142 (β-carboline carboxamide). Experiments in conditions of free behavior were performed on outbred white male rats, in which the release of dopamine in the prefrontal cortex was determined by microdialysis. It was established that the Antibody preparation in homeopathic ultra-high dilution of C200 antibodies to FG-7142 increase the release of dopamine in the rat prefrontal cortex, exhibiting anxiogenic properties.

 Example 101. Antibodies to CGS-8216. The experiments were carried out on outbred white male rats using the technique of a conflict situation in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. It was found that the administration of anti-CGS-8216 antibodies to rats The preparation of antibodies in homeopathic ultra-high dilution C200 reduces (by 35%) the number of water taken from the drinker, despite receiving pain irritation (punishable by the rat taking water), which indicates the anxiogenic effect of antibodies to substance.

 Example 102. Antibodies to β-CCE. The experiments were carried out on outbred white male rats under the conditions of the technique for developing a conditioned passive avoidance reflex. It was found that antibodies to β-CCE improve memory processes. Rats in the control group remember that the usually preferred dark compartment has become dangerous. For this reason, they enter it with a high latency period and spend little time in it. Antibody preparation in homeopathic ultra-high dilution of C200 Antibodies to β-CCE further increase the latency period of the first entry into the dark chamber and shorten the time spent in it. Therefore, they stimulate the processes of memorization.

 Example 103. Antibodies to β-CCM. The experiments were carried out on outbred white male rats under the conditions of the methodology for developing a conditioned reflex of active avoidance, according to which the animals were trained for 5 days in a shuttle chamber, separated by a partition with a hole in the middle. Sound (10 s) served as a conditioned stimulus, and a current (10 s), which was alternately applied to different halves of the chamber 5 s after the start of the conditioned stimulus, served as an unconditioned stimulus; the intersignal period was 40 s. The rat, located in one of the compartments, had to move to another compartment by a conditional signal. Otherwise, she received punishment through sex. It was found that antibodies to β-CCM Antibody preparation in homeopathic ultra-high dilution C200 improves training in the shuttle chamber, accelerating the development of the skill.

Antibodies to benzodiazepine receptor antagonists
Example 104. Antibodies to the central benzodiazepine receptor antagonist flumazenil (RO 15-1788). The experiments were performed on outbred white male rats under the conditions of a conflict situation technique. According to this technique, direct agonists of benzodiazepine receptors (diazepam, phenazepam, etc.) increase the number of punished water takes. It was established that antibodies to flumazenil The preparation of antibodies in homeopathic ultra-high dilution of C200 blocks the anti-conflict effect of the direct agonist of the benzodiazepine diazepam receptors, exhibiting the properties of an antagonist to benzodiazepine receptors.

 Example 105. Antibodies to the central benzodiazepine receptor antagonist ZK-91296. The experiments were performed on outbred white male rats under the conditions of a conflict situation technique. According to this technique, direct agonists of benzodiazepine receptors (diazepam, phenazepam, etc.) increase the number of punishable water takes. It was found that antibodies to ZK-91296 The preparation of antibodies in homeopathic ultra-high dilution of C200 blocks the anti-conflict effect of the direct agonist of the benzodiazepine diazepam receptors, exhibiting the properties of an antagonist to benzodiazepine receptors.

 Example 106. Antibodies to the central benzodiazepine receptor antagonist harman. The experiments were performed on outbred white male rats under the conditions of a conflict situation technique. According to this technique, direct agonists of benzodiazepine receptors (diazepam, phenazepam, etc.) increase the number of punishable water takes. It was found that antibodies to harman in homeopathic dilution of C200, when 0.1 ml is administered, orally block the anti-conflict effect of the direct agonist of the benzodiazepine diazepam receptors, exhibiting the properties of an antagonist to benzodiazepine receptors.

 Example 107. Antibodies to the central benzodiazepine receptor antagonist β-CCP. The experiments were performed on outbred white male rats under the conditions of a conflict situation technique. According to this technique, direct agonists of benzodiazepine receptors (diazepam, phenazepam, etc.) increase the number of punishable water takes. It was found that antibodies to β-CCP Antibody drug in homeopathic ultra-high dilutions of C200, when administered in 0.1 ml, orally block the anti-conflict effect of the direct agonist of the benzodiazepine diazepam receptors, exhibiting the properties of an antagonist to benzodiazepine receptors.

Antibodies to substances that weaken the function of GABA _A -ergic system
Antibodies to GABA _A Receptor Antagonists
Example 108. Antibodies to the GABA _A receptor antagonist bicucullin. The experiments were performed on outbred white male mice. It was found that antibodies to bicucullin when administered systemically with 0.1 ml of an oral solution of antibodies in homeopathic ultra-high dilution of C200 each cause convulsions.

Antibodies to GABA _A receptor chlorine channel blockers
Example 109. Antibodies to the chlorine channel blocker GABA _A receptor picrotoxin. The experiments were performed on outbred white male rats, in which postsynaptic potentials in the cerebral cortex were studied using the electrophysiological method using intracellular microelectrodes. It was found that antibodies to picrotoxin when administered 0.1 ml orally in homeopathic dilution of C200 reduce the amplitude and duration of inhibitory postsynaptic potentials that occur in the cerebral cortex of rats during peripheral stimulation.

Antibodies to GABA Synthesis Inhibitors
Example 110. Antibodies to the inhibitor of the synthesis of GABA thiosemicarbazide. The experiments were performed on outbred white male mice. It was found that antibodies to thiosemicarbazide in homeopathic ultra-high dilutions of C200 cause seizures in white mice when administered 0.1 ml orally.

 Example 111. Antibodies to the inhibitor of the synthesis of GABA 4-deoxypyridoxine. The experiments were carried out on outbred white male rats, in which under general anesthesia holes were drilled in the skull above the sensorimotor cortex. It was established that the preparation of antibodies in homeopathic dilution of C200 causes seizures with local application of 0.1 ml per rat cerebral cortex.

 Example 112. Antibodies to an inhibitor of the synthesis of GABA isoniazid. The experiments were performed on outbred white male rats, which under general anesthesia were cannulated stereotactically into the hippocampus. It was found that antibodies to isoniazid in homeopathic dilution of C200 cause seizures when 0.1 ml of rats are introduced into the hippocampus.

Antibodies to substances that enhance the function of GABA _B- ergic system
Antibodies to GABA _B receptor agonists
Example 113. Antibodies to the GABA _B receptor agonist baclofen. The experiments were conducted under conditions of free behavior on outbred white male rats with electrodes implanted in the hippocampus. Using the electrophysiological method, it was found that antibodies to baclofen in homeopathic ultra-high dilutions of C200 cause a decrease in the frequency of rhythmic electroactivity of the hippocampus after administration of 0.1 ml orally.

Example 114. Antibodies to the GABA _B Phenibut Receptor Agonist. The experiments were carried out on outbred white male rats using the technique of a conflict situation in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. It was found that administration of 0.1 ml ml of oral anti-phenibut rats in homeopathic ultra-high dilutions of C200 orally increases (by 35%) the number of water taken from the drinker, despite receiving pain irritation (punishable by rat water taking), which indicates an anxiolytic effect antibodies to the substance.

 Example 115. Antibodies to phenotropyl. The experiments were carried out on outbred white male rats under the conditions of the technique for developing a conditioned passive avoidance reflex. It was found that the preparation of antibodies in homeopathic ultra-high dilution of C200 improves memory processes. Rats in the control group remember that the usually preferred dark compartment has become dangerous. For this reason, they enter it with a high latency period and spend little time in it. Antibodies to phenotropil when administered 0.1 ml orally increase the latency period of the first entry into the dark chamber and shorten the time spent in it. Therefore, they stimulate the processes of memorization.

Antibodies to substances that weaken the function of GABA _B- ergic system
Antibodies to GABA _B receptor blockers
Example 116. Antibodies to the GABA _B receptor blocker baclofen. The experiments were performed on isolated synaptosomes of the rat cerebral cortex using neurochemical methods in which the release of somatostatin was inhibited by the GABA _B receptor agonist baclofen. It was found that antibodies to baclofen when introduced into the incubation medium until the final dilution of C200 eliminate the inhibitory effect of baclofen on the release of somatostatin in rat synaptosomes of the cerebral cortex.

Example 117. Antibodies to the GABA _B receptor blocker baclofen. The experiments were performed on outbred white male rats, in which, using the electrophysiological method, intracellular electrodes were used to study the characteristics of inhibitory postsynaptic potentials arising in the rat cortex with various types of stimulation. It was found that when 0.1 ml of the anti-baclofen antibody is administered orally in homeopathic ultra-high dilution C200, the amplitude of slow inhibitory postsynaptic potentials resulting from stimulation is reduced.

Example 118. Antibodies to the blocker of GABA _B receptors of δ-amino-N-valeric acid. The experiments were carried out on hippocampal preparations extracted from the brain and placed in a nutrient solution. Using intracellular microelectrodes, they studied the characteristics of inhibitory postsynaptic potentials that arise in the hippocampus upon stimulation of afferents. It was found that antibodies to δ-amino-N-valeric acid, introduced into the incubation medium in a homeopathic dilution of C200, block the slow inhibitory postsynaptic potentials of the hippocampus.

Antibodies to dopaminergic substances
Antibodies to Dopamine Receptor Antagonists
Antibodies to antagonists of dopamine receptors type D ₂
Example 119. Antibodies to the dopamine receptor antagonist type D2 chlorpromazine. The experiments were performed on outbred white male rats using the methodology for evaluating its cataleptogenic effect. At the same time, the ability of antibodies to chlorpromazine to rats to immobility in uncomfortable positions was evaluated. The severity of the effect was evaluated on a 4-point scale. It was found that when 0.1 ml of the anti-chlorpromazine antibody is administered orally, homeopathic dilution of C200 causes catalepsy close to maximum (3 points out of 4).

 Example 120. Antibodies to chlorpromazine. The experiments were performed on outbred white male rats using the method of recording motor activity in an Opto Varimex actometer (USA). Rats in groups of 5 were placed in the chamber of the device and their activity was recorded for 5 min. It was found that antibodies to chlorpromazine have a sedative effect when administered orally at 0.2 ml in a homeopathic dilution of C200, significantly (35-50%) reducing the number of movements of animals along the chamber of the device.

Example 121. Antibodies to a selective dopamine receptor antagonist type D ₂ haloperidol. The experiments were performed on outbred white male rats using the methodology for evaluating its cataleptogenic effect. In this case, the ability of antibodies to haloperidol to cause rats to be immobilized in uncomfortable positions was evaluated. The severity of the effect was evaluated on a 4-point scale. It was found that antibodies to haloperidol cause maximum catalepsy (4 points out of 4) with the introduction of 0.1 ml of an oral solution in homeopathic dilution of C400.

 Example 122. Antibodies to haloperidol. The experiments were performed on outbred white male rats using the method of recording motor activity in an Opto Varimex actometer (USA). Rats in groups of 5 were placed in the chamber of the device and their activity was recorded for 5 min. It was found that antibodies to haloperidol when administered 0.1 ml orally in the form of a solution in homeopathic dilution of C400 have a pronounced sedative effect, significantly (by 45-65%) reducing the number of movements of animals along the chamber of the device.

Antibodies to antagonists of dopamine receptors type D ₃
Example 123. Antibodies to the highly effective antagonist of dopamine receptors of types D ₃ nafadotride. The experiments were performed on outbred white male rats, which were stereotyped using the dopamine agonist apomorphine, administered at a dose of 0.3-1 mg / kg (subcutaneously). It was found that antibodies to nafadotride when administered 0.1 ml orally in the form of a solution in homeopathic dilution of C400 inhibit the stereotype caused by apomorphine.

Antibodies to dopamine receptor antagonists of type D ₂ -D ₄
Example 124. Antibodies to the highly effective dopamine receptor antagonist types D ₂ -D ₄ nemonapride. The experiments were performed on outbred white male rats, which were stereotyped using the dopamine agonist apomorphine, administered at a dose of 0.3-1 mg / kg (subcutaneously). It was found that antibodies to nemonapride inhibit by 37% the stereotype caused by apomorphine when administered 0.1 ml orally in the form of a solution in homeopathic dilution of C400.

Example 125. Antibodies to the highly effective dopamine receptor antagonist types D ₂ -D ₄ racloprid. The experiments were performed on outbred white male rats, which were stereotyped using the dopamine agonist apomorphine, administered at a dose of 0.3-1 mg / kg (subcutaneously). It was found that antibodies to racloprid when administered 0.1 ml orally as a solution in homeopathic dilution of C400 inhibit 49% stereotype caused by apomorphine.

Example 126. Antibodies to the highly effective dopamine receptor antagonist types D ₂ -D ₄ spiperone. The experiments were carried out using the radioligand binding technique. It was found that antibodies to spiperone in homeopathic dilution of C200 intensively (K _i <0.5 nmol) displace labeled dopamine from the binding sites located in striatum.

Example 127. Antibodies to the antagonist of dopamine receptors of types D ₂ -D ₄ (-) - sulpiride. The experiments were carried out using the radioligand binding technique. It was found that antibodies to (-) - sulpiride in homeopathic dilution of C400 displace labeled ligands, preventing their binding to receptors in n.striatum ventralis.

Antibodies to dopamine receptor antagonists of type D ₂ -D ₄
Example 128. Antibodies to the dopamine receptor antagonist types D ₁ and D ₅ SCH23390. The experiments were carried out using the radioligand binding technique. It was found that antibodies to SCH23390 displace labeled dopamine from the receptors it occupies in the dorsal striatum, as indicated by a decrease in the radioactivity of the drug in the presence of an antibody solution in homeopathic dilution of C400.

Antibodies to dopamine receptor agonists
Antibodies to dopamine receptor agonists type D ₂ -D ₄
Example 129. Antibodies to the dopamine receptor agonist type D ₂ -D ₄ apomorphine. Patient B. 45 years old has been suffering from Parkinsonism for 15 years. Marked increased stiffness of the hands, twitching of the head, impaired mental activity. Traditional methods of treatment are ineffective. Antibodies to apomorphine reduced the severity of symptoms and led to remission when taking 1 ml orally in the form of a solution in homeopathic dilution of C400 1 time per day for 7 days.

Antibodies to dopamine receptor agonists type D ₂ -D ₃
Example 130. Antibodies to the dopamine receptor agonist types D ₂ -D ₃ bromocriptine. Patient K., 52 years old, has been suffering from Parkinsonism for 8 years. Complaints of increased stiffness of the extremities, tremor of the head and hands, impaired mental activity and emotional sphere. Traditional methods of treatment failed. Antibodies to bromocriptine led to a reduction in symptoms when taking 1 ml orally in the form of a solution in homeopathic dilution of C400 1 time per day for 7 days.

Example 131. Antibodies to the dopamine receptor agonist type D ₃ 7-OH-DPAT (7-hydroxydipropylaminotetralin). The experiments were carried out using the radioligand binding technique. It was found that antibodies to 7-OH-DPAT in homeopathic dilution of C400 displace the labeled ligand [ ³ H] 7-OH-DPAT, preventing its binding to receptors in n.striatum ventralis.

Antibodies to dopamine receptor agonists type D ₃ -D ₄
Example 132. Antibodies to a moderate dopamine receptor agonist type D ₃ -D ₄ quinpirol. The experiments were carried out using the radioligand binding technique. It was found that antibodies to quinpirol displace the labeled ligand [ ³ H] NGD941, preventing its binding to recombinant receptors in homeopathic dilution of C200.

Antibodies to dopamine receptor agonists type D ₁ -D ₅
Example 133. Antibodies to a selective dopamine receptor agonist type D ₁ , D ₅ SKF 38393. The experiments were carried out using the radioligand binding technique. It was found that antibodies to SKF 38393 in homeopathic dilution of C400 displace the labeled [ ³ H] SCH23390 ligand in an experiment on rat brain homogenate, preventing its binding to recombinant receptors.

Antibodies to Dopamine Precursors
Example 134. Antibodies to the dopamine precursor L-DOPA. Patient I. 39 years old has been suffering from Parkinsonism for 12 years. Severe tremors of the head and hands, disorders of the emotional sphere and mental activity. Traditional treatments have not led to improvement. Antibodies to L-DOPA led to a relief of the patient's condition when taking 1 ml orally in the form of a solution in homeopathic dilution of C400 1 time per day for 7 days.

Antibodies to serotonergic substances
Antibodies to serotonergic receptor agonists
Antibodies to serotonin receptor agonists type 5-HT _1a
Example 135. Antibodies to the 5-HT _1a agonist of serotonergic receptors buspiron. The experiments were carried out on outbred white male rats using the technique of a conflict situation in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. It was found that administering 0.1 ml of the anti-buspirone antibody to rats orally in the form of a solution in homeopathic dilution of C400 once a day for 3 days increases (by 40%) the number of water taken from the drinker, despite receiving pain irritation (punishable taking rats water), which indicates the anxiolytic effect of antibodies to the substance.

Example 136. Antibodies to the 5HT _1a agonist of serotonergic receptors ipsapiron. The experiments were carried out on outbred white male rats using the technique of a conflict situation in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. It was found that administering 0.1 ml of the anti-ipsapiron antibody to rats orally in the form of a solution in homeopathic dilution of C400 1 time per day for 2 days increases (by 42%) the number of water taken from the drinker, despite receiving pain irritation (punishable taking rats water), which indicates the anxiolytic effect of antibodies to the substance.

Example 137. Antibodies to the 5HT _1a agonist of the serotonergic receptors 8-OH-DPAT (8-hydroxy-2- (di-n-propyl-amino) tetralin). The experiments were performed on outbred white male rats using the forced swimming technique in a vessel with freely rotating wheels. In accordance with the methodology of the rat, after placing them in a vessel with water, they unsuccessfully try to get out of it by rotating the wheels. The number of revolutions is a measure of the antidepressant effect of a substance. It was found that antibodies to 8-OH-DPAT with a single dose of 0.1 ml orally in the form of a solution in homeopathic dilution of C400 increase (by 25%) the number of wheel revolutions, exerting an antidepressant effect.

Antibodies to agonists of serotonin receptors type 5HT _1b ,
Example 138. Antibodies to the 5HT _1b agonist of serotonergic receptors sumatriptan. The experiments were carried out using the radioligand binding technique. It was found that antibodies to sumatriptan in the form of a solution in homeopathic dilution of C400 displace the labeled ligand ([ ³ H] serotonin), preventing its binding to receptors in the basal ganglia of rats, reducing the radioactivity of the label.

Antibodies to agonists of serotonin receptors of type 5HT _1d
Example 139. Antibodies to the 5HT _1d serotonergic receptor agonist cyanopindolol. The experiments were carried out using the method for determining the release of labeled serotonin mediator. It was found that antibodies to cyanopindolol inhibit the release of labeled serotonin from the nerve terminals of the guinea pig cortex when a solution is introduced into the incubation medium in homeopathic dilution of C400.

Example 140. Antibodies to the 5HT _1d serotonergic receptor agonist metergoline. Using neurochemical methods, experiments were carried out to determine the activity of adenylyl cyclase in homogenates of substantia nigra guinea pig. It was established that antibodies to metergoline in homeopathic dilution of C200 cause inhibition of adenylyl cyclase activity in substantia nigra homogenates.

Antibodies to agonists of serotonin receptors type 5HT _2a
Example 141. Antibodies to the 5HT _2a agonist of serotonergic α-methyl-5-hydroxytryptamine receptors. The experiments were performed on isolated sections of the cortex of the cerebral hemispheres using electrophysiological methods. It was found that antibodies to α-methyl-5-hydroxytryptamine cause excitation of pyramidal cells of the cortex in the homeopathic dilution of C400.

Antibodies to agonists of serotonin receptors type 5HT _2c
Example 142. Antibodies to the 5HT _2c agonist of serotonergic receptors bufotenin. The experiments were performed on outbred white male rats, in which, when observed in pairs for 5 min, the number and duration of active agonistic contacts were recorded. It was found that antibodies to bufotenin inhibit zoosocial interactions when 0.1 ml is administered orally in the form of a solution in homeopathic dilution of C400 1 time per day for 7 days, which manifests itself in a decrease in the number (1.3 times) and duration (by 25 %) active contacts between animals.

Antibodies to agonists of serotonin receptors type 5HT ₃
Example 143. Antibodies to the 5HT ₃ serotonergic receptor agonist phenylbiguanide. The experiments were performed on outbred white male rats under the conditions of the conflict method, in which substances with the anxiolytic component of the action cause an increase in the number of punishable water take. It was found that antibodies to phenylbiguanide cause a decrease in the number of punishable water intake by rats when 0.2 ml is administered orally in the form of a solution in homeopathic dilution of C200. Thus, they have a pro-conflict effect, characteristic for the activation of 5HT ₃ receptors.

Antibodies to Serotonergic Receptor Antagonists
Antibodies to serotonin receptor antagonists type 5HT _1a
Example 144. Antibodies to the 5HT _1a antagonist of serotonergic receptors spiperone. The experiments were carried out using the radioligand binding technique. It was established that antibodies to spiperone in homeopathic dilution of C200 displace the labeled ligand ([ ³ H] 8-OH-DPAT), preventing its binding to receptors in the hippocampal homogenates.

Antibodies to antagonists of serotonin receptors type 5HT _1b
Example 145. Antibodies to the 5HT _1b antagonist of serotonergic receptors mianserin. Using neurochemical methods, experiments were carried out to determine the effect of a substance on the activity of adenylyl cyclase in the homogenates of rat substantia nigra. It was found that antibodies to mianserin in homeopathic dilution of C200 cause a significant activation of this enzyme by 20%.

Antibodies to antagonists of serotonin receptors of type 5HT _1d
Example 146. Antibodies to the 5HT _1d antagonist of serotonergic receptors GR 127935 (N- [methoxy-3- (4-methyl-1-piperazinyl) phenyl] -2'-methyl-4 '- (5-methyl-1,2,4 -oxadiazol-3-yl) [1,1-biphenyl] -4-carboxamide). The experiments were carried out using the radioligand binding technique. It was found that antibodies to GR 127935 in homeopathic dilution of C 100 displace the labeled ligand ([ ³ H] sumatripan), preventing its binding to receptors in sections of the guinea pig cortex.

Antibodies to antagonists of serotonin receptors of type 5HT _2a
Example 147. Antibodies to the 5HT _2a antagonist of serotonergic receptors ketanserin. The experiments were carried out on outbred white male rats using the technique of a conflict situation in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. It was found that administering 0.1 ml of an antibody to ketanserin to rats orally in the form of a solution in homeopathic dilution of C400 1 time per day for 3 days increases (by 38%) the number of water taken from the drinker, despite receiving pain irritation (punishable taking rats water), which indicates the anxiolytic effect of antibodies to the substance.

Antibodies to antagonists of serotonin receptors of type 5HT _2b
Example 148. Antibodies to the 5HT _2b antagonist of serotonergic receptors SB 204741. The experiments were performed on preparations of an isolated rat stomach. It was found that antibodies to SB 204741, when a 1% solution in the homeopathic dilution of C400 is introduced into the incubation shade, eliminates drug contractions.

Antibodies to agonists of serotonin receptors type 5HT _2c
Example 149. Antibodies to the 5HT _2c antagonist of serotonergic receptors cyproheptadine. The experiments were performed on outbred white male rats in which spontaneous locomotor activity was recorded using an Opto Varimex actometer (USA). It was established that antibodies to cyproheptadine when administered orally in 0.1 ml orally in the form of a solution in homeopathic dilution of C400 1 time per day for 7 days increase (by 30%) motor activity, reduced after administration of the 5HT _2c agonist MK 212 receptors (6 -chloro-2- (1-piperazinyl) pyrazine).

Antibodies to agonists of serotonin receptors of type 5HT ₃
Example 150. Antibodies to the 5HT ₃ antagonist _of serotonergic ondansetron receptors. The experiments were carried out on outbred white male rats using the technique of a conflict situation in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. It was found that administering 0.1 ml of anti-ondansetron antibodies to rats orally in the form of a solution in homeopathic dilution of C400 1 time per day for 4 days increases (by 51%) the number of water taken from the drinker, despite receiving pain irritation (punishable taking rats water), which indicates the anxiolytic effect of antibodies to the substance.

Antibodies to adrenergic substances
Antibodies to adrenergic receptor agonists
Antibodies to α ₁ -adrenergic receptor agonists
Example 151. Antibodies to the agonist of α _1A- adrenergic receptors oxymetazoline. The experiments were performed on preparations of an isolated rat vas deferens. It has been established that antibodies to oxymetazoline enhance rat contraction of the vas deferens when their solution is introduced into the incubation medium in homeopathic dilution of C200.

Example 152. Antibodies to the agonist of α _1A- adrenergic receptors A61603. The experiments were performed on preparations of isolated rat renal artery segments. It was established that antibodies to A61603 enhance the contraction of isolated segments of the rat renal artery when they are introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200.

Example 153. Antibodies to the α _1B -adrenoreceptor agonist norepinephrine. The experiments were performed on preparations of an isolated rat spleen. It was found that the introduction into the incubation medium of a 5% solution of anti-norepinephrine antibodies in homeopathic dilution of C400 enhances the contraction of the isolated rat spleen.

Example 154. Antibodies to the α _1D -adrenoreceptor agonist phenylephrine. The experiments were performed on preparations of isolated rat aortic segments. It was found that antibodies to phenylephrine enhance the contraction of isolated rat aortic segments when a 1% solution in homeopathic dilution of C200 is introduced into the incubation medium.

Antibodies to α ₂ -adrenergic receptor agonists
Example 155. Antibodies to the α _2A -adrenoreceptor agonist α-methyl-radrenaline. The experiment was performed on preparations of an isolated rabbit vas deferens. It was found that antibodies to α-methyl-radrenaline increase the contraction of the isolated vas deferens of the rabbit by adding their 5% solution to the incubation medium in homeopathic dilution C200.

Example 156. Antibodies to the agonist of α _2A- adrenergic receptors, quantafacin. In experiments on HT29 cell culture using neurochemical methods, the effect of antibodies to quantfacin on adenylate cyclase activity was studied. It was found that antibodies to quantafacin in homeopathic dilution of C200 inhibit the activity of adenylate cyclase in HT29 cell culture by 20%.

Example 157. Antibodies to the agonist of α _2A- adrenergic receptors dexmedetomidine. The experiments were performed on isolated v. saphenous, extracted from the body and placed in a nutrient solution. It was found that antibodies to dexmethedine in homeopathic dilution of C200 enhance the contraction of isolated v segments. saphenous dogs by 30%.

Example 158. Antibodies to the agonist of α _2B- adrenergic receptors clonidine. Experiments were conducted to study the effect of antibodies on adenylate cyclase activity in NG 108 cell culture using neurochemical methods. It was found that antibodies to clonidine in homeopathic dilution of C200 cause inhibition of adenylate cyclase activity in the culture of NG 108 cell line by 30%.

Example 159. Antibodies to the α _2C -adrenoreceptor agonist α-methyl radrenrenaline. The experiments were conducted on isolated tissue samples of human kidneys placed in a nutrient medium. Using neurochemical methods, it was found that antibodies to α-methyl-radrenrenaline in homeopathic dilution of C200 cause inhibition of the release of mediators in human kidney preparations.

Example 160. Antibodies to the α _2C -adrenoreceptor agonist dexmethomidine. Experiments to determine the activity of adenylate cyclase using neurochemical methods were carried out on a culture of isolated cells of the Y79 line. It was found that antibodies to dexmethomidine in homeopathic dilution of C200 cause inhibition of adenylate cyclase activity in Y79 cell line cultures.

Antibodies to β-adrenergic receptor agonists
Example 161. Antibodies to the β ₁ -adrenoreceptor agonist denopamine. The experiments were carried out using the method of recording contractions of the isolated atrium of guinea pig. It was found that antibodies to denopamine increase the reduction in the isolated atrial of guinea pig in homeopathic dilution of C200 by 40%.

Example 162. Antibodies to the β ₁ -adrenoreceptor agonist xamoterol. The experiments were carried out using the method of registration of contractions of the isolated atrium of a rat. It was found that antibodies to xamoterol in homeopathic dilution of C200 increase the frequency of contractions of the isolated rat atrium by 20%.

Example 163. Antibodies to β ₂ -adrenoreceptor agonist salmeterol. The experiments were carried out using the method of recording contractions of isolated segments of the guinea pig trachea placed in a nutrient medium. It was established that antibodies to salmeterol in homeopathic dilution of C200 cause relaxation of the isolated guinea pig trachea.

Example 164. Antibodies to the β ₂ -adrenoreceptor agonist salbutamol. The experiments were carried out using the method of registration of contractions of an isolated rat ureter placed in a nutrient medium. It was found that antibodies to salbutamol cause relaxation of the isolated rat ureter in homeopathic dilution of C100.

Example 165. Antibodies to β ₃ -adrenoreceptor agonist BRL 37344. The experiments were carried out using the method of registering the rate of lipolysis in rat adipose tissue. It was found that antibodies to BRL 37344, administered orally at 0.1 ml in a homeopathic dilution of C200, cause after 30 minutes an increase in lipolysis in rat adipose tissue.

Example 166. Antibodies to the β ₃ -adrenoreceptor agonist CGP 12177. The experiments were carried out using the method of registration of motility of rat large intestine segments, isolated from the body and placed in a nutrient medium. It was found that antibodies to CGP 12177 in homeopathic dilution of C200 cause relaxation of isolated segments of the rat large intestine.

Example 167. Antibodies to the β ₃ -adrenoreceptor agonist CL 316243. The experiments were carried out using the radioligand binding technique. It was found that antibodies to CL 316243 in homeopathic dilution of C200 displace the labeled [ ³ H] -dihydroalprenolol ligand in rat brown adipose tissue receptors from receptors, reducing label radioactivity by 30%.

Example 168. Antibodies to the β ₄ -adrenoreceptor agonist iodocyanopindolol. The experiments were carried out on outbred white male rats, in which the heart rate was recorded. It was established that antibodies to iodocyanopindolol when administered orally at 0.2 ml in homeopathic dilution of C200 cause an increase in heart rate in rats by 10% after 10 minutes.

Antibodies to Adrenergic Receptor Antagonists
Antibodies to α ₁ -adrenergic receptor antagonists
Example 169. Antibodies to the antagonist of α _1A -adrenergic receptors (+) - nigaldipine. The experiments were carried out using the registration technique of the contractions of the vas deferens of a rat isolated from the body and placed in a nutrient medium. It was found that a 5% solution of antibodies to nigaldepine in homeopathic dilution of C200 prevents the contractions of an isolated rat vas deferens.

Example 170. Antibodies to the α _1A -adrenoreceptor antagonist of (5) -methyluradipil. The experiments were carried out using the technique of recording contractions of rat tail caudal segments isolated from the body and placed in a nutrient medium. It was established that antibodies to methyluradipil in homeopathic dilution of C200 block the contraction of isolated segments of the rat tail artery.

Example 171. Antibodies to the antagonist of α _1B- adrenergic receptors of chloroethylclonidine. The experiments were carried out using a technique for registering rat spleen contractions isolated from the body and placed in a nutrient medium. Antibodies to chloroethylclonidine have been found to inhibit the contraction of an isolated rat spleen in homeopathic dilution of C400 after 5 minutes of incubation.

Example 172. Antibodies to the antagonist of α _1D- adrenergic receptors BMY7378. The experiments were carried out using the technique of recording contractions of rat aortic segments isolated from the body and placed in a nutrient
Wednesday It was found that antibodies to BMY7378 in homeopathic dilution of C200 prevent contractions of isolated rat aortic segments.

Example 173. Antibodies to the α _1D -adrenoreceptor antagonist SKF105854. The experiments were carried out using the radioligand binding technique. It was found that antibodies to SKF105854 in homeopathic dilution of C200 displace the labeled [ ³ H] -prazosin ligand from receptors in the rat aorta, reducing the radioactivity of the drug by 20%.

Antibodies to α ₂ -adrenergic receptor antagonists
Example 174. Antibodies to the α _2A -adrenoreceptor antagonist BRL 44408. The experiments were carried out using the method of registration of contractions of the vas deferens of a rabbit isolated from the body and placed in a nutrient medium. It was found that antibodies to BRL 44408 prevent contractions of an isolated rabbit vas deferens in homeopathic dilution of C200.

Example 175. Antibodies to the antagonist of α _2A- adrenergic receptors BRL 48962. The experiments were carried out using methods for recording contractions of the atria of guinea pigs, isolated from the body and placed in a nutrient medium. It was found that antibodies to BRL 48962 in homeopathic dilution of C200 inhibit the reduction of isolated guinea pig atrium by 30%.

Example 176. Antibodies to the α _2B -adrenoreceptor antagonist imiloxane. The experiments were carried out using neurochemical methods on a culture of cells of the NG 108 line, in which the activity of adenylate cyclase was suppressed as a result of the administration of a clonidine adrenergic agonist. It was established that antibodies to imiloxane introduced into the incubation medium in homeopathic dilution of C200 stop the inhibition of adenylate cyclase activity caused by the adrenoreceptor agonist clonidine in the cell culture of the NG 108 line.

Example 177. Antibodies to the α _2C- adrenoreceptor antagonist rauwolfscin. The experiments were carried out using the radioligand binding technique in Hep-G2 cell culture. It was found that antibodies to Rauwolfscin in homeopathic dilution of C200 displace the labeled ligand [ ¹²⁵ I] iodoclonidine from receptors in the Hep-G2 cell culture by 40%.

Antibodies to β ₁ -adrenergic receptor antagonists
Example 178. Antibodies to the β ₁ -adrenoreceptor antagonist atenolol. The experiments were carried out using a technique for recording atrial contractions of a guinea pig, isolated from the body and placed in a nutrient medium. It was found that antibodies to atenolol in homeopathic dilution of C200 reduce the frequency of contractions of the isolated atrium of guinea pig by 30%.

Example 179. Antibodies to the β ₁ -adrenoreceptor antagonist bisoprolol. The experiments were carried out using the radioligand binding technique. It was found that antibodies to bisoprolol in homeopathic dilution of C200 displace the labeled ligand [ ¹²⁵ I] -iodocyanopindolol from receptors in the rat ventricle.

Example 180. Antibodies to the β ₁ -adrenoreceptor antagonist praktolol. The experiments were carried out using the method of recording atrial contractions of a rat isolated from the body and placed in a nutrient medium. It was found that antibodies to praktolol in homeopathic dilution of C200 reduce the frequency of contractions of the isolated rat atrium by 40%.

Antibodies to β ₂ -adrenergic receptor antagonists
Example 181. Antibodies to the β ₂ -adrenoreceptor antagonist ICI 118551. The experiments were carried out using the method of recording stress segments of the guinea pig trachea, isolated from the body and placed in a nutrient medium. It was found that antibodies to ICI 118551 prevent the relaxation of isolated segments of the guinea pig trachea in homeopathic dilution of C200.

Antibodies to β ₃ -adrenergic receptor antagonists
Example 182. Antibodies to the β ₃ -adrenoreceptor antagonist SR 59230A. The experiments were carried out using the registration technique of motility of rat large intestine segments isolated from the body and placed in a nutrient medium. It was found that antibodies to SR 59230A in homeopathic dilution of C400 prevent the relaxation of isolated segments of the rat large intestine.

Antibodies to β ₄ -adrenergic receptor antagonists
Example 183. Antibodies to the antagonist of β ₄ -adrenoreceptors bupranolol. The experiments were carried out on rat heart tissues excised from the body and placed in a nutrient medium. It was found that antibodies to bupranolol in homeopathic dilution of C200 introduced into the incubation medium to a final concentration of 1% cause negative inotropic responses in isolated rat cardiac tissues.

Antibodies to Purinergic Substances
Antibodies to adenosine substances (P ₁ purinergic)
Antibodies to A ₁ Adenosine Receptor Agonists
Example 184. Antibodies to the agonist A ₁ receptor CPA. The experiments were performed on isolated sections of the cerebral cortex of the rat, in which the release of mediators was determined using neurochemical methods. It was found that antibodies to CPA in homeopathic dilution of C200 inhibit neurotransmission in the drug by 30%.

Example 185. Antibodies to the A ₁ receptor agonist cyclohexyl adenosine. The experiments were performed on isolated sections of the rat hippocampus, in which the release of mediators was determined using neurochemical methods. It has been established that antibodies to CPA in homeopathic dilution of C200 inhibit neurotransmission in the hippocampus by 20%.

Antibodies to A ₁ Adenosine Receptor Antagonists
Example 186. Antibodies to the A ₁ receptor antagonist of caffeine. The experiments were carried out on outbred white male rats in which spontaneous locomotor activity was recorded in groups of 5 individuals using an Opto Varimex actometer (USA). It was found that antibodies to caffeine cause a significant (65%) increase in spontaneous motor activity upon oral administration of 0.1 ml of a solution in homeopathic dilution of C200.

Example 187. Antibodies to the theophylline A ₁ receptor antagonist. The experiments were performed on outbred white male mice in which the convulsions and death due to hypoxic stress were delayed after the administration of adenosine agonists (adenosine, 2-chloradenosine, etc.). It was found that antibodies to theophylline stop the protective effect of adenosine agonists upon oral administration of 0.1 ml of a solution of antibodies in homeopathic dilution of C200.

Antibodies to A _2A Adenosine Receptor Agonists
Example 188. Antibodies to agonist A _2A of CGS 21860 receptors. Experiments were performed on isolated vessels of the guinea pig heart. It was found that antibodies to CGS 21860 in homeopathic dilution of C400 cause relaxation of the heart vessels after 5 minutes of incubation.

Example 189. Antibodies to the AEC receptor agonist A _2A . The experiments were carried out on isolated vessels of the heart of a guinea pig. It was found that antibodies to APEC in homeopathic dilution of C400 cause relaxation of the blood vessels of the heart by 40%.

Antibodies to A _2A Adenosine Receptor Antagonists
Example 190. Antibodies to the antagonist And _2A receptors SCH58261. The experiments were carried out on isolated vessels of the heart of a guinea pig. It was found that antibodies to SCH58261 in homeopathic dilution of C200 cause contraction of the heart vessels after 4 minutes of incubation.

Example 191. Antibodies to the CSC receptor antagonist A _2A . The experiments were carried out on isolated vessels of the heart of a guinea pig. It was found that antibodies to CSC in homeopathic dilution of C400 cause a reduction in blood vessels of the heart by 50% after 10 minutes of incubation.

Antibodies to A _2B Adenosine Receptor Agonists
Example 192. Antibodies to agonist A _2B of NECA receptors. Experiments using neurochemical methods were performed on isolated sections of the cerebral cortex of the rat brain. It was found that antibodies to NECA with the introduction of a 1% solution in homeopathic dilution of C400 increase the accumulation of cAMP in sections of rat cerebral cortex by 40%.

Antibodies to A _2B Adenosine Receptor Antagonists
Example 193. Antibodies to the antagonist of A _2B receptors alloxazine. Experiments using neurochemical methods were performed on isolated sections of the cerebral cortex of the rat brain. It was found that a 1% solution of antibodies to alloxazine in homeopathic dilution of C400 reduces the accumulation of cAMP in sections of the rat cerebral cortex by 20% after 5 minutes of incubation.

Antibodies to A ₃ Adenosine Receptor Agonists
Example 194. Antibodies to agonist A ₃ receptors CI-IB-MECA. The experiments were performed using neurochemical methods on isolated rat RBL-2H3 cell cultures. It was found that antibodies to CI-IB-MECA in homeopathic dilution of C200 increase the release of β-hexosaminidase from RBL-2H3 culture cells by 30% after 15 minutes of incubation.

Antibodies to A ₃ Adenosine Receptor Antagonists
Example 195. Antibodies to antagonist A ₃ receptor MRS1191. The experiments were performed using neurochemical methods on isolated rat RBL-2H3 cell cultures. It was found that antibodies to MRS1191 in homeopathic dilution of C400 weaken the release of β-hexosaminidase from RBL-2H3 culture cells and prevent the facilitating effect of the agonist A ₃ receptors CI-IB-MECA on this process.

Antibodies to P ₂ purinergic receptors
Antibodies to P _2X Purinoreceptor Agonists
Example 196. Antibodies to the P _2X αβ-MeATP receptor agonist. The experiments were conducted on the rabbit’s ear artery. It was found that antibodies to αβ-MeATP in homeopathic dilution of C400 cause contractions of the ear artery preparation after 10 minutes of incubation.

Antibodies to P _2X Purinoreceptor Antagonists
Example 197. Antibodies to the antagonist of P _2X receptors ANAPP ₃ . The experiments were performed on rat brain using radioligand methods. It was found that antibodies to ANAPP ₃ displace the labeled [ ³ H] D - αβ-MeATP ligand from receptors in homeopathic dilution of C200, which leads to a 30% decrease in label radioactivity.

Antibodies to P _2Y purinoreceptor agonists
Example 198. Antibodies to the agonist P _2Y receptor 2-MeSATP. The experiments were carried out using neurochemical methods on preparations of an isolated aorta of a guinea pig. It was found that antibodies to 2-MeSATP in homeopathic dilution of C400 reduce the content of cAMP in the drug by 30%.

Antibodies to P _2Y purinoreceptor antagonists
Example 199. Antibodies to the antagonist of the P _2Y receptor suramin. The experiments were carried out on turkey red blood cells using radioligand methods. It was found that antibodies to suramin in homeopathic dilution of C200 displace the labeled [ ³⁵ S] ADPβS ligand from the receptors, which leads to a decrease in the radioactivity of the label by 20%.

Antibodies to P _2U Purinoreceptor Agonists
Example 200. Antibodies to the P _2U UTP receptor agonist. The experiments were carried out using electrophysiological methods on isolated sections of cardiac tissue. It was found that introducing into the incubation medium a 5% solution of antibodies to UTP in homeopathic dilution of C200 enhances the currents of Ca ²⁺ and K ⁺
Antibodies to P _2T Purinoreceptor Agonists
Example 201. Antibodies to the P _2T ADP receptor agonist. The experiments were carried out using biochemical methods on blood cells. It was found that the introduction into the incubation medium of a 1% solution of antibodies to ADP in homeopathic dilution of C200 contribute to an increase in the level of cAMP in platelets by 15% after 10 minutes of incubation.

Antibodies to P _2T Purinoreceptor Antagonists
Example 202. Antibodies to the antagonist of p _2t ATP receptors. The experiments were carried out using radioligand methods on human blood cells. It was found that antibodies to ATP in homeopathic dilution of C400 displace the labeled β [ ³² P] 2-MeSADP ligand from platelet receptors, reducing cell radioactivity by 30%.

Antibodies to P _2Z Purinoreceptor Agonists
Example 203. Antibodies to the P _2Z ATP ^4- receptor agonist. The experiments were carried out on an isolated preparation of the vas deferens duct of a guinea pig. It was found that antibodies to ATP ^4- in homeopathic dilution of C400 stimulate drug contractions by 20% after 5 minutes of incubation.

Example 204. Antibodies to the agonist of P _2D receptors Ap ₄ A. Experiments were performed using neurochemical methods on isolated synaptosomes of rat brain. It was found that introducing into the incubation medium 1% of antibodies to Ap ₄ A in the homeopathic dilution of C400 increases the Ca ²⁺ content in synaptosomes by 10%.

Antibodies to histaminergic substances
Antibodies to histamine receptor agonists
Antibodies to histamine H ₁ receptor agonists
Example 205. Antibodies to the histamine H ₁ receptor agonist 2-thiazolylethylamine. The experiments were carried out on isolated segments of the intestine of guinea pig placed in a nutrient medium. It was found that introducing into the incubation medium a 5% solution of antibodies to 2-thiazolylethylamine in homeopathic dilution of C200 stimulates contraction of the isolated intestine of guinea pig by 20%.

Antibodies to histamine H ₂ receptor agonists
Example 206. Antibodies to the histamine H ₁ receptor agonist dimaprit. The experiments were carried out using neurochemical methods on isolated sections of the hippocampus of guinea pig. It was found that antibodies to dimaprit contribute to the accumulation of cAMP in slices of the hippocampus of guinea pig when a 1% solution in homeopathic dilution of C400 is introduced into the incubation medium.

Antibodies to histamine H ₃ receptor agonists
Example 207. Antibodies to imetitis. The experiments were performed on isolated sections of the cortex of the cerebral hemispheres of the rat, placed in a nutrient medium. It was found that antibodies to imetitis in homeopathic dilution of C200 inhibit the release of histamine in sections of the cerebral cortex of the rat brain.

Antibodies to histamine receptor antagonists
Antibodies to histamine H ₁ receptor antagonists
Example 208. Antibodies to the histamine H ₁ receptor antagonist mepiramine. The experiments were carried out using neurochemical methods on isolated sections of the cortex of the cerebral hemispheres. It was found that antibodies to mepiramine in homeopathic dilution of C400 inhibit the hydrolysis of phospholipids in the cerebral cortex of the guinea pig by 20% after 30 minutes of incubation.

Antibodies to histamine H ₂ receptor antagonists
Example 209. Antibodies to cimetidine. The experiments were performed on isolated guinea pig atria placed in a nutrient medium. It was found that antibodies to cimetidine in homeopathic dilution of C400 reduce the frequency of contractions in the preparation of isolated guinea pig atrial by 30%.

Antibodies to histamine H ₃ receptor antagonists
Example 210. Antibodies to thioperamide. The experiments were carried out using isolated sections of the cerebral cortex of the rat brain, placed in a nutrient medium. It was found that antibodies to thioperamide stimulate the release of histamine in the studied structure in homeopathic dilution of C400
Antibodies to histamine release inhibitors
Example 211. Antibodies to ketotifen. Patient R., 52 years old, complained of asthma attacks. Traditional methods of treatment have been ineffective. After a course of treatment with antibodies to ketotifen, 1 teaspoon of the solution in homeopathic dilution of C400 2 times a day for 7 days improved. It is proposed to continue treatment in order to prevent relapse of the disease.

Antibodies to activators of diamine oxidase - an enzyme of histamine deactivation
Example 212. Antibodies to fencarol. Patient I., 37 years old, complained of neurodermatitis. Since traditional methods of treatment caused pronounced hypnotic and sedative effects in the patient, it was proposed to conduct a course of treatment with antibodies to fencarol (1 teaspoon of the solution in homeopathic dilution C200 2 times a day for 7 days), devoid of these side effects. After treatment with antibodies to fencarone, the signs of the disease reduced and disappeared.

Antibodies to substances of the endogenous kinurenin system
Example 213. Antibodies to endogenous quinolenic acid, which is a selective agonist of NMDA receptors and is formed from kinurinine under the influence of the kinureninaminotransferase enzyme. It was shown that in experiments on mice, the administration of antibodies to quinolenic acid orally in a 0.1 ml solution in homeopathic dilution of C400 causes convulsive twitching in animals once, and with an increase in dose - convulsions.

 Example 214. Antibodies to kinurenic acid, an antagonist of strychnine insensitive glycine receptor. In experiments on mice, it was shown that the administration of antibodies to kinurenic acid orally in a 0.1 ml solution in homeopathic dilution of C400 once calms the animals and reduces their motor activity (by 33%) in the Opto-varimex unit.

 Example 215. It was found that antibodies to 4-kinurenin (an antagonist of the glycine portion of the NMDA receptor complex) cause a decrease in motor activity, especially horizontal activity, in mice in an open field test with a single oral administration of 0.1 ml of a solution in homeopathic dilution of C200.

 Example 216. Antibodies to 7-chlorothiokinurenic acid (an antagonist of the glycine portion of the NMDA receptor complex) have a neuroprotective effect. Studies using morphohistochemical methods have shown that antibodies to 7-chlorothiokinurenic acid when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution C200 reduce apoptosis in the cell culture of hippocampal neurons during experimental chemical hypoxia caused by dinitrophenol (200 μmol).

Antibodies to neurotransmitter reuptake inhibitors
Antibodies to Dopamine Reuptake Inhibitors
Example 217. Antibodies to RTI-113 (3β- (4-chlorophenyl) tropan-2β-carboxylic acid phenyl ester), a selective dopamine reuptake inhibitor. The experiments were performed under conditions of free behavior on outbred white male rats with implanted intravenous catheters. They developed a self-administration reaction of cocaine. It was found that antibodies to RTI-113, administered orally in 0.1 ml each at homeopathic dilution of C200, significantly (63%) suppress the self-administration of cocaine.

Antibodies to Norepinephrine Reuptake Inhibitors
Example 218. Antibodies to the serotonin and norepinephrine reuptake inhibitor milnacipran. Patient D., 39 years old, complained of low mood, chronic fatigue, lack of interest in life, emotional dullness. After a course of treatment with antibodies to milnacipran, 1 tablespoon of the solution in homeopathic dilution of C400 3 times a day for 7 days, these symptoms were reduced, the patient returned to his usual way of life.

Antibodies to serotonin reuptake inhibitors
Example 219. Antibodies to trazodone. Patient K., 36 years old, complained of low mood, lack of interest in the environment, difficulties in mental and emotional spheres. After prolonged administration of antibodies to trazodone in a 10 ml solution in homeopathic dilution of C400 2 times a day for 10 days, an improvement in mood was noted, interest in the environment appeared, and the emotional state improved.

 Example 220. Antibodies to paroxetine. Patient U., 47 years old, complained of low mood, lack of interest in the environment, difficulties in mental and emotional spheres. After prolonged oral administration of antibodies to paroxetine (15 ml each solution in homeopathic dilution C200 3 times a day for 7 days), an improvement in mood was noted, interest in the environment appeared, and the emotional state improved.

Antibodies to GABA reuptake inhibitors
Example 221. Antibodies to the GABA reuptake inhibitor SKF 100330. The experiments were performed on outbred white male mice that were convulsed with corazole. It was found that antibodies to SKF 100330 have an anticonvulsant effect in convulsions caused by corazole. Under the influence of oral administration (0.1 ml each solution in homeopathic dilution of C400 once) of antibodies to SKF 100330, an increase (by 90%) in the latent period of seizures and a decrease in the duration of clonic seizures (by 55%) were noted.

Antibodies to substances that affect monoamine oxidase activity
Antibodies to MAO-A inhibitors
Example 222. Antibodies to nialamide - an irreversible and non-selective MAO inhibitor. Patient N., 58 years old with a diagnosis of cyclotymic depression, a course (30 days) of antibodies to nialamide was prescribed. After the course application of the substance (1 teaspoon of the solution in homeopathic dilution of C400 2 times a day), the patient showed a significant decrease in the manifestations of the depressive state, a decrease in lethargy, lethargy, and lack of initiative.

 Example 223. Antibodies to pyrazidol, a selective and reversible MAO-A inhibitor. Patient V., 53 years old, with a diagnosis of manic-depressive psychosis, a course of antibodies to pyrazidol was prescribed. It was shown that after the course use of the substance (1 teaspoon of the solution in homeopathic dilution of C400 2 times a day for 7 days), the patient showed a significant improvement - a decrease in the manifestations of the depressive state, a decrease in anxiety-depressive, asthenic and hypochondria symptoms.

Antibodies to MAO-B inhibitors
Example 224. Antibodies to rasagiline. In studies on old outbred rats aged 24 months, there was a violation of the processes of recording information and extracting a memorable trace. The use of antibodies to rasagiline (oral 0.1 ml solution in homeopathic dilution of C400 for 7 days) caused an improvement in memory in old animals, facilitated the learning process and reduced neurological deficits. Under the influence of the substance, an improvement in the process of training animals in the defensive reflex was observed, which was expressed in a decrease in the latent period of the reflex execution and in a decrease in the number of trainings (by 25%) needed to develop the reflex compared to control animals of the same age.

 Example 225. Antibodies to SL-25.1188. In studies on old outbred rats 24 months of age, there was a violation of the processes of recording information and extracting a memorable trace. The use of antibodies to SL-25.1188 (oral solution of 0.1 ml in homeopathic dilution C200 for 10 days) caused an improvement in memory in old animals, facilitated the learning process and reduced neurological deficits.

Antibodies to substances that affect ion currents in the membranes of cells of the nervous system
Antibodies to sodium channel blockers.

 Example 226. Antibodies to lamotrigine. The studies were carried out in experiments on mice in which a convulsive seizure was caused by conducting a maximum electroconvulsive seizure through corneal electrodes. The introduction of anti-lamotrigine antibodies to animals (0.1 ml oral solution in a homeopathic dilution of C400) before the maximum electroshock prevented the development of a convulsive seizure, significantly reduced the duration and severity of tonic-clonic seizures, and increased the latent time of their onset, and reduced the death rate of animals.

 Example 227. Antibodies to BW-619C89. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was established that the introduction of antibodies to BW-619C89 before the operation (0.1 ml solution in homeopathic dilution of C400) reduces the infarction zone, improves the general condition of animals, their neurological status.

 Example 228. Antibodies to MS-153. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 70% hippocampal cell death. The introduction (orally in 0.1 ml of a solution in homeopathic dilution of C200) antibodies to MS-153 led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 40%.

 Example 229. Antibodies to tetrodotoxin. In experiments on sections of rat hippocampus in anoxia using neurochemical methods, it was found that antibodies to tetrodotoxin when introduced into the incubation medium as a 1% solution in homeopathic dilution C200 reduced the decrease in ATP concentration and improved recovery of granular neurons and CA1 pyramidal neurons.

 Example 230. Antibodies to lidocaine or procaine. In experiments on slices of the hippocampus of rats using neurochemical methods, it was found that antibodies to lidocaine or procaine when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C400 restored synaptic functions, prevented damage to the pyramidal cells caused by 15-minute hypoxia.

 Example 231. Antibodies to QX-314. In experiments on slices of the hippocampus of rats using neurochemical methods, it was found that antibodies to QX-314 when introduced into the incubation medium in the form of a 5% solution in homeopathic dilution of C200 prevented pyramidal cell damage caused by 12-minute anoxia or aglycemia.

 Example 232. Antibodies to riluzole. Studies on rats with bilateral compression of carotid arteries by neurochemical, behavioral and electrophysiological methods found that antibodies to riluzole (0.1 ml oral solution in homeopathic dilution C400) improved memory impaired in animals, reduced hippocampal cell degeneration and improved EEG pattern. After a course of therapy (2 weeks), rats were better trained in the conditioned reflex of passive avoidance, as evidenced by a decrease (by 25%) in the latent time of the reflex.

 Example 233. Antibodies to lubeluzole. Patient N with acute cerebral ischemia was prescribed antibodies to lubeluzole for 3 weeks once daily, 5 ml orally in the form of a solution in homeopathic dilution C200. After treatment, the patient had an improvement in neurological status, an improvement in memory, especially memory for current events, an increase in overall life activity.

Antibodies to potassium channel opening enhancers
Example 234. Antibodies to cromacoline, an ATP-sensitive potassium channel opener. Using neurochemical methods, it was shown that the introduction of 0.01 ml antibodies to cromacoline into the rat ventricles in a homeopathic dilution of C400 before ischemia and during reperfusion blocked the expression of c-foc, c-jun proteins and the beta-amyloid protein precursor in rat hippocampus through 20 minutes after experimental forebrain ischemia.

 Example 235. Antibodies to nicoraldin, an ATP-sensitive potassium channel opener. Using morphohistochemical methods, it was found that the introduction of antibodies to nicoraldin into the ventricles of the brain led to protection against hippocampal neurons from neuronal death, preventing their degeneration.

 Example 236. Antibodies to pinacidil, ATP-sensitive potassium channel opener. Using neurochemical methods, it was shown that the introduction of antibodies to pinacidil into the ventricles of the brain before ischemia and during the reperfusion period blocked the expression of c-foc, c-jun proteins and the beta-amyloid protein precursor in rat hippocampus 20 minutes after experimental forebrain ischemia.

 Example 237. Antibodies to levoromacalin. Using morphohistochemical methods, it was found that the introduction of antibodies to levoromacalin into the ventricles of the brain 20 minutes before ischemia protected hippocampal neurons from neurodegeneration and delayed neuronal death.

 Example 238. Antibodies to apricaline. In experiments with modeling of myocardial ischemia in experiments on rats by morphohistochemical methods, it was shown that antibodies to apricaline reduced the size of the heart attack zone in the heart by 20% when administered before surgery (0.1 ml of the solution in homeopathic dilution C200 orally.

Antibodies to substances that affect the function of calcium channels
Antibodies to substances that affect the function of calcium channels of the L-type
Antibodies to L-type calcium channel agonists
Example 239. Antibodies to the calcium channel agonist of the L-type Bay K 8644. The experiments were performed on outbred white male mice, which were injected with substances into the lateral ventricle of the brain under conditions of free behavior. It was found that antibodies to Bay K 8644 cause autoaggression in mice - bites of their own paws.

 Example 240. Antibodies to the calcium channel agonist of L-type FPL64176. The experiments were carried out on outbred white male mice, which, under conditions of free behavior, were injected through the cannula into the lateral ventricle of the brain. It was found that antibodies to FPL64176 cause autoaggression in mice - bites of their own paws.

Calcium Blocker Antibodies
Example 241. Antibodies to the calcium release blocker ryanodine. The experiments were performed on isolated preparations of the rat visual cortex, in which the reactions of calcium channels to depolarization of the drug were enhanced under the influence of neurotrophin-4. It was found that antibodies to ryanodine when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 block the effect of neurotrophin-4.

 Example 242. Antibodies to the calcium ejection blocker dantrolene. The experiments were performed on preparations of an isolated rat heart, in which the frequency of contractions was impaired as a result of the administration of a toxic dose of propranolol. It was found that antibodies to dantrolene when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 restore the normal heart rate disturbed by propranolol.

Antibodies to L-Type Calcium Channel Antagonists
Example 243. Antibodies to the calcium channel antagonist of the L-type verapamil. The experiments were performed on isolated strips of rat heart tissue, in which the β-adrenoagonist isoprenaline caused a positive inotropic effect. It was found that antibodies to verapamil when introduced into the incubation medium in the form of a 5% solution in homeopathic dilution of C200 stop the effect of isoprenaline.

 Example 244. Antibodies to the calcium channel antagonist of L-type nifedepine. The experiments were performed on outbred white male mice that were autoaggressed by administering a calcium channel agonist, Bay K 8644. It was found that the administration of antibodies to nifedepine (0.1 ml oral solution in homeopathic dilution C200) suppresses the autoaggression caused by Bay K 8644 .

 Example 245. Antibodies to the L-type calcium channel antagonist diltiazem. The experiments were performed on outbred white male rats, in which nerve cell death resulting from general cerebral ischemia after chest compression was studied. It was found that antibodies to diltiazem had a neuroprotective effect when administered before surgery (0.1 ml of a solution in homeopathic dilution of C200 orally).

Antibodies to N-Type Calcium Channel Antagonists
Example 246. Antibodies to the calcium channel antagonist of the N-type ω-conotoxin GVIA. The experiments were carried out on outbred white male rats, which were administered antibodies to GVIA ω-conotoxin under oral conditions of free behavior for 2 weeks (0.1 ml oral solution in C200 homeopathic dilution). It was established that antibodies to ω-conotoxin GVIA reduce spontaneous motor activity, reduce rotational asymmetry and cause increased sensitivity to apomorphine.

Antibodies to P-type calcium channel antagonists
Example 247. Antibodies to the calcium channel antagonist P-type ω-agatoxin IVA. The experiments were carried out on an isolated iliac artery preparation, the neurogenic contractions of which were caused by electrical stimulation of the nerve. It was found that antibodies to ω-agatoxin IVA when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 eliminate arterial contractions.

Antibodies to Q-type calcium channel antagonists
Example 248. Antibodies to the calcium channel antagonist of Q-type ω-conotoxin MVIIC. The experiments were carried out on an isolated iliac artery preparation, the neurogenic contractions of which were caused by electrical stimulation of the nerve. It was found that antibodies to MVIIC ω-conotoxin, when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C400, eliminate arterial contractions.

Antibodies to specific lipids of the nervous tissue
Antibodies to lipids of brain nerve cells
Example 249. Antibodies to cholesterol. In experiments on nerve cell biomembranes by neurochemical and physicochemical methods, it was found that antibodies, when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200, are embedded in the phospholipid bilayer and cause a violation of the quasicrystalline packaging of the chains and a decrease in their mobility. The ability of antibodies to change the liquidity of the membrane and the processes associated with it, such as activation of ATPases, calcium-mediated release of mediators from synaptic terminals, and the process of ligand binding to receptors, has been shown. It was found that when antibodies to cholesterol are added to the membrane of nerve cells, the area of the lecithin molecule decreases from 0.96 to 0.71 nm ²
Example 250. Antibodies to cerebrosides. In experiments on nerve cell biomembranes by neurochemical and physicochemical methods, the ability of antibodies, when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution C200, to change the liquidity of the rat hippocampal nerve membrane was shown.

 Example 251. Antibodies to sulfatides (sulfocerebrosides). It is known that the sulfate group of cerebroside sulfate is part of the active center of opiate receptors. In vivo experiments have shown that antibodies to cerebroside sulfate introduced into the brain of a rat eliminate the narcotic effect of morphine. Neurochemical and physicochemical methods have shown the ability of antibodies, when introduced into the incubation medium of rat neurons in the form of a 5% solution in homeopathic dilution C200, to change the membrane fluidity and related processes, such as activation of ATPases, calcium-induced release of mediators from synaptic terminals, the process of ligand binding to receptors .

Antibodies to Nerve Cell Phospholipids
Example 252. Antibodies to cytidine 5-diphosphocholine (cyticholine, CDP-choline). In experiments on white adult rats, the anti-anamnestic activity of antibodies to cytidine 5-diphosphocholine was shown. Administration of scopolamine to rats immediately prior to training in the conditioned reflex of passive avoidance in a dark-bright chamber caused a disturbance in the process of reproduction of the reflex 24 hours after training. A single use of antibodies (0.1 ml oral solution in a homeopathic dilution of C200) caused the elimination of the amnesic effect of scopolamine, which was expressed in a decrease (1.5 times) in the time spent in a dark dangerous chamber.

 Administration of antibodies (0.1 ml oral solution in C200 homeopathic dilution) for 3 months to old rats 24 months old led to the restoration of impaired motor skills and to improved learning processes. Under the influence of the drug, the number of mistakes made decreased (by 32%) and the latent time was reduced during the development of the reflex in the T-shaped labyrinth.

Example 253. Antibodies to phosphatidylcholine. In vitro experiments on nerve cell biomembranes by neurochemical methods have shown the ability of antibodies to phosphatidylcholine when they are introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 to cause activation of membrane enzymes Na ⁺ , K ⁺ -ATPase and monoamine oxidase in rat CNS membranes.

Example 254. Antibodies to lysophosphatidylcholine. In vitro experiments on biomembranes of nerve cells by neurochemical methods showed the ability of antibodies to phosphatidylcholine when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 to cause activation of membrane enzymes Na ⁺ , K ⁺ -ATPase in biomembranes of animal brain by 20%.

Example 255. Antibodies to sphingomyelin. In vitro experiments on biomembranes of nerve cells by neurochemical methods showed the ability of antibodies to sphingomyelin when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 to activate membrane enzymes - Na ⁺ , K ⁺ -ATPase in rat brain biomembranes.

Example 256. Antibodies to phosphotidylserine. In vitro experiments on nerve cell biomembranes by neurochemical methods have shown the ability of antibodies to sphingomyelin when introduced into the incubation medium in the form of a 5% solution in homeopathic dilution of C400 to activate membrane enzymes - protein kinases C, adenylate cyclase and Na ⁺ , K ⁺ -ATPase in the head biomembranes rat brain.

 Example 257. Antibodies to phosphoinositides (phosphotidylinositol) - regulators of calcium ion transport through the membrane. In vitro studies on biomembranes of nerve cells by neurochemical methods have shown that upon depolarization of the membrane, arachidonic acid is rapidly released from phosphoinositides. Antibodies to phosphoinositides and their metabolic products also have the ability to regulate calcium transport. Antibodies to 1,2-diacylglycerol when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 stimulate the activity of protein kinase C, which phosphorylates the calcium channel protein, and antibodies to triphosphoinositol have the ability to bind divalent cations and thereby stimulate calcium transport.

Example 258. Antibodies to phosphatidylethanolamine. In vitro experiments on biomembranes of nerve cells by neurochemical methods have shown the ability of antibodies to phosphatidylcholine when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 to trigger the activation of Na ⁺ , K ⁺ -ATPase membrane enzymes in rat brain biomembranes.

Ganglioside Antibodies
Example 259. Antibodies to ganglioside GM1. In in vitro experiments in the nerve tissue of the cerebral cortex, receptor binding methods have shown the affinity of antibodies to the GM1 ganglioside to the ligand - dopamine. When they are introduced into the incubation medium of rat neurons in the form of a 1% solution in homeopathic dilution of C200, displacement of labeled dopamine from neurons by 20% is observed. In vivo studies have shown that antibodies to GM1 monosialoganglioside restore neurochemical parameters of dopaminergic neurons after a violation of the nigrostriatal system, enhance dopamine uptake and tyrosine hydroxylase activity. The substance normalizes the imbalance between the activity of dopamine and serotonergic neurons, caused in the experiment by the introduction of apomorphine. Under the influence of the substance, a decrease in cerebral edema and restoration of ion balance after a brain injury in an experiment in rats are observed.

 Example 260. Antibodies to monosialoganglioside — GM1 and disialoganglioside —GD1b, having an affinity for the ligand — cholera toxin. In experiments on tissue culture by neurochemical methods, it was shown that the oligosaccharide part of the monosialoganglioside binds to the recognition molecule of cholera toxin - protomer B, which causes an increase in the local density of gangliosides and their micelle formation. Ganglioside micelles interact with the regulatory unit of cholera toxin - protomer A, which has ADP-ribosylating activity. ADP-ribosylation of slow receptors leads to activation of adenylate cyclase. Antibodies to monosialoganglioside - GM1, when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200, trigger a similar cascade of events, leading to 30% activation of adenylate cyclase.

 Example 261. Antibodies to the gangliosides GQ1b, GD1b, GT1b. In in vitro experiments in the nerve tissue of the cerebral cortex, receptor binding methods have shown the affinity of antibodies to the gangliosides GQ1b, GD1b, GT1b to the ligand - tetanus toxin, which is manifested in their ability to displace 3H-tetanus toxin from the binding sites on rat neurons and decrease the radioactivity of samples on 30% when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution C200.

 Example 262. Antibodies to ganglioside GT1b. In in vitro experiments in the nerve tissue of the cerebral cortex, receptor binding methods have shown the affinity of antibodies to the GTlb ganglioside to the ligand - botulinum toxin, which is manifested in their ability to displace 3H-toxin from the binding sites on rat neurons and decrease the radioactivity of samples by 30% when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution C200.

 Example 263. Antibodies to ganglioside GM1. In in vitro experiments, receptor binding methods have shown the affinity of antibodies to the ganglioside GM1 to the ligand - E. Coli toxin, which is manifested in their ability to displace 3H-toxin from the binding sites on rat neurons and to reduce the radioactivity of samples by 20% when introduced into the incubation medium in as a 1% solution in homeopathic dilution C200.

 Example 264. Antibodies to gangliosides GP1, GQ1b, GT1a. In in vitro experiments in the nerve tissue of the cerebral cortex, receptor binding methods showed the affinity of antibodies to the gangliosides GP1, GQlb, GTla to the ligand - Sendai virus, which manifests itself in their ability to displace the virus from binding sites on rat neurons by 20% when introduced into the medium incubation in the form of a 1% solution in homeopathic dilution C200.

 Example 265. Antibodies to gangliosides GD1b, GT1b. In in vitro experiments in the nerve tissue of the cerebral cortex, receptor binding methods showed the affinity of antibodies to the gangliosides GD1b, GT1b to the ligand - the influenza virus, which manifests itself in their ability to displace the virus from the binding sites on rat neurons by 30% when introduced into the incubation medium in as a 1% solution in homeopathic dilution C200.

 Example 266. Antibodies to ganglioside GD3. In in vitro experiments in the nerve tissue of the cerebral cortex, receptor binding methods have shown the affinity of antibodies to the ganglioside GD3 to the ligand - serotonin, which is manifested in their ability to displace labeled serotonin from the binding sites on rat neurons by 20% when antibodies are introduced into the incubation medium in the form of 1 % solution in homeopathic dilution C200.

 Example 267. Antibodies to gangliosides GM2, GT1. In in vitro experiments in the nervous tissue, receptor binding methods have shown the affinity of antibodies to gangliosides GM2, GT1 to the ligand - interferon, which is manifested in their ability to displace interferon from binding sites on rat neurons by 20% when antibodies are introduced into the incubation medium in the form of a 5% solution in homeopathic dilution C200.

 Example 268. Antibodies to gangliosides GM1, GD1b, GT1b. In in vitro experiments in the nerve tissue of the cerebral cortex, receptor binding methods have shown the affinity of antibodies to the gangliosides GM1, GD1b, GT1b to the ligand - thyrotropin, which is manifested in their ability to displace thyrotropin from the binding sites on rat neurons by 30% when antibodies are introduced into the incubation medium in the form of a 1% solution in homeopathic dilution C200.

 Example 269. Antibodies to gangliosides GD1b, GT1b. In in vitro experiments, receptor binding methods have shown the affinity of antibodies to the gangliosides GD1b, GT1b to the ligand - luteotropin, which is manifested in their ability to displace luteotropin from binding sites on rat neurons by 20% when introduced into the incubation medium as a 1% solution in homeopathic dilution C200.

 Example 270. Antibodies to ganglioside GT1b. In in vitro experiments, receptor binding methods have shown the affinity of antibodies to ganglioside GT1b to the ligand - gonadotropin, which is manifested in their ability to displace 3H-gonadotropin from the binding sites on rat neurons by 30% when introduced into the incubation medium as a 2% solution in a homeopathic dilution of C200 .

 Example 271. Antibodies to gangliosides GD1a, GT1. In in vitro experiments in the nerve tissue of the cerebral cortex, receptor binding methods have shown the affinity of antibodies to the gangliosides GD1a, GT1 to the ligand - fibronectin, which manifests itself in their ability to displace fluorescently labeled fibronectin from the binding sites on rat neurons when antibodies are introduced into the incubation medium in the form of 1% solution in homeopathic dilution C200.

Antibodies to specific amino acids, peptides and proteins of the nervous tissue
Antibodies to the free amino acids of the nervous system
Example 272. Antibodies to glutamic acid. Patient K., aged 48 years old, with depression with symptoms of exhaustion, was injected with antibodies to glutamic acid (1 teaspoon of the solution in homeopathic dilution of C400 2 times a day) for a month's course. The patient's mood improved significantly, a desire to work appeared, general health improved, and signs of nervous system depletion disappeared.

 Example 273. Antibodies to gamma-aminobutyric acid. In experiments on rats, the introduction of antibodies to gamma-aminobutyric acid directly into the ventricles of the brain of 0.01 ml in the form of a solution in homeopathic dilution of C200 calmed the animal, reduced the motor activity recorded in the open field test.

 Example 274. Antibodies to proline. In experiments on rats, it was shown that the introduction of antibodies to proline (0.1 ml of solution in a homeopathic dilution of C400 orally) causes the learning of animals to deteriorate the conditioned reflex of active avoidance in a two-section shuttle-box chamber using a light signal as a conditioned stimulus, and in as an unconditioned irritant - pain irritation through the electrode floor.

 Example 275. Antibodies to methionine. In vitro experiments on neural tissue culture using neurochemical methods have shown that antibodies to methionine contribute to the synthesis of choline and restore impaired synthesis of phospholipids from fats.

 Example 276. Antibodies to cysteine. Patient S., aged 57 with an initial form of age-related cataract, was used anti-cysteine antibodies, which are involved in the metabolism of the lens of the eye, and the changes that occur during cataracts are associated with a violation of the content of this amino acid in the lens. The use of antibodies in 1 teaspoon of the solution in homeopathic dilution of C200 1 time per day for 7 months led to a significant therapeutic effect - a delay in the development of cataracts.

 Example 277. Antibodies to histidine. The use of antibodies to histidine in 1 teaspoon of the solution in homeopathic dilution of C400 2 times a day for a long course (3 months) in a patient B., aged 62, suffering from a moderate form of atherosclerosis, led to the normalization of lipoprotein metabolism, improved memory, attention, general well-being.

 Example 278. Antibodies to N-acetyl aspartic acid, glutamine, aspartic acid, cystothionine, alanine, glutathione, serine, phenylalanine, tyrosine, threonine, tryptophan, valine, lysine, asparagine, isoleucine, leucine. In vitro studies on rat nervous tissue culture using neurochemical methods showed the ability of antibodies to these amino acids when they are introduced into the incubation medium in the form of a 2% solution in homeopathic dilution of C200 to provide the plastic and energy needs of the cell, increase the concentration of acetylcholine and norepinephrine in the synaptic cleft.

 Example 279. Antibodies to taurine - 2-aminoethanesulfonic acid. In experiments on sexually mature white rats, it was shown that antibodies to taurine have an anticonvulsant, anti-aggressive effect. It is established that when a pair of rats is placed on the electrode floor, to which electric current is supplied, it causes fights in animals. The use of antibodies to taurine (oral solution of 0.1 ml in homeopathic dilution C200) reduces the number of episodes of fights by 30% and the duration of one episode (by 45%).

 Example 280. Antibodies to glycine. It was shown that the introduction of antibodies to glycine in mature rats for 7 days (0.1 ml of solution in a homeopathic dilution of C200 orally) causes an improvement in the process of fixation of the memorial trail during the development of the reflex in the U-shaped complex maze. Under the influence of a substance, an improvement in orientation, a decrease in the number of errors (by 30%) and an acceleration of the reflex are observed.

Antibodies to neurospecific proteins
Antibodies to beta-amyloid peptide (APβ) and substances that affect APβ (playing a key role in the etiopathogenesis of neurodegeneration, including in Alzheimer's disease).

Antibodies to beta-amyloid peptide and its precursors
Example 281. Antibodies to beta-amyloid peptide (APβ), which plays a key role in the etiopathogenesis of Alzheimer's disease. Antibodies to ARβ are considered as a marker for the diagnosis of Alzheimer's disease. In experiments on transgenic mice (PDAPP line) with an increased production of APβ42 and an increased level of deposition of amyloid plaques, it was found that the oral administration of 0.1 ml of a solution of antibodies in homeopathic dilution of C200 to APβ42 amyloid leads to the prevention of deposition of amyloid plaques in young animals and leads to significant reducing the number and size of plaques in old animals, prevents memory loss.

 Example 282. Antibodies to fragments of the protein APP. It was shown that antibodies to IgM508 to fragments of the APP protein are able to block the formation of insoluble APβ aggregates and dissolve already formed amyloid fibrils upon oral administration to mice of 0.1 ml antibody solution in homeopathic dilution C200 10 days.

 Example 283. Antibodies to the synthetic form AP432 (preparation AN-1792). It has been shown that the substance prevents, and in some animals, reverses the formation of amyloid formations by oral administration to mice of 0.1 ml of antibody solution in homeopathic dilution of C200 for 7 days.

Antibodies to inhibitors of the formation of beta-amyloid peptide
Antibodies to inhibitors of the formation of beta-amyloid peptide (APβ) from the protein of the APP precursor, the expression of which is stimulated by a number of endogenous factors, for example, cytokines, some neurotrophic factors (BFGF, EGF), estrogens, stressful conditions.

Example 284. Antibodies to calpain proteases, cathepsin D, specific blockers of the formation of β-synthetase, affecting the formation of APβ from the protein of the precursor APP. In vitro experiments by neurochemical methods have shown that antibodies to them when introduced into the incubation medium in the form of a 2% solution in a homeopathic dilution of C200 affect the first stage of the formation of APβ, namely they stimulate 30% intracellular proteolysis by β-secretases that form amino -term residue ARβ.
Example 285. Antibodies to the protein presenilin I. In in vitro experiments by neurochemical methods it was found that antibodies to presenilin I, when introduced into the incubation medium of rat neurons in the form of a 2% solution in homeopathic dilution C200, inhibit the activity of the calpain II enzyme, which has a neurotoxic effect on cell level.

 Example 286. Antibodies to monensin. In in vitro experiments on nerve cell culture using neurochemical methods, it was found that antibodies, when introduced into the incubation medium as a 2% solution in homeopathic dilution of C200, reduce the formation of APβ, causing destabilization of the pH gradient and vesicular transport.

Example 287. Antibodies to Brefeldin A. In in vitro experiments on a culture of nerve cells by neurochemical methods, it was found that when antibodies are added to the incubation medium as a 2% solution in homeopathic dilution of C200, the formation of APβ is reduced.
Example 288. Antibodies to bafilomycin A and its analogues. In experiments on the culture of nerve cells by neurochemical methods, it was found that antibodies to bafilomycin A when they are introduced into the incubation medium as a 1% solution in homeopathic dilution of C200 selectively block the formation of APβ by the mechanism of indirect inhibition of β-secretase activity, and prevent lysosomal acidification by inhibition of ATP- V-type basics. The EC50 of the blocking effect of the substances is 50 nM.

 Example 289. Antibodies to the peptides leupeptin (MDL-28170) and E-64. In vitro experiments using neurochemical methods have shown that antibodies to leupeptin, when introduced into the incubation medium in the form of a 2% solution in a homeopathic dilution of C200, stabilize the C-terminal fragment of APβ and cause a decrease in the level of APβ in the brain by direct or indirect inhibition of γ-secretase activity.

 Example 290. Antibodies to esters of N-arylalanine. In in vivo experiments on transgenic mice with neurochemical methods, it was found that oral administration of antibodies to N-arylalanine esters in a homeopathic dilution of C200 in 0.1 ml once causes inhibition of γ-secretase activity and, due to this effect, a decrease in the level of APβ in the brain of animals is observed.

Antibodies to substances affecting the processes of aggregation-disaggregation of APβ and binding to APβ
Example 291. Antibodies to peptides representing abbreviated or modified variants of APβ: pentapeptide KLVFF, which is a fragment of APβ: with a sequence of amino acids 16-20, and its modified analogues: LPFFD, LPYFD, RDLPFYPVPID. In experiments on the culture of nervous tissue by neurochemical methods, it was shown that antibodies to the KLVFF pentapeptide when they are introduced into the incubation medium as a 1% solution in homeopathic dilution of C200 slow down the process of conversion of APβ from a soluble form to an aggregated one, i.e. prevent the conversion of APβ into a form exhibiting neurodegenerative properties. In vitro experiments by morphohistochemical methods showed the ability of these peptides to influence the process of APβ fibrillation by attenuating the formation of β-folded aggregates. Under the influence of antibodies, the ability of APβ to form β-folded oligomeric structures is weakened.

 Example 292. Antibodies to endogenous proteoglycans and glucosaminoglycans. It was found that in experiments on tissue cultures in vitro by morphohistochemical methods, it was shown that antibodies, when introduced into the incubation medium as a 2% solution in homeopathic dilution of C200, reduce the aggregation and deposition of fibrillar formations of APβ in the brain. In experiments on cell culture, it was shown that antibodies to glycoprotein, laminin, expressed in the brain after an injury, block the formation of β-fibrils and induce their disaggregation.

 Example 293. Antibodies to the protein apoJ. Using morphohistochemical methods, it was shown that antibodies to the apoJ protein stimulate the accumulation in the central nervous system of rats of the trophic form of sAPPα amyloid (when administered orally with 0.2 ml of antibody solution in homeopathic dilution C200 for 10 days) and, thus, affect apoE / apoJ -regulated process of formation and deposition of amyloid fibrils in the brain.

 Example 294. Antibodies to apolipoprotein E (isoforms E2, E3, E4). Using morphohistochemical and neurochemical methods on rat nerve cell culture, it was shown that antibodies to apolipoprotein E, when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution C200, have a neurodegenerative effect, which is experimentally proved by their ability to enhance APβ fibrillogenesis and reduce the elimination of APβ from intercellular space.

 Antibodies to non-enzymatic neuro-specific calcium-binding proteins.

Example 295. Antibodies to the S-100 protein, which is a heterogeneous acidic calcium-binding protein, found mainly in glia. With the introduction of antibodies to the S-100 protein in the ventricles of rat brain, 0.01 ml of a solution of antibodies in homeopathic dilution of C200 changes the process of developing an active avoidance reflex in a two-section chamber. A correlation was found between the amount of S-100 protein in the brain of inbred line mice and learning ability - the higher the protein content, the better the training. During the formation of conditioned reflexes in the learning process, the biosynthesis of S-100 protein is enhanced. The introduction of antibodies to the S-100 protein improves learning. Under the influence of a substance, the number of mistakes made when performing a reflex decreases by 37% and the number of combinations necessary to achieve the learning criterion decreases
Example 296. Antibodies to calmodulin - the main regulator and mediator of the effects of calcium. In experiments using neurochemical methods, it was shown that antibodies to calmodulin, when introduced into the incubation medium of rat neurons in the form of a 2% solution in homeopathic dilution of C200, activate calcium-dependent protein kinases.

 Example 297. Antibodies to calcineurin, a protein that controls the functions of calmodulin. In experiments using neurochemical methods, it was shown that antibodies to calcineurin when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 have the ability to inhibit calmodulin activity by 30% and have protein phosphatase activity.

 Example 298. Antibodies to fosfomyristin - a protein that can bind and reserve calmodulin. In experiments using neurochemical methods on rat nerve cell culture, it was shown that antibodies to phosphomyristin are able to bind and reserve calmodulin in a dephosphorylated state when introduced into the incubation medium in the form of a 2% solution in homeopathic dilution of C200, and after its phosphorylation, release calmodulin.

 Example 299. Antibodies to sialoglycoprotein GP-350 (has a high content of glutamic and aspartic acids). In experiments using neurochemical methods, the ability of antibodies to the GP-350 sialoglycoprotein to bind calcium was shown when they were introduced into the neuron incubation medium in the form of a 5% solution in homeopathic dilution of C200.

 Example 300. Antibodies to protein B-50, one of the main phosphorylated proteins of synaptic (mainly presynaptic) membranes. Using neurochemical methods, it was found that antibodies to protein B-50, when introduced into the incubation medium in the form of a 2% solution in homeopathic dilution of C200, improve interneuron transmission, affect calcium-dependent protein kinase C, stimulate the phosphorylation of protein B-50, which leads to a long-term change charge and state of the channel of the postsynaptic membrane, causing the beat of the synapse.

 Example 301. Antibodies to fodrin, a structural protein of the postsynaptic membranes of glutamate synapses, which is a substrate for calpein neurons. In experiments using radioligand binding methods, it was found that antibodies to fodrin block glutamate receptors when introduced into the incubation medium as a 2% solution in homeopathic dilution of C200, which leads to a 20% decrease in the binding of labeled glutamate to rat neurons.

 Example 302. Antibodies to calpein, a membrane calcium-dependent proteinase that activates when the concentration of calcium ions near the postsynaptic membrane increases and cleaves fodrin. Using methods of neurochemical analysis, it was shown that antibodies to calpein, when introduced into the incubation medium in the form of a 1% solution in a homeopathic dilution of C200, cleave fodrin and release the active glutamate receptors, previously closed, bound by fodrin and thus increase the synapse conductivity.

 Example 303. Antibodies to phosphoprotein F 1-20. Using methods of neurochemical analysis, it was shown that antibodies to phosphoprotein F 1-20, when introduced into the incubation medium of rat neurons in the form of a 2% solution in homeopathic dilution C200, activate glutamate receptors and are, like fodrin, a substrate for calpein neuron.

Antibodies to non-enzymatic neurospecific proteins associated with the functions of vesicles in nerve endings
Example 304. Antibodies to synapsins (a family of phosphoproteins) associated with the functions of vesicles in nerve endings. It was shown that dephosphorylated synapsin, binding to the membranes of the vesicles, promotes their connection with actin filaments (actin), as a result of which a reserve, inactive pool is formed. Using methods of neurochemical analysis, it was shown that antibodies to synapsins, when introduced into the incubation medium of rat neurons in the form of a 2% solution in homeopathic dilution of C200, contribute to the phosphorylation of synapsins with increasing calcium concentration in the terminal, which reduces the affinity of synapsins to vesicle membranes, freeing them from communication with actin filaments, as a result of which the vesicle “melts” and passes from the reserve to the active state and ensures the release of norepinephrine into the medium.

 Example 305. Antibodies to synaptic proteins synaptobrevin, synaptophysin, synthexin, synaptogamine. Using methods of neurochemical analysis, it was shown that antibodies to these synaptic proteins, when introduced into the incubation medium in the form of a 2% solution in a homeopathic dilution of C200, regulate the melting process of the vesicles and modulate the release of dopamine from neurons in cell culture.

 Example 306. Antibodies to synaptoporin. Using methods of neurochemical analysis, it was shown that antibodies to synaptoporin, when introduced into the incubation medium of rat neurons in the form of a 1% solution in homeopathic dilution of C200, contribute to the formation of a pore, a channel through which the contents (neurotransmitter) of the vesicles exit. The environment increases by 30% the concentration of dopamine.

Antibodies to non-enzymatic neurospecific proteins responsible for adhesion and intercellular recognition processes
Example 307. Antibodies to glycoproteins consisting of peptide and carbohydrate moieties. Using methods of neurochemical analysis, it was shown that antibodies to glycoproteins when introduced into the incubation medium in the form of a 2% solution in homeopathic dilution of C200 stimulate the formation of specific contacts between neurons, their mutual recognition, facilitate synaptic transmission, memory formation.

 Example 308. Antibodies to surface glycoproteins involved in cell adhesion. Using methods of neurochemical analysis, it was shown that antibodies to D2, N-CAM, K4, BSP-2, when introduced into the incubation medium as a 1% solution in homeopathic dilution of C200, stimulate homotypic adhesion between neurons in rat cell culture by 20%.

 Example 309. Antibodies to glycoproteins Ng-CAM and L-1. Using methods of neurochemical analysis, it was shown that antibodies to the Ng-CAM and L-1 glycoproteins, when introduced into the incubation medium as a 2% solution in homeopathic dilution of C200, stimulate heterotypic calcium-independent adhesion between neurons and glial cells in cell culture.

 Example 310. Antibodies to glycoproteins located in postsynaptic seals and in areas of synaptic compounds. Using methods of neurochemical analysis, it was found that antibodies to glycoproteins NSA-3, MBA-2, Thy-1, when introduced into the incubation medium of rat neurons in the form of a 1% solution in homeopathic dilution of C200, are a substrate for proteinases and sialidases, causing local modifications of the glycoprotein structure in response to a change in the functional state of the synapse.

Cytoskeletal and contractile proteins of the nervous tissue
Example 311. Antibodies to neurotubulin, which is part of microtubules (neurotubules) - specific contractile proteins involved in self-assembly and decay, as well as in the transport of nucleic acids, proteins, lipids along the axon from the neuron body to synaptic endings. In vitro experiments using neurochemical analysis methods showed that antibodies to neurotubulin when introduced into the incubation medium in the form of a 1% solution in homeopathic dilution of C200 have phosphokinase and protein kinase activity.

 Example 312. Antibodies to neurosterol, related to actomyosin-like proteins (contractile proteins of the nervous tissue), which are part of the neurofilaments. Using methods of neurochemical analysis in studies on tissue culture, it was shown that antibodies to neurosterol when introduced into the incubation medium in the form of a 2% solution in homeopathic dilution of C200 have ATPase activity and stimulate the opening of vesicles, which contributes to the release of the neurotransmitter into the cytoplasm and synaptic cleft.

 Example 313. Antibodies to kinesin (contractile protein of neurons) are a cytoplasmic translator providing anterograde axonal current. In experiments using methods of neurochemical analysis, it was shown that antibodies to kinesin in homeopathic dilution of C200 hydrolyze ATP and the energy released is sufficient to move intracellular organelles along microtubules (in axons).

 Example 314. Antibodies to dynein. Using methods of neurochemical analysis, it was found that antibodies to dynein in homeopathic dilution of C200 provide a retrograde axonal current in the cell culture of rat hippocampal neurons.

 Example 315. Antibodies to spectrin and ankyrin are components of the cytoskeleton of a nerve cell, which, interacting with other proteins of the cytoskeleton, reduce the mobility of proteins in the membrane plane. In experiments on brain tissue culture by neurochemical analysis, it was shown that antibodies to spectrin in homeopathic dilution of C200 alter the distribution of potassium and sodium ions on the surface of the membranes of excitable cells.

 Example 316. Antibodies to the clathrin protein, forming a multicellular clathrin case in the form of a basket-like network on the surface of the vesicles and providing fast intracellular transport of substances. Using methods of neurochemical analysis in rat neuron culture, it was shown that antibodies to clathrin in homeopathic dilution of C200 provide internalization - entry into the cytoplasm of large groups of peptide receptors that bind to their ligand, i.e. carry out in a special way the introduction of information through the membrane into the cytoplasm of the cell.

Neurospecific proteins - enzymes
Example 317. Antibodies to protein 14-3-2 (enzyme enolase), which is localized in neurons. Protein 14-3-2, aldolase, arylsulfatase, and BB-isozyme creatine kinase are the brain isomers of known enzymes. Using methods of neurochemical analysis, it was shown that antibodies to these brain isomers of known enzymes in homeopathic dilution of C200 stimulate the synthesis and inhibit the degradation of norepinephrine in rat nerve cell culture.

Secreted regulatory and transport neurospecific proteins
Example 318. Antibodies to neurophysins (NF1, NFP, NFS) - proteins carriers of peptide regulators located in the posterior lobe of the pituitary gland and gitotalamus. In an intact state, NFs are in a strong complex with oxytocin or vasopressin and provide their protection. Using NMR, it was shown that antibodies to NF in homeopathic dilution of C200 enhance the fast (5 · 10 ^-8 s) exchange between the NF-oxytocin or NF-vasopressin complexes and the free hormone in the rat brain tissue homogenate.

 Example 319. Antibodies to secreted proteins ependymine. In experiments on goldfish, it was shown that antibodies to ependymines when administered 0.1 ml of a solution of antibodies in homeopathic dilution of C200 each time reinforce the adaptation of fish to new swimming conditions, which indicates their participation in the mechanisms of formation of long-term memory.

Antibodies to neurospecific glia proteins
Example 320. Antibodies to alpha2-glycoprotein and glial fibrillar acidic protein (GFA). Methods of neurochemical analysis showed the stimulating effect of antibodies in homeopathic dilution of C200 on the construction of myelin in rat nervous tissue culture.

Antibodies to regulators of growth and proliferation of nerve tissue
Antibodies to neurotrophins - growth and trophic factors
Example 321. Antibodies to nerve growth factor (NGF) located on cholinergic neurons. In experiments on white outbred rats, it was shown that administering to the animals antibodies to NGF orally in 0.1 ml of a solution in homeopathic dilution of C200 leads to an improvement in the learning process of the conditioned reflex of active avoidance of electric pain irritation in a two-section chamber. Under the influence of a substance, a decrease in latent periods of the reflex and a decrease in the number of combinations necessary to achieve the criterion for the development of a conditioned reflex are observed.

 Example 322. Antibodies to brain-specific neurotrophic factor (BDNF) located on cholinergic neurons. In vivo experiments showed that antibodies to BDNF after a single oral administration to rats of 0.1 ml of a solution of antibodies in homeopathic dilution of C200 stimulate neuronal transmission in the cortex, in particular, responses from II / III to the IY layer of the visual cortex, and this effect is blocked by K252a - a specific TrkB receptor blocker whose agonist is BDNF. The use of antibodies to BDNF modulates the increase in the level of AMPA receptor proteins, which indicates the effect of the substance on the process of converting silent neurons into functional ones.

 Example 323. Antibodies to neurotrophin 3 (NT-3), located on the hippocampal neurons. In experiments in vivo and in vitro by morphochemical methods, it was shown that antibodies to NT-3 support neuronal survival and growth of neurons, are involved in the restoration of connections between neurons during the development and maturation of nervous tissue and after trauma after a single oral administration to rats of 0.1 ml a solution of antibodies in homeopathic dilution C200.

 Example 324. Antibodies to neurotrophin 4/5 (NT4 / 5). In vivo and in vitro experiments have shown that antibodies to NT-4/5 support neuronal survival and are involved in the restoration of neuronal connections after trauma after a single oral administration to rats of 0.1 ml antibody solution in homeopathic dilution C200. Electrophysiological methods have shown that antibodies are involved in the process of synaptic plasticity by the type of prolonged potentiation.

 Example 325. Antibodies to erythropoietin. Patient T., 36 years old, with complaints of fatigue and weakness. The presence of a reduced level of hemoglobin made it possible to diagnose iron deficiency anemia. The use of antibodies to erythropoietin for 3 weeks orally in a 10 ml solution in homeopathic dilution of C400 2 times a day significantly reduced dizziness, fatigue, and increased hemoglobin level.

 Example 326. Antibodies to vascular growth factor. Patient A., 59 years old, with a diagnosis of coronary heart disease and arrhythmia, was prescribed 3 times a day for 2 weeks, antibodies to vascular growth factor, 1 teaspoon of the solution in homeopathic dilution C400. As a result of therapy, the patient's condition improved significantly, the severity of arrhythmia and angina pectoris decreased.

 Example 327. Antibodies to platelet growth factor. Patient S., 71 years old with multiple petechiae, received antibodies to platelet growth factor for two weeks. Course treatment (5 ml of a solution orally in a homeopathic dilution of C400 2 times a day for 7 days) led to a decrease in the formation of subcutaneous hemorrhage.

 Example 328. Antibodies to endothelial growth factor. In experiments on tissue culture by neurochemical methods, it was found that antibodies to endothelium, when introduced into the incubation medium in the form of a 2% solution in homeopathic dilution of C200, stimulate cell proliferation by 18%, which indicates the activation of endothelial growth.

Antibodies to cytokines, interleukins
Example 329. Antibodies to IL-1. It has been shown that a cytokine is synthesized in the brain when brain tissue is damaged or during infection. Using morphohistochemical methods, it was shown that under the influence of antibodies to IL-1, after oral administration to rats of 0.1 ml of a solution of antibodies in homeopathic dilution of C200 each rat, the synthesis of nerve growth factor increases and the neurovascularization of the brain improves.

 Example 330. Antibodies to IL-2, a cytokine that is synthesized in the brain when brain damage or infection occurs. On a model of brain injury in rats, it was shown that the introduction of antibodies to IL-2 before exposure to an oral solution of 0.1 ml of antibody solution in homeopathic dilution of C200 improved cerebral blood flow and prevented neurodegeneration after an injury, as evidenced by morphohistochemical studies.

 Example 331. Antibodies to IL-6 - a cytokine, which is synthesized in the brain with damage to brain tissue or infection. Using morphohistochemical methods, it was shown that the introduction of antibodies to IL-6 when they are introduced into the incubation medium in the form of a 2% solution in homeopathic dilution of C200 inhibits excitoxic lesions in the cell.

 Example 332. Antibodies to TNF-α-cytokine, which is synthesized in the brain with damage to brain tissue or infection. In a rat brain injury model, administration of anti-TNF-α antibodies orally with 0.1 ml of a solution of antibodies in homeopathic dilution of C200 improved cerebral blood flow and prevented neurodegeneration after injury, as evidenced by morphohistochemical studies.

Antibodies to Neuroimmunotrophins
Example 333. Antibodies to cerebrolysin. In experiments on the culture of nerve cells using neurochemical methods, it was found that antibodies to cerebrolysin, when introduced into the incubation medium in the form of a 2% solution in homeopathic dilution C200, have an inhibitory effect on calpain II, an enzyme that has a neurotoxic effect at the cell level in the pathological processing of APP - protein precursor ARβ.
Antibodies to cyclooxygenase 2 inhibitors (COX-2)
Example 334. Antibodies to rofexoxib. Patient K., aged 75 years, suffering from Alzheimer's disease, was prescribed orally antibodies to rofexoxib in 1 teaspoon of a solution in homeopathic dilution of C400 2 times a day for 30 days. The patient has improved memory for current events, attention, orientation in situations, increased overall life activity.

 Example 335. Antibodies to selexoxib. Patient M., aged 70, suffering from Alzheimer's disease, was prescribed 1 teaspoon of a solution of anti-selexoxib antibodies in a homeopathic dilution of C400 2 times a day for 4 months. The patient has improved memory for current events, attention, orientation in situations, increased overall life activity.

Antibodies to Neurotrophins
Example 336. Antibodies to lethrin. In experiments using neurochemical methods, it was found that antibodies to letrinin cause an increase in neurotrophic effects, an improvement in brain metabolism, and energy metabolism after a single oral administration to rats of 0.1 ml of an antibody solution in homeopathic dilution of C200.

 Example 337. Antibodies to SER-1347. In experiments using neurochemical methods, an increase in neurotrophic effects, an improvement in brain metabolism, and energy metabolism under the influence of antibodies to SER-1347 after a single oral administration to rats of 0.1 ml of antibody solution in homeopathic dilution C200 were established.

 Example 338. Antibodies to NDD-094. Under the influence of antibodies to NDD-094 in experiments using neurochemical methods, an increase in neurotrophic effects, an improvement in brain metabolism, and energy metabolism after a single oral administration to rats of 0.1 ml of a solution of antibodies in homeopathic dilution of C200 were established.

Antibodies to tertiary neural transmission messengers
Antibodies to inhibitors of NO synthetase (NOS)
Example 339. Antibodies to methyl ester of nitro-L-arginine (L-NAME). It was found that in the period immediately following brain ischemia, there is an increase in NO production in the vascular endothelium and perivascular nerves, which improves blood flow and promotes neuroprotection. Infusion with L-NAME antibodies intravenously at 0.1 ml in homeopathic dilution of C200 causes a decrease in the stroke zone and leads to an improvement in the electrocorticogram and cerebral blood flow in rats.

 Example 340. Antibodies to nitro-L-arginine (L-NA). Studies on mutant mice lacking the expression of endothelial or neuronal NOS isoforms on a stroke model with occlusion of the middle cerebral artery showed that administration of antibodies to L-NA orally with 0.1 ml of antibody solution in homeopathic dilution C200 reduces the size of the infarct zone and reduces neurological deficiency 24 hours after a stroke.

 Example 341. Antibodies to monomethyl-L-arginine (L-NMMA). On the model of ischemia of the middle cerebral artery in rats, it was shown that the administration of antibodies to L-NMMA orally in 0.1 ml of antibody solution in homeopathic dilution of C200 leads to a decrease in the infarction zone by 15% and neuroprotective effect.

Antibodies to Neuropeptides
Antibodies to hypothalamic liberins and statins
Antibodies to Liberians
Example 342. Antibodies to tyroliberin. The experiments were carried out on outbred white rats under the conditions of the method of forced swimming of rats in a vessel with freely rotating wheels, which is a modification of the Porsolt method and is used along with it to find substances with antidepressant activity. In accordance with it, rats are placed in a vessel with water, from which they unsuccessfully try to get out using the wheels. Wheel speed is a measure of antidepressant activity. As a result of the studies, it was found that 3-day administration to rats of 0.1 ml of a solution of antibodies to tyroliberin in homeopathic dilution of C200 orally, like antidepressants and stimulants, significantly increases the number of wheel revolutions. However, unlike stimulants and like antidepressants, they increase the correlation coefficient between the number of wheel revolutions in the first and second 5 min of observation. Thus, antibodies to tyroliberin have an antidepressant effect.

 Example 343. Antibodies to tyroliberin have a moderate activating effect. The experiments were carried out on outbred white rats, which were placed in groups of 5 individuals in the chamber of the Opto Varimex instrument (Columbus Instr., USA). The introduction of a single oral administration of 0.1 ml of a solution of antibodies to thyroliberin in homeopathic dilution of C200 increases (1.4 times) the number of movements of animals along the cell of the device.

 Example 344. Antibodies to tyroliberin exert the properties of an opioid antagonist. In outbred white male rats, morphine was used to induce analgesia, which was manifested by an increase in its thresholds of vocalization caused by electrical irritation of the base of the tail. Oral administration to rats of 0.1 ml of a solution of antibodies to tyroliberin in homeopathic dilution of C200 weakens the analgesic effect of morphine, as indicated by a decrease in pain response thresholds increased after administration of morphine.

 Example 345. Antibodies to corticoliberin. The experiments were carried out on outbred white rats, which were placed in groups of 5 individuals in the chamber of the Opto Varimex instrument (Columbus Instr., USA). A single oral administration of a solution of antibodies to corticoliberin in a homeopathic dilution of C400 with 0.1 ml orally increases (1.3 times) the number of movements of animals, increasing spontaneous motor activity.

 Example 346. Antibodies to gonadotropin. The experiments were carried out on white male rats, to which females were planted at the stage of oestrus or proestrus. It was found that the administration to rats of 0.1 ml of a solution of antibodies to gonadotropin orally in homeopathic dilution of C200 for 5 days significantly increased the erectile function of males, significantly and statistically significantly increasing the main indicators of this process (the number of cages with pressure and especially the cages with intromissions). Compared to control animals, in which, during the 30-minute observation period, there was almost no cage with intromissions, antibodies to gonadotropin caused not only their appearance, but also their significant number, most of which ended with the introduction of the penis into the vagina.

Antibodies to statins
Example 347. Antibodies to somatostatin. The experiments were performed on outbred white male rats, which in groups of 5 individuals were placed in the chamber of the Opto Varimex instrument (Columbus Instr., USA). It was found that antibodies to somatostatin when administered to rats orally with 0.1 ml of a solution in homeopathic dilution of C200 significantly (1.8 times) suppress the spontaneous motor activity of outbred white male rats, showing sedative properties.

 Example 348. Antibodies to melanostatin. The experiments were carried out on outbred white rats under the conditions of the method of forced swimming of rats in a vessel with freely rotating wheels, which is a modification of the Porsolt method and is used along with it to find substances with antidepressant activity. In accordance with it, rats are placed in a vessel with water, from which they unsuccessfully try to get out using the wheels. Wheel speed is a measure of antidepressant activity. As a result of the studies, it was found that the administration to rats for 5 days of oral administration of 0.1 ml of a solution of antibodies to melanostatin in homeopathic dilution of C200, like antidepressants and stimulants, significantly increases the speed of the wheels. However, unlike stimulants and like antidepressants, antibodies increase the correlation coefficient between the number of wheel revolutions in the first and second 5 min of observation. Thus, antibodies to melanostatin have an antidepressant effect.

 Example 349. Antibodies to melanostatin. The experiments were performed on outbred white male rats, which in groups of 5 individuals were placed in the chamber of the Opto Varimex instrument (Columbus Instr., USA). It was found that antibodies to melanostatin, once administered to rats orally in a dose of 0.1 ml in a solution in homeopathic dilution C200, activate (1.4 times) the behavior of rats, increasing spontaneous motor activity.

Antibodies to Opioid Peptides
Enkephaline Opioid Antibodies
Example 350. Antibodies to met-enkephalin. The experiments were performed on outbred white male rats under the conditions of the methodology for assessing the pain threshold for the occurrence of vocalization during electrical stimulation of the base of the tail. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before electrostimulation. It was found that antibodies to met-enkephalin increase (by 30%) the thresholds of pain reaction, thus exerting an analgesic effect.

 Example 351. Antibodies to leukenkephalin. The experiments were performed on outbred white male rats under the conditions of the methodology for assessing the pain threshold for the occurrence of vocalization during electrical stimulation of the base of the tail. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C400 before electrostimulation. It was found that antibodies to leu-enkephalin increase (by 35%) the thresholds of a pain reaction, thus exerting an analgesic effect.

 Example 352. Antibodies to leukenkephalin. The experiments were carried out on outbred white male rats with electrodes implanted in the zones of positive reinforcement of the hypothalamus, under the conditions of a self-stimulation technique with pressing the lever to obtain positive reinforcement. Rats were orally administered with 0.1 ml of homeopathic dilution of C200 antibody solution for 7 days. It was found that antibodies to leu-enkephalin facilitate the self-stimulation reaction, increasing the number of clicks on the lever by 2.1 times, which indicates the activation of positive reinforcement systems under their influence.

 Example 353. Antibodies to β-endorphin. The experiments were performed on outbred white male rats under the conditions of the methodology for assessing the pain threshold for the occurrence of vocalization during electrical stimulation of the base of the tail. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before electrostimulation. It was found that antibodies to β-endorphin have an analgesic effect, increasing (by 1.4 times) the thresholds of vocalization caused by electro-irritation of the tail.

 Example 354. Antibodies to β-endorphin. The experiments were carried out on outbred white male rats with electrodes implanted in the zones of positive reinforcement of the hypothalamus, under the conditions of a self-stimulation technique with pressing the lever to obtain positive reinforcement. Rats were orally administered with 0.1 ml of homeopathic dilution of C200 antibody solution for 5 days. It was found that antibodies to β-endorphin facilitate the self-stimulation reaction, increasing the number of lever presses by 1.7 times, which indicates the activation of positive reinforcement systems under their influence.

 Example 355. Antibodies to β-endorphin. The experiments were carried out on outbred white male rats under the conditions of the technique for developing a conditioned passive avoidance reflex. It was established that antibodies to β-endorphin have an amnestic effect. The rats of the control groups remember that the usually preferred dark compartment of the chamber becomes dangerous, and do not go into it during testing, as evidenced by the long latent period of the first entry into the dark chamber and the short residence time in it. Animals that received antibodies to β-endorphin orally in 0.1 ml of solution in homeopathic dilution of C400 after developing a reflex on the first day of the experiment, on the contrary, go into the dark compartment with a short latent period and spend a long time in it. This indicates the formation of retrograde amnesia under the influence of β-endorphin.

 Example 356. Antibodies to γ-endorphin. The experiments were performed on outbred white male rats under the conditions of a method for assessing the ability of antibodies to γ-endorphin to induce catalepsy in animals - fading in uncomfortable positions, characteristic of antipsychotics. Rats were once orally administered with 0.1 ml of homeopathic dilution of C200 antibody solution. It was found that antibodies to γ-endorphin have a moderate antipsychotic effect, since moderate catalepsy developed under their influence - the animals died in a pose when the fore and hind limbs were fixed at a height of 5 cm above the surface of the experimental table.

 Example 357. Antibodies to α-endorphin. The experiments were performed on outbred white male rats, which were placed in groups of 5 individuals in the chamber of an Opto Varimex instrument (Columbus Instr., USA) to assess the effect of the substance on spontaneous locomotor activity. Rats were orally administered 0.1 ml of antibody solution in homeopathic dilution of C400 for 5 days. It was found that antibodies to the neuropeptide cause activation of animal behavior, increasing (1.5 times) the number of movements in the recorder chamber.

 Example 358. Antibodies to α-neoendorphin. The experiments were performed on outbred white male rats under the conditions of the methodology for assessing the pain threshold for the occurrence of vocalization during electrical stimulation of the base of the tail. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before electrostimulation. It was found that antibodies to α-neoendorfin have a pronounced analgesic effect, increasing 1.3 times the thresholds of the pain reaction.

 Example 359. Antibodies to α-neoendorphin. The experiments were performed on outbred white male rats under open field techniques. Rats were once orally administered with 0.1 ml of homeopathic dilution of C200 antibody solution. It was found that antibodies to α-neoendorphin inhibit the behavior of animals in an open field, in particular vertical activity, reducing it by 1.5 times, and examining holes, which indicates a decrease in research behavior.

 Example 360. Antibodies to dinorphin. The experiments were carried out on outbred white male rats in groups of 5 individuals, each placed in the chamber of an Opto Varimex instrument (Columbus Instr., USA). Rats were once orally administered with 0.1 ml of homeopathic dilution of C200 antibody solution. It was shown that antibodies to dinorphin inhibit the locomotor (motor) activity of animals 1.4 times, which indicates the presence of a sedative component in its mechanism of action.

 Example 361. Antibodies to dinorphin. The experiments were performed on outbred white male rats under open field conditions. Rats were orally administered with 0.1 ml antibody solution in homeopathic dilution of C200 for 4 days. As a result of the studies, it was found that antibodies to dinorphin significantly inhibit the behavior of animals in an open field, and all its components are suppressed. This suggests that antibodies to dinorphin exhibit a sedative effect.

 Example 362. Antibodies to met-enkephalin-RGL and met-enkephalin-RF. The experiments were performed on outbred white male rats under the conditions of the methodology for assessing the analgesic effect of morphine. Morphine analgesia was judged by an increase in pain threshold. The criterion for the pain response was vocalization, which occurs in response to electrical stimulation of the base of the tail. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before electrostimulation. It was found that antibodies to both substances reduce (1.7 times) the thresholds for pain reactions increased under the influence of morphine, that is, they exhibit the properties of opioid antagonists.

Antibodies to Melanocortins
Antibodies to Corticotropins
Example 363. Antibodies to adrenocorticotropin. The experiments were carried out on outbred white male rats under the conditions of the technique for developing a conditioned passive avoidance reflex. It was established that the rats of the control group on the day of testing remember that the day before they received punishment in a dark cell. Therefore, they enter it with a long latent period and spend little time in it. Rats were orally administered 0.1 ml of antibody solution in homeopathic dilution of C200 for 5 days. Animals receiving antibodies to adrenocorticotropin enter the dark chamber with an even longer latent period and spend even less time in it. This indicates the activation of memorization processes under the influence of a substance.

Antibodies to melanotropins
Example 364. Antibodies to α-melanotropin. The experiments were performed on outbred white male rats, which in groups of 5 individuals were placed in the chamber of the Opto Varimex instrument (Columbus Instr., USA). Rats were once orally administered with 0.1 ml of homeopathic dilution of C200 antibody solution. It was found that antibodies to α-melanotropin increase (by 30%) the number of movements of animals, which indicates the possibility of the presence of an activating component in the spectrum of their pharmacological activity.

 Example 365. Antibodies to α-melanotropin. The experiments were performed on outbred white male rats under open field conditions. Rats were orally administered with 0.1 ml of a solution of antibodies in homeopathic dilution C200 10 days. It was found that the antibody preparation increases motor activity, including vertical (by 40%). This indicates activation under his influence of emotional behavior.

 Example 366. Antibodies to α-melanotropin. The experiments were carried out on outbred white male rats under the conditions of the technique for developing a conditioned passive avoidance reflex. Rats were orally administered with 0.1 ml of antibody solution in homeopathic dilution of C200 for 7 days. It has been established that antibodies to α-melanotropin improve memory processes. As indicated earlier, the rats in the control group remember that the usually preferred dark compartment has become dangerous. For this reason, they enter it with a high latency period and spend little time in it. Antibodies to α-melanotropin further increase the latency period of the first entry into the dark chamber and shorten the time spent in it. Therefore, they stimulate the processes of memorization.

Antibodies to vasopressin-tocin
Antibodies to vasopressins
Example 367. Antibodies to vasopressin. The experiments were carried out on outbred white male rats under the conditions of the technique for developing a conditioned passive avoidance reflex. To cause amnesia, convulsions were used, caused by maximum electric shock immediately after the development of a reflex. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before electrostimulation. It has been established that antibodies to vasopressin have an antiamnestic effect. The rats of the control group remember that the usually preferred dark compartment of the chamber becomes dangerous, and do not go into it during testing, as evidenced by the long latent period of the first entry into the dark chamber and the short residence time in it. The animals receiving the maximum electric shock after developing a reflex on the first day of the experiment, on the contrary, enter the dark compartment with a short latent period and spend a long time in it. This indicates the formation of retrograde amnesia under the influence of maximum electric shock. Rats that received antibodies to vasopressin along with the maximum electroshock, like control animals of the first group, remembered the punishment received the day before in a dark chamber, and entered it with a long latent period and spent little time in it. This indicates activation under the influence of antibodies to vasopressin of memory consolidation, impaired by maximum electroshock.

Tocin Antibodies
Example 368. Antibodies to oxytocin. The experiments were carried out on outbred white male rats under the conditions of the technique for developing a conditioned passive avoidance reflex. Rats were orally administered with 0.1 ml of antibody solution in homeopathic dilution of C200 for 7 days. It was established that antibodies to oxytocin have a proamnestic effect, making it difficult to develop a conditioned reflex of passive avoidance. This is indicated by a decrease in the duration of the latent period in the dark compartment of the chamber and an increase in the duration of stay in it in animals treated with oxytocin, compared with the control.

Antibodies to Pancreatic Peptides
Example 369. Antibodies to neuropeptide Y. The experiments were performed on outbred white male rats using a conflict situation technique in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before electrostimulation. It was found that the administration of anti-neuropeptide Y antibodies to rats increases (by a factor of 2.3) the number of water taken from the drinker, despite the receipt of pain irritation (punished by the rat taking water), which indicates the anxiolytic effect of antibodies to the substance.

Antibodies to peptides similar to gastrin
Example 370. Antibodies to cholecystokinin-8. The experiments were carried out on outbred white male rats under the conditions of a method for evaluating the cataleptogenic effect of a substance — its ability to make a rat maintain an uncomfortable posture. Rats were once orally administered with 0.1 ml of homeopathic dilution of C200 antibody solution. Antibodies to cholecystokinin-8 have been found to cause moderate catalepsy. After their introduction, the rat freezes on the crossbars at a height of 5 cm above the experimental table. Thus, antibodies to cholecystokinin-8 exhibit antipsychotic properties.

 Example 371. Antibodies to cholecystokinin-4. The experiments were carried out on outbred white male rats using the technique of a conflict situation in which rats subjected to drinking deprivation are punished by electric shock when trying to satisfy their thirst. Rats were orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before electrostimulation. It was found that administration of anti-cholecystokinin-4 antibodies to rats increases (by 75%) the number of water taken from the drinker, despite receiving pain irritation (punished by rat water taking), which indicates the anxiolytic effect of antibodies to the substance.

Antibodies to tachykinins
Example 372. Antibodies to substance P. The experiments were carried out on outbred male white rats, in which, using the electrophysiological method, acute conditions were used to record evoked potentials (primary responses) arising in the sensorimotor cortex of white rats during peripheral electrical stimulation. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C400 before electrostimulation. It was found that antibodies to substance P reduce the amplitude of evoked potentials. Thus, they affect the conduct of sensory impulses.

Antibodies to Neurotensins
Example 373. Antibodies to neurotensin. The experiments were carried out on outbred white male rats with electrodes implanted in the zones of positive reinforcement of the hypothalamus, under the conditions of a self-stimulation technique with pressing the lever to obtain positive reinforcement. Rats were orally administered 0.1 ml of antibody solution in homeopathic dilution of C200 for 5 days. It has been established that antibodies to neurotensin facilitate the self-stimulation reaction, increasing the number of clicks on the lever by 2.5 times, which indicates the activation of positive reinforcement systems under their influence.

Antibodies to bombesins
Example 374. Antibodies to bombesin. The experiments were performed on outbred white male rats under conditions of a rectal temperature recording procedure. Rats were once orally administered with 0.1 ml of homeopathic dilution of C200 antibody solution. It was found that antibodies to bombesin have a significant hypothermic effect, significantly (by 20%) lowering body temperature 1 hour after administration.

Antibodies to kinins
Example 375. Antibodies to bradykinin. The experiments were carried out on outbred white male rats, in which, under the conditions of a sharp experiment, the spontaneous activity of sensitive spinal cord neurons was recorded by electrophysiological methods. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before the introduction of the electrodes. It was found that antibodies to bradykinin cause a significant increase in the spontaneous impulse of sensitive spinal cord neurons, which indicates the effect of antibodies to the substance on the modulation of pain sensitivity.

Antibodies to Angiotensins
Example 376. Antibodies to angiotensin II. The experiments were performed on outbred white male rats in which the pressure in the caudal artery was measured using an implanted catheter. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before measuring pressure. It was found that antibodies to angiotensin II cause significant (15%) hypertension.

 Example 377. Antibodies to angiotensin II. The experiments were performed on outbred white male rats, which were kept in cages with free access to drinking bowls. Rats were orally administered with 0.1 ml of antibody solution in homeopathic dilution of C200 for 3 days. It was found that antibodies to angiotensin II cause thirst, as indicated by the activation under their influence of drinking behavior and an increase in the volume of fluid consumed.

Antibodies to endozepines
Example 378. Antibodies to endosepine. The experiments were performed on outbred white male rats under the conditions of a technique of a conflict situation caused by electric shock. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before electrostimulation. It was found that antibodies to endosepine reduce the number of punishable water intake in rats in a conflict situation compared with the control. This suggests that they have anxiogenic, pro-conflict action.

Example 379. Antibodies to DBI (peptide - diazepam binding inhibitor). Experiments to study the effect of antibodies to DBI on GABA _A receptors were performed on a culture of central mammalian brain neurons using intracellular microelectrodes. It was found that antibodies to DBI when introduced into the incubation medium in the form of a 2% solution in homeopathic dilution of C200 cause a reversible decrease in the responses of neurons to the applied GABA, exhibiting the properties of its antagonist.

Antibodies to galanin
Example 380. Antibodies to galanin. The experiments were performed on outbred white male rats housed in cages with free access to food and water. Rats were orally administered with 0.1 ml antibody solution in homeopathic dilution of C200 for 4 days. It was found that antibodies to galanin stimulate eating behavior and increase the amount of food consumed by 20%.

Antibodies to the peptide - inducer of slow wave sleep (DSIP)
Example 381. Antibodies to DSIP. The experiments were carried out using electrophysiological methods in conditions of free behavior on outbred white male rats with electrodes implanted in the cerebral cortex, hippocampus and cervical muscles. Rats were orally administered 0.1 ml of antibody solution in homeopathic dilution of C200 for 5 days. When registering sleep-wake cycles, it was found that antibodies to DSIP reduce the duration of wakefulness and increase the percentage of slow-wave sleep, without affecting the duration of fast (paradoxical) sleep.

Antibodies to Prolyl Endopeptidase Inhibitors
Example 382. Antibodies to Z-pyroglutamyl proline. In experiments on rats, it was shown that antibodies to Z-pyroglutamyl-proinal have a pronounced antiamnestic effect. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before electrostimulation. The substance, when administered once, eliminates the amnesia caused by the maximum electroconvulsive seizure immediately after learning the conditioned reflex of passive avoidance in the dark-light chamber test. Under the influence of the substance, the latent time of entry into the dark dangerous compartment increased and the time spent in it decreased.

 Example 383. The antibody to the proline derivative is Ono-1603. The studies were carried out in experiments on old rats aged 24 months, in which there was a deterioration in the formation of a commemorative trace and neurological deficits. The three-month administration of 0.1 ml of anti-Ono-1603 antibodies orally in homeopathic dilution of C400 caused a significant improvement in the learning process of the conditioned reflex of active avoidance in the shuttle box bilateral chamber, which was manifested in a faster reflex with shorter latent periods and eliminated nephrological deficits.

 Example 384. Antibodies to JTP-4819. The studies were carried out in experiments on adult rats with impaired memory, which was caused by the introduction of scopolamine. It was shown that antibodies to JTP-4819 had a pronounced and statistically significant antiamnestic effect. Rats were once orally administered with 0.1 ml of homeopathic dilution of C200 antibody solution before scopolamine administration. The substance, when administered once, eliminated the amnesia caused by the introduction of scopolamine immediately before learning the conditioned reflex of passive avoidance in the dark-light chamber test. Under the influence of the substance, the latent time of entry into the dangerous dark chamber increased and the time spent there was reduced.

 Example 385. Antibodies to S-17092-1. In experiments on old rats 24 months old, in which learning processes were impaired, it was found that the administration of antibodies to S-17092-1 orally in the form of a solution in homeopathic dilution of C200 in 0.1 ml for 3 months caused a significant improvement in the learning process of conditioned reflex active avoidance in the double-sided shuttle-box chamber, which was expressed in a faster execution of the reflex with shorter latent periods.

Antibodies to substances with antioxidant mechanism of action
Example 386. Antibodies to alpha tocopherol. A patient M. with muscular dystrophy was prescribed a course (3 months) of antibodies to alpha-tocopherol (1 teaspoon 2 times a day in homeopathic dilution C200). The patient's condition improved, muscle mass increased, indicators of neuromuscular conduction improved, mood and general well-being improved.

 Example 387. Antibodies to uric acid. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before experimental hypoxia of the brain. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery for 48 hours, it was found that the introduction of antibodies to uric acid reduces the infarction zone by 50%.

 Example 388. Antibodies to CP traps PBN, DMPO. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before ischemic exposure. In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery for 48 hours, it was found that the introduction of antibodies to CP-traps PBN, DMPO reduces the infarction zone by 45 and 55%, respectively.

 Example 389. Antibodies to catechin-flavinoid. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 75% hippocampal cell death and increased free radical oxidation processes. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before vascular compression. The introduction of antibodies to the catechin-flavinoid led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 30%, and an antioxidant effect.

 Example 390. Antibodies to Recombinant Superoxide Dismutase. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 5 minutes, which caused 80% death of C1 hippocampal cells. Rats were orally administered with 0.1 ml antibody solution in homeopathic dilution of C400 prior to ischemia. The introduction of antibodies to recombinant superoxide dismutase led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 25%.

 Example 391. Antibodies to liposomal superoxide dismutase. Prior to the experiment, 0.1 ml of a solution of antibodies in homeopathic dilution of C200 was orally administered to rats once. In an experiment on outbred white rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that administration of antibodies to liposomal superoxide dismutase reduces the infarction zone by 40%.

 Example 392. Antibodies to MCI-186. A model of global cerebral ischemia was used in experiments on rats with complete vascular constriction for 10 minutes, which caused 70% death of the pyramidal C1 hippocampal cells and activation of free radical processes. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before ischemia. The introduction of antibodies to MCI-186 led to a neuroprotective effect, which was expressed in the restoration of hippocampal cells by 50% and a decrease in free radical oxidation.

 Example 393. Antibodies to U-74006F (21 aminosteroids). In an experiment on white outbred rats using a model of focal cerebral ischemia with compression of the middle cerebral artery, it was found that the introduction of antibodies to U-74006F reduces the infarction zone and reduces hippocampal cell damage by 30%. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before ischemic exposure.

 Example 394. Antibodies to desmethyldeprenyl. Rats were once orally administered with 0.1 ml of a solution of antibody in homeopathic dilution of C200 before squeezing the cerebral arteries. Using morphohistochemical methods, it was found that administration of antibodies to desmethyldepenyl reduces neuronal apoptosis caused by experimental cerebral ischemia and causes activation of a new protein synthesis.

 Example 395. Antibodies to N-acetylcysteine. Rats were once orally administered with 0.1 ml of a solution of homeopathic dilution of C400 antibody before ischemic exposure. Using morphohistochemical methods, it was found that the administration of antibodies to N-acetylcysteine reduces neuronal apoptosis by 50% and causes the activation of new protein synthesis in preapoptotic nerve cells after clamping the cerebral arteries.

Claims (135)

 1. A drug for providing a neuropsychotropic effect, characterized in that it contains an activated form of ultra-low doses of monoclonal, polyclonal immune antibodies to an exogenous or endogenous substance that has a neuropsychotropic effect, while the activated form is obtained by repeated serial dilution and external exposure mainly by homeopathic technology.  2. The drug according to claim 1, characterized in that use antibodies to acetylcholinesterase inhibitors.  3. The drug according to claim 1, characterized in that use antibodies to M1 agonists of the acetylcholine subtype of the receptor.  4. The drug according to claim 1, characterized in that the use of antibodies to antagonists of M1 acetylcholine receptor subtype.  5. The drug according to claim 1, characterized in that use antibodies to antagonists of M2 acetylcholine receptor subtype.  6. The drug according to claim 1, characterized in that use antibodies to antagonists of M3 acetylcholine receptor subtype.  7. The drug according to claim 1, characterized in that use antibodies to antagonists of M4 acetylcholine receptor subtype.  8. The drug according to claim 1, characterized in that use antibodies to nicotinic receptor agonists.  9. The drug according to claim 1, characterized in that antibodies are used to substances that increase the concentration of acetylcholine in the synaptic cleft.  10. The drug according to claim 1, characterized in that use antibodies to endogenous ligands of glutamate receptors.  11. The drug according to claim 1, characterized in that the use of antibodies to competitive antagonists of NMDA receptors.  12. The drug according to claim 1, characterized in that use antibodies to non-competitive antagonists of NMDA receptors.  13. The drug according to claim 1, characterized in that use antibodies to blockers of the NMDA receptor channel.  14. The drug according to claim 1, characterized in that the use of antibodies to antagonists of the glycine site of the glutamate receptor.  15. The drug according to claim 1, characterized in that the use of antibodies to agonists of the glycine site of the glutamate receptor.  16. The drug according to claim 1, characterized in that antibodies are used to antagonists of the polyamine portion of the NMDA receptor complex and NMDAR2B-selective antagonists.  17. The drug according to claim 1, characterized in that use antibodies to agonists, antagonists and positive modulators of AMPA receptors. 18. The drug according to claim 1, characterized in that use antibodies to substances that enhance the function of GABA _A -ergic system. 19. The drug according to claim 1, characterized in that the use of antibodies to agonists of GABA _A receptors.  20. The drug according to claim 1, characterized in that the use of antibodies to GABA deactivation inhibitors.  21. The drug according to claim 1, characterized in that use antibodies to substances that increase the content of GABA.  22. The drug according to claim 1, characterized in that use antibodies to benzodiazepine receptor agonists.  23. The drug according to claim 1, characterized in that antibodies are used to complete agonists of benzodiazepine receptors.  24. The drug according to claim 1, characterized in that use antibodies to partial agonists of benzodiazepine receptors.  25. The drug according to claim 1, characterized in that use antibodies to the inverse (inverse) agonists of benzodiazepine receptors.  26. The drug according to claim 1, characterized in that the use of antibodies to antagonists of benzodiazepine receptors. 27. The drug according to claim 1, characterized in that use antibodies to substances that weaken the function of GABA _A -ergic system. 28. The drug according to claim 1, characterized in that the use of antibodies to antagonists of GABA _A receptors. 29. The medicine according to claim 1, characterized in that antibodies are used against the GABA _A receptor chlorine channel blockers.  30. The drug according to claim 1, characterized in that the use of antibodies to inhibitors of the synthesis of GABA. 31. The drug according to claim 1, characterized in that antibodies are used to substances that enhance the function of GABA _B- ergic system. 32. The drug according to claim 1, characterized in that the use of antibodies to GABA _B receptor agonists. 33. The drug according to claim 1, characterized in that antibodies are used to substances that weaken the function of GMAK _B- ergic system. 34. The drug according to claim 1, characterized in that the use of antibodies to GABA _B receptor blockers.  35. The drug according to claim 1, characterized in that the use of antibodies to dopamine receptor antagonists. 36. The drug according to claim 1, characterized in that the use of antibodies to dopamine receptor antagonists of type D ₂ . 37. The drug according to claim 1, characterized in that antibodies are used against dopamine receptor antagonists of type D ₃ . 38. The drug according to claim 1, characterized in that the use of antibodies to dopamine receptor antagonists of type D ₂ -D ₄ . 39. The drug according to claim 1, characterized in that antibodies are used against dopamine receptor antagonists of type D ₁ and D ₅ .  40. The drug according to claim 1, characterized in that the use of antibodies to dopamine receptor agonists. 41. The drug according to claim 1, characterized in that antibodies are used against dopamine receptor agonists of type D ₂ -D ₄ . 42. The drug according to claim 1, characterized in that antibodies are used against dopamine receptor agonists of type D ₂ -D ₃ . 43. The drug according to claim 1, characterized in that the use of antibodies to dopamine receptor agonists of type D ₃ -D ₄ . 44. The drug according to claim 1, characterized in that antibodies are used against dopamine receptor agonists of type D ₁ -D ₅ .  45. The drug according to claim 1, characterized in that the use of antibodies to dopamine precursors.  46. The drug according to claim 1, characterized in that antibodies are used against serotonergic receptor agonists. 47. The drug according to claim 1, characterized in that antibodies are used to agonists of serotonin receptors of type 5-HT _1A . 48. The drug according to p. 1, characterized in that the use of antibodies to serotonin receptor agonists of type 5HT _1b . 49. The drug according to claim 1, characterized in that antibodies are used to agonists of serotonin receptors of type 5HT _1d . 50. The drug according to claim 1, characterized in that antibodies are used to agonists of serotonin receptors of type 5HT _2A . 51. The drug according to claim 1, characterized in that antibodies are used against serotonin receptor agonists of type 5HT _2c . 52. The drug according to claim 1, characterized in that antibodies are used to agonists of serotonin receptors of type 5HT ₃ .  53. The drug according to claim 1, characterized in that antibodies are used to antagonists of serotonergic receptors. 54. The drug according to claim 1, characterized in that antibodies are used to antagonists of serotonin receptors of type 5HT _1A . 55. The drug according to claim 1, characterized in that antibodies are used against serotonin receptor antagonists of type 5HT _1b . 56. The drug according to p. 1, characterized in that the use of antibodies to serotonin receptor antagonists of type 5HT _1d . 57. The drug according to claim 1, characterized in that antibodies are used against serotonin receptor antagonists of type 5HT _2a . 58. The drug according to claim 1, characterized in that antibodies are used to antagonists of serotonin receptors of type 5HT _2b . 59. The drug according to claim 1, characterized in that antibodies are used to agonists of serotonin receptors of type 5HT _2C . 60. The drug according to claim 1, characterized in that antibodies are used to agonists of serotonin receptors of type 5HT ₃ .  61. The drug according to claim 1, characterized in that the use of antibodies to adrenergic receptor agonists. 62. The drug according to claim 1, characterized in that antibodies are used to agonists of α ₁ -adrenergic receptors. 63. The drug according to p. 1, characterized in that the use of antibodies to agonists of α ₂ -adrenergic receptors.  64. The drug according to claim 1, characterized in that antibodies are used to agonists of β-adrenergic receptors.  65. The drug according to p. 1, characterized in that the use of antibodies to antagonists of adrenergic receptors. 66. The drug according to claim 1, characterized in that the use of antibodies to antagonists of α ₁ -adrenergic receptors. 67. The drug according to claim 1, characterized in that the use of antibodies to antagonists of α ₂ -adrenergic receptors. 68. The drug according to p. 1, characterized in that the use of antibodies to antagonists of β ₁ -adrenergic receptors. 69. The drug according to p. 1, characterized in that the use of antibodies to antagonists of β ₂ -adrenergic receptors. 70. The drug according to claim 1, characterized in that the use of antibodies to antagonists of β ₃ -adrenergic receptors. 71. The drug according to claim 1, characterized in that the use of antibodies to antagonists of β ₄ -adrenergic receptors. 72. The medicine according to claim 1, characterized in that antibodies to adenosine substances (P ₁ purinergic) are used. 73. The drug according to claim 1, characterized in that antibodies are used against a ₁ adenosine receptor agonists. 74. The drug according to p. 1, characterized in that the use of antibodies to antagonists of A ₁ adenosine receptors. 75. The drug according to p. 1, characterized in that the use of antibodies to agonists A _2A adenosine receptors. 76. The drug according to p. 1, characterized in that the use of antibodies to antagonists of A _2A adenosine receptors. 77. The drug according to claim 1, characterized in that antibodies are used against A _2B adenosine receptor agonists. 78. The drug according to p. 1, characterized in that the use of antibodies to antagonists of A _2B adenosine receptors. 79. The drug according to claim 1, characterized in that antibodies are used against agonists of A ₃ adenosine receptors. 80. The drug according to p. 1, characterized in that the use of antibodies to antagonists of A ₃ adenosine receptors. 81. The medicine according to claim 1, characterized in that antibodies to P ₂ purinergic receptors are used. 82. The medicine according to claim 1, characterized in that antibodies to P _2X purinoreceptor agonists are used. 83. The drug according to claim 1, characterized in that antibodies are used against P _2X purinoreceptor antagonists. 84. The medicine according to claim 1, characterized in that antibodies to P _2Y purinoreceptor agonists _are used. 85. The drug according to claim 1, characterized in that antibodies are used against P _2Y purinoreceptor antagonists. 86. The medicine according to claim 1, characterized in that antibodies to P _2U purinoreceptor agonists are used. 87. The drug according to claim 1, characterized in that antibodies are used against P _2T purinoreceptor agonists. 88. The drug according to claim 1, characterized in that antibodies are used against P _2T purinoreceptor antagonists. 89. The medicine according to claim 1, characterized in that antibodies to P _2Z purinoreceptor agonists are used.  90. The drug according to claim 1, characterized in that the use of antibodies to histamine receptor agonists. 91. The drug according to claim 1, characterized in that the use of antibodies to histamine H ₁ receptor agonists. 92. The drug according to claim 1, characterized in that the use of antibodies to histamine H ₂ receptor agonists. 93. The drug according to claim 1, characterized in that the use of antibodies to histamine H ₃ receptor agonists.  94. The drug according to claim 1, characterized in that the use of antibodies to histamine receptor antagonists. 95. The drug according to claim 1, characterized in that antibodies are used against histamine H ₁ receptor antagonists. 96. The drug according to claim 1, characterized in that antibodies are used against histamine H ₂ receptor antagonists. 97. The drug according to claim 1, characterized in that antibodies are used against histamine H ₃ receptor antagonists.  98. The drug according to claim 1, characterized in that antibodies are used against histamine release inhibitors.  99. The drug according to claim 1, characterized in that antibodies are used against activators of diamine oxidase, the histamine deactivation enzyme.  100. The drug according to claim 1, characterized in that use antibodies to dopamine reuptake inhibitors.  101. The drug according to claim 1, characterized in that the use of antibodies to norepinephrine reuptake inhibitors.  102. The drug according to claim 1, characterized in that the use of antibodies to serotonin reuptake inhibitors.  103. The drug according to claim 1, characterized in that the use of antibodies to GABA reuptake inhibitors.  104. The drug according to claim 1, characterized in that use antibodies to substances that affect the function of calcium channels.  105. The drug according to claim 1, characterized in that use antibodies to substances that affect the function of calcium channels of the L-type.  106. The drug according to claim 1, characterized in that the use of antibodies to L-type calcium channel agonists.  107. The drug according to claim 1, characterized in that use antibodies to calcium blockers.  108. The drug according to claim 1, characterized in that use antibodies to L-type calcium channel antagonists.  109. The drug according to claim 1, characterized in that the use of antibodies to antagonists of calcium channel N-type.  110. The drug according to claim 1, characterized in that the use of antibodies to antagonists of calcium channel P-type.  111. The drug according to claim 1, characterized in that the use of antibodies to antagonists of calcium channels of Q-type.  112. The drug according to claim 1, characterized in that use antibodies to hypothalamic liberins and statins.  113. The drug according to claim 1, characterized in that use antibodies to liberins.  114. The drug according to claim 1, characterized in that the use of antibodies to statins.  115. The drug according to claim 1, characterized in that the use of antibodies to opioid peptides.  116. The drug according to claim 1, characterized in that use antibodies to enkephalin opioids.  117. The drug according to claim 1, characterized in that use antibodies to melanocortins.  118. The medicine according to claim 1, characterized in that antibodies to corticotropins are used.  119. The drug according to claim 1, characterized in that use antibodies to melanotropins.  120. The medicine according to claim 1, characterized in that antibodies to vasopressin-tocins are used.  121. The drug according to claim 1, characterized in that antibodies to vasopressins are used.  122. The drug according to claim 1, characterized in that use antibodies to tocins.  123. The drug according to claim 1, characterized in that the use of antibodies to "pancreatic" peptides.  124. The drug according to claim 1, characterized in that use antibodies to peptides similar to gastrin.  125. The drug according to claim 1, characterized in that use antibodies to tachykinins.  126. The drug according to claim 1, characterized in that the use of antibodies to neurotensins.  127. The drug according to claim 1, characterized in that use antibodies to bombesins.  128. The drug according to claim 1, characterized in that use antibodies to kinins.  129. The drug according to claim 1, characterized in that use antibodies to angiotensins.  130. The drug according to claim 1, characterized in that use antibodies to endosepins.  131. The drug according to claim 1, characterized in that use antibodies to galanin.  132. The drug according to claim 1, characterized in that use antibodies to the peptide - inducer of slow wave sleep (DSIP).  133. The drug according to claim 1, characterized in that use antibodies to prolyl endopeptidase inhibitors.  134. The drug according to claim 1, characterized in that use antibodies to substances with an antioxidant mechanism of action.  135. The medicine according to claims 1-134, characterized in that mixtures of various, mainly hundred, homeopathic dilutions are used.