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Keywords: alcohol, a nervous tissue, a CNS, nervous system, ethanol, alcohol, a histology, the abstract, the report, alkogolizm, a destruction of neurones, infringement of a microstructure of neurocytes at influence of alcohol, radioprotektornoe action of ethanol

the Author: Poljanskaja O.V.

INFLUENCE OF ALCOHOL ON THE NERVOUS TISSUE

At introduction of ethanol series of interneuronalic contacts have various reactive changes as a swelling aksonalnoj parts of synapses, changes of amount, the form osmiofilnosti and locatings of vesicles.

Alongside with it there are contacts aksonnyh terminalej with shipikami the dendrites, having changes of the destructive character. Basically the involution meets for light phylum. Thus it is observed not only change of amount of vesicles, but also their dimensions, the form, osmiofilii. Change of sinaps vesicles is marked and at a chronic drunkenness. At a threshold dose of alcohol the augmentation of amount of the synapses degenerating for dark phylum is apparent. Thus the presynaptic department diminished in the dimension, osmiofilen and is overflown with vesicles that testifies to blockage of a mediator.

The important value has also change shipikovogo the device, t. To. To this formation, alongside with synaptic membranes, attaches the important value during perception and formations of time connections. For action of alcohol downstroke informativnosti transneuronal contacts is rather typical, that morfologicheski is determined by decrease of the area of engagement of awake regions of synaptic membranes and dilating of a synaptic gap. In all cases around of changed mezhnejralnyh contacts the edema astrotsitarnoj glias is observed. It is confirmed also with biochemical methods, is especial at introduction trankvilizirujushchej doses of alcohol.

Thus, at an acute drunkenness in connection with changes in synapses particulate interdigitation of interneuronalic ensembles and as consequence of it, occurs morfofunktsionalnaja a basis of development of alcoholic illness and asotsialnogo behaviour of an individual is observed.

In scientific, and in fiction the opinion on radioprotective action of alcohol is sustained. In this connection investigated a state of interneuronalic integration of a brain at the combined action of ethanol and an ionizing radiation. Experiment was carried out on rats - samtsah of line Vistar in mass 250г which head irradiated with scales - quantums in a dose 50 gr. For 2 minutes. Up to or right after irradiatings vnutribrjushinno introduced 15 %-s' solution of ethanol. In 100 minutes. After influence of animals dekapitirovali. It was found out, that changes of synapses as at action of an ionizing radiation, and ethanol are same and are not specific. More radical changes at action of ethanol in comparison with scale an irradiating are observed in shipikovom the device which is intimately connected to an engram of memory.

Effects of the combined action of investigated factors depend on sequence of their influence and a dose of ethanol. Introduction of ethanol up to a gamma-irradiation of a head essentially did not modify radiative changes of synapses. Action of small doses of ethanol after an irradiating of a head also did not render significant influence on radiative lesions of synapses. At action of the big doses of alcohol the legible effect of a synergy with an ionizing radiation is received: at conservation of number of the changed synapses in them more rasping changes are marked. Disintegration of mitochondrions in presynaptic departments of interneuronalic contacts is constantly observed. The destruction of mitochondrions, probably, descends very quickly, t. To. Their one pole looks the turgent, and the second conserves densely packed kristy. Change of an inner membrane of mitochondrions which twists in mielinopodobnye complexes is typical. Such state of mitochondrions can result in essential infringement of process of development of energy and difficulty of function of synapses. Ethanol has also fixed effect provoking an edema. Minimum concentration of ethanol itself did not invoke alterations hydration a profile of a brain, but at action after an irradiating invoked an edema in a brainstem. Higher concentration of ethanol already in itself result ined overhydratations in a brainstem, and after an irradiating the edema arose already in all investigated departments of a brain. The authentic augmentation of water content in a brain well correlates with a swelling revealed at ultrastructural research presynaptic terminalej and prilezhashchih astrocytes.

Thus, more rasping changes of synapses. Connected, probably, with infringement of power supply and an overhydratation, are observed at introduction of ethanol after an irradiating of a head. The similar circumstance demands the cautious approach to the data on medical action of ethanol at an irradiating. The numerous data testify to awake nocuous action of ethanol, that brightly shows in morphological changes.

The microstructure of neurocytes of a sensomotor bark and a hippocampus of rats has been investigated at action of ethanol.

The majority of neurocytes of a sensomotor bark is characterized by the large dimensions, correct and legible contours, the spherical or weakly extended form. As a rule, it is swept well up aksonnyj holmik and sometimes – dendrites. The nucleus of a nervous cell has the correct form, acyanotically painted and in most cases contains round, is intensive bazofilnoe a nucleolus borrowing the central position. In cytoplasm the moderate level of a basophilia caused by presence uniform shallow glybok of ribonucleoproteins is determined. Similar frame have also a neurocyte of a hippocampus though in them the fillet of cytoplasm around of a nucleus is a little already, and aksonnyj holmik, as a rule, it is swept weakly up. Such cells name "normohromnymi" neurocytes. They compound 86,79 % of all nervous cells in a parietofrontal bark and 62,09 % - in a hippocampus of intact rats. Regarding neurocytes some structural changes are determined. Nervous cells with the expressed non-uniformity of a basophilia of cytoplasm or with presence of the shallow locuses of regions of a chromatolysis are marked. Diffusely posed in cytoplasm or localized around of a nucleus or on periphery of a cell. Such neurocytes have routinely excentricly posed nucleoluses and smooth contours tsitolemmy. These structural changes can be appreciated as exhibiting of a chromatolysis. The small part of nervous cells differs roughness of contours of cytoplasm and a nucleus. Thus the cell, as a rule, has the extended form, it is marked more than a twofold interrelation of maximal and minimum diameters. Cytoplasm in these cells has a high level of a basophilia. Glybki chromatophilous material are integrated. And a nucleus more dark with a large excentricly posed nucleolus. These cells can be attributed to hyperchromatic cells.

The small lobe of neurocytes looks sharply hyperchromatic, corrugated, with shtoporoobrazno a gyrose initial part of an axon. The frames conforming to a nucleus or a nucleolus, in them are not determined. Such neurocytes consider piknomorfnymi.

At introduction of ethanol in a dose of 1,5 g / kg there is a rising amount piknomorfnyh neurocytes of a hippocampus in 10-17 minutes. In 35-60 minutes significant downstroke of amount normohromnyh neurocytes with augmentation of the maintenance piknomorfnyh cells is marked.

The degree of manifestation of changes on the part of neurocytes of a sensomotor bark at action of ethanol has legible dozovuju dependence. On the part of nervous cells of a hippocampus dozovaja dependence is not marked. Structural changes of neurocytes of a hippocampus it is carried out mainly for the account piknomorfnyh neurocytes. Absence dozovoj dependences at action of ethanol on a hippocampus, probably, is connected to appearance of higher excitation threshold of neurocytes.

Under action of ethanol the number of neurocytes in all layers of a bark decreases. The kept nervous cells are in a state kariotsitoliza. Swellings and shrinkages. In a dentate nucleus of a cerebellum alongside with kariotsitolizom there were neurones a vacuolation of cytoplasm, a karyopyknosis and a karyorrhexis. In a glia of a brain there is an expressed proliferation and dystrophic changes. The greatest structural changes were marked in a bark of the big hemispheres, nucleus of a cerebellum and a striate body.

Influence of ethanol on power and carbohydrate metabolism

At an acute and chronic drunkenness there are infringements of a metabolism of cells what it is possible to judge on change of activity of enzymes of a tricarbonic acid cycle and a glycolysis and accumulation of intermediate products of a metabolism in a tissue of a brain. The degree of these changes depends on amount of ethanol and duration of his introduction.

Infringement of oxidative processes in a tissue of a brain is one of early reactions to acute toxic action of ethanol. At chronic introduction of small doses of ethanol there is a rearrangement of activity of ferment systems in a brain, testifying about incorporation of the compensator mechanisms directed on regeneration of damages, connected with change of a permeability of membranes and an inactivation of ferment systems.

Influence of ethanol on respiration intensity of a brain.

The chronic drunkenness results in infringement of a digestion of Oxygenium by a tissue of a brain. Sharp oppression of histic respiration is found out in a bark of the big hemispheres, subtalamic range, a cerebellum and myelencephalon. Low concentrations routinely enlarge by 10 % respiration of sections of a brain in vitro. Respiration of sections of a brain drops only at influence of rather high concentrations of ethanol.

Sensitivity of sections of a bark of the big hemispheres to action of ethanol increases in the much greater degree at addition of ions of a potassium or a stimulation an electric current, (respiration is oppressed much more strongly).

Influence of ethanol on a glycolysis in nervous cells.

Action of ethanol on respiration of a brain is connected to his influence on the bonds being an energy source for function activity of nervous cells.

A glucose - the most specific substrate of a metabolism in a brain which in vivo for 1 hour consumes 18 mkmol glucoses on 1 g of a tissue.

Low concentrations of ethanol will activate an aerobic glycolysis and depress process of oxidation of a glucose. Introduction of ethanol promotes augmentation in a brain of a glucose, фруктозо-1-1,6-дифосфата, a-Glycerophosphatum and lactic acid with simultaneous downstroke of levels of pyruvic acid, a glycogen and dioksiatsetonfosfata.

At a drunkenness as a result of downstroke of rate of a glycolysis and rate of reactions in a tricarbonic acid cycle the maintenance in a brain of pyroracemic and lactescent acids, a glycogen and a coenzyme And (KoA) drops. The augmentation of disintegration of a glycogen in a brain, probably, is caused by an activation of the phosphorylase freed under action of ethanol. Toxic doses of ethanol invoke appreciable downstroke of salvaging of a glucose in a brain in vivo with rising its concentration in tissues of this organ.

Activity of oxidation-reduction enzymes in a brain at a drunkenness.

The mechanism of action of ethanol on ferment systems of a tricarbonic acid cycle in a brain for the present is not clear. It is possible, that changes in concentration of intermediate products of this cycle it is caused by augmentation Рсо2 during a drunkenness.

At single-pass introduction of ethanol activity Sodium lactatum – and suktsinatdegidrogenazy in a brain grew in 1 hour. Single-pass introduction of ethanol promotes rising of activity alanine – and aspartat-aminotransferazy in subcellular fractions of a brain. At the small doses of ethanol rendering a promoting effect on an organism, the individual sensibility to action of ethanol which is levelled by depressive action of his high doses shows. Reception of the big doses of ethanol invokes downstroke of activity of enzymes of a tricarbonic acid cycle. This infringement of oxidative processes in mitochondrions of a brain is one of early reactions to acute toxic action of ethanol at which the transamination of amino acids in a brain also is broken. It is possible, that influence of ethanol on transport and an exchange of amino acids in nervous cells is caused by changes in properties of their membranes.

Long action of small doses of ethanol reduces activity глюкозо-6-фосфатдегидрогеазы and rises activity of a malate dehydrogenase and SDG in a bark of the big hemispheres, in ependime ventricles, in a mild meninx and in cells of vascular plexuses. At the chronic use ethanol invokes augmentation of activity of dehydrogenases of a brain.

The chronic intoxication ethanol results in intensifying compensator mechanisms, in result the metabolism in nervous cells is sustained at the fixed reduced level. Thus substantial growth of activity of some glycoclastic and oxidative enzymes is found out: a-glitserofosfatdegidrogenazy, MDG, nuclear heating plant. Activity глюкозо-6-фосфатдегидрогеназы drops.

Ferment systems of oxidation-reduction processes function as the highly organized complexes connected to a cellular membrane. Small doses of ethanol invoke augmentation of the maintenance recovered ABOVE, mediate doses rendered various action, and big always invoked oxidation of a coenzyme. This action of the big doses of the ethanol, invoking augmentation of the maintenance oxidated ABOVE, seems unexpected as ethanol stimulates a glycogenolysis connected to augmentation of amount recovered ABOVE. Action of ethanol thus is accompanied by sharp rising of the maintenance of a glucose in a brain and downstroke of its exchange.

But as oxidation ABOVE, apparently, is connected to circulation in a nem of the acetaldehyde delivered with a blood from a liver, that, most likely, ethanol does not invoke appreciable changes in redox potential of a brain.

Ethanol and makroergicheskie bonds in a brain.

The majority of explorers denies the data that ethanol influences synthesis of high-energy Natrii phosphases. Ethanol is not the uncoupler of oxidative phosphorylation and does not depress formation ATF. The maintenances given about augmentation makroergicheskih bonds in a brain after reception of ethanol testify to depressive action of alcohol on a nervous tissue and a metabolism in it owing to what salvaging ATF and a creatine phosphate decreases.

Results of researches with sections of a brain, with isolated mitochondrions and in vivo show experiences, that ethanol does not influence synthesis makroergicheskih Natrii phosphases in a brain, but inhibits their salvaging. Action of alcohol on practically able-bodied people and on the persons, suffering an alcoholism, shows in infringement of an external respiration and in downstroke of rate of a cerebral circulation.

The data of biochemical analysises of biological fluids of the patients, suffering an alcoholism, show downstroke of activity глюкозо-6-фосфотазы and accumulation PVK that testifies to infringement of a normal path of oxidation of a glucose and about difficulty of its digestion a tissue of a brain.

Influence of ethanol on an exchange of amino acids, proteins and nucleic acids in a brain.

The urgency of studying of influence of ethanol on an exchange of amino acids speaks not only their value for synthesis of proteins, but also a role of some amino acids as neuromediators. Proteins and nucleic acids play a part during education and memory which infringement fixed at an alcoholism.

Transport and an exchange of amino acids in nervous cells at a drunkenness.

Strengthening ethanol in a blood promotes entering in a brain only the amino acids keeping an appreciable neutral radical. The drunkenness enlarges the maintenance of dicarboxylic amino acids and reduces the maintenance of a glutamine in a tissue of a brain. The augmentation of a glycolysis in a tissue of a brain can cause accumulation of dicarboxylic amino acids.

The dose of ethanol rendering excitant action on a CNS, invokes rising the maintenance of a glutamine in a cerebellum on 40 %. Rising of a dose of alcohol results in weakening glutamic acid in a cerebellum, and at terminal states, as a result of a venenating with ethanol, and in the big parencephalons.

Most likely, character of influence of ethanol on transport and an exchange of amino acids in a tissue of a brain is caused by changes which are invoked with ethanol in a membrane of nervous cells. The augmentation of hydrophoby in series of aliphatic alcohols invokes progressing downstroke sinaptosomalnogo transport a piperidic acid and glutamic acid that grows out interactions of moleculas of alcohol with a lipoid part of a membrane of synaptosomes. At introduction of ethanol downstroke of the maintenance of quick-response SH-bunches is observed. The long use of ethanol results in augmentation of the maintenance of these bunches at 12-16 % that testifies to compensator structurally functional transformations of membranes at a chronic drunkenness.

the Exchange of proteins of a brain at a drunkenness.

At an acute and chronic alcoholic venenating in a brain the maintenance of nitrogen of the general and solvable proteins and amidnogo nitrogen of crude proteins with simultaneous augmentation of concentration of ammonia and not albuminous and aminnogo nitrogen decreases. The greatest changes in an exchange of proteins at acute action of ethanol are marked in gray matter of the big hemispheres, and at a chronic drunkenness as well in a cerebellum.

For function activity of a CNS and sinaps processes the important value has influence of ethanol on aksonalnyj transport of protein which promotes delivery of the bonds necessary for synthesis of enzymes, responsible for synthesis or destruction of sinaps neuromediators. Neither single-pass, nor chronic introduction of ethanol does not influence transport of solvable proteins of nervous cells and on a sluggish component of axoplasmatic transport of the proteins responsible for a matrix membranous and tubuljarnogo of an atomy of an axon.

Influence of ethanol on a RNA of cells of a brain.

On the maintenance and an exchange of nucleic acids in a brain it is not enough data on influence of ethanol. The Romanian explorers have noticed, that the moderate doses of ethanol promoting hyperactivity of a CNS and rising of a motor performance, result in decrease of the maintenance of a DNA and rising of the maintenance of a RNA.

the Nuclear RNA.In a nucleus it is synthesized mRNK. Gomopolinukleotid, Acidum adenylicum, has essential value for synthesis of this kind of a RNA. At the use of alcohol there is an inhibition of formation of Acidum adenylicum and decrease mRNK. This decrease can be result of dropped synthesis and (or) damages of its native frame. Thus, retardation of synthesis of Acidum adenylicum under influence of ethanol results in infringement of synthesis mRNK and protein cells of a brain in conditions of a drunkenness.

Acceptor RNA.Under action of ethanol there is a retardation of synthesis tRNK, that can result in downstroke of synthesis of proteins for the lack of necessary amounts of this RNA at a stage of labilizing of amino acids.

the Ribosomal RNA.At the chronic use of ethanol synthesis rRNK considerably decreases, the yield of loose ribosomes drops up to 83 %; padding introduction of an admixture of amino acids does not variate rate of synthesis of protein.

Mitohondrialnaja a RNA.Under action of ethanol the permeability of a mitochondrial membrane for precursors of a RNA can drop, result of that can be time-lagged incorporation of precursors in a ribosomal RNA or tRNK mitochondrions.

Thus, chronic consumption of ethanol results in damage of a membrane of nucleus of nervous cells and the mechanism of transport mRNK and to accumulation of this material in a nucleus in the season of his initial influence. In connection with decrease of amount tsitoplazmaticheskoj tRNK and a ribosomal RNA activity of the RNK-POLYMERASE in a nucleus that entails downstroke of the maintenance mRNK in a nucleus and infringement of the general exchange in nervous cells starts to drop. The damaging effect of ethanol can be connected to weakening ions Мg participating in formation of RNK-POLYMER by means of the DNK-DEPENDENT RNK-POLYMERASE. Chronic influence of ethanol reduces also a permeability of a mitochondrial membrane for precursors of a RNA and, probably, inhibits a transcriptional mitohondrialnoj a RNA.

These changes in an exchange of a RNA of nervous cells influence synthesis of protein of neurones which infringement shows in change of normal function activity of a CNS, structural integration of nervous cells and their general metabolism. These defects in an exchange of a RNA of a brain in part explain infringements of memory, processes of processing of the information and the general behaviour of the person and animals.

the Lipide exchange in a brain at an alcoholic venenating.

After reception of ethanol concentration in a brain of the general lipids, cerebrosides, gangliosides, sulfatides, poliglitserofosfolipidov, lecithines and etanolaminfosfolipidov is enlarged. Alongside with it downstroke of the maintenance monofosfoinozitidov and U-phosphotides is marked. At a long intoxication the maintenance of all fractions of phosphotides increases, is especial sphingomyelins. The proportional augmentation as acidic, and nejralnyh phosphotides promotes conservation of a constance of quotient of the attitude of these phosphotides in a tissue of a brain. Conservation of quantitative interrelations is the kompensatorno-adaptive mechanism directed on maintenance of normal functioning of a CNS in conditions of a chronic alcoholic venenating.

Some words about a pathology.

The maintenance of neutral lipids and a cholesterin in white matter of a brain is reduced. In gray matter the maintenance of cerebrosides mainly drops. Composition of fatty acids variates. In gray matter of a brain the maintenance stearinic and nervonovoj acids drops, and palmitic and myristic grows. In white matter the maintenance of stearic acid dropped, and nervonovoj-enlarges. Decrease of fatty acids is typical of degenerative processes in a brain with the lengthy chain in cerebrosides, sphingomyelins and fosfatidiletanolaminah gray matter of a bark. In cerebrosides and sphingomyelins of white matter the maintenance of unsaturated fatty acids with the lengthy carbon chain - linoleic, linolenic and arachidonic drops. In fosfatidilatanolaminah the maintenance of fatty acids not meeting, as a rule, in norm with a plenty of unsaturated bonds is enlarged.

Action of ethanol on neuromediators.

Acetylcholinum.

Appearance of changes in behaviour, emotional distresses and signs of psychopathologic states, characteristic for an alcoholism, have a feedforward with infringement of neuromediator systems.

The augmentation of frequency and voltage of biological potentials of electroencephalogram (EEG) and miniature potentials at action of low doses of ethanol, apparently, is connected to remission of Acetylcholinum. Center and high doses of ethanol reduce frequency of potentials with appearance of spindles medlennovolnovoj activity. In a brain ethanol inhibits more often, than stimulates atsetilholinovye synapses on pre-and postsinaps levels. At a drunkenness the maintenance of Acetylcholinum in a brain is faded out.

Assume, that the appetence to alcohol educes at the fixed interdependent participation holinergicheskoj and serotoninergicheskoj systems. There are assumptions of immediate participation holinergicheskoj systems in mechanisms of originating of preference to ethanol that occurs the fixed maintenance of Acetylcholinum and in weakening activity of an acetylcholinesterase in a tissue of a brain. It is possible, that initial action of ethanol shows in decrease of the maintenance in a brain of Acetylcholinum and downstroke of activity holinatsetilazy. The subsequent decrease of activity of an acetylcholinesterase is the kompensatorno-adaptive process promoting conservation of function activity of a CNS in conditions of the poor maintenance of Acetylcholinum in a brain as a result of chronic reception of alcohol.

the Piperidic acid.

The piperidic acid (piperidic acid) and ethanol render depressive action on function activity of nervous frames. Finding-out of mutual relations between these two bonds and interest to system a piperidic acid at a drunkenness are connected to its role as mediator of inhibition in a CNS, close interrelation with a tricarbonic acid cycle and its application as a medicinal agent for treatment of nervous and mental diseases.

The acute intoxication ethanol invoked augmentation of the maintenance a piperidic acid in gray matter of the big hemispheres and a cerebellum.

Series of authors have not found changes of the maintenance a piperidic acid in a brain at an acute drunkenness.

Alongside with it downstroke of the maintenance a piperidic acid in a cerebellum which was accompanied by hypotaxia at alcoholic intoxication fixed.

Contradictions about concentration a piperidic acid in a brain at acute action of ethanol can be explained by methodical conditions of experiments.

Apparently, in dependence on features of model of a chronic drunkenness the maintenance the piperidic acid in a brain can be enlarged, drop or remain without changes.

After a cancellation of alcohol the maintenance the piperidic acid in a brain is sharply enlarged. This augmentation is surveyed as compensator reaction of an organism.

Stressful influence of alcohol invokes balance upset between synthesis and salvaging a piperidic acid with distinct downstroke of activity glutamatdekarboksilazy. Alterations in an exchange a piperidic acid in a brain at single-pass introduction of ethanol correspond to phasal nature of change of a function state of the CNS caused by a dose of ethanol. Chronic introduction of ethanol results in intensifying compensator opportunities of the organism directed on maintenance of a metabolism of nervous cells at a fixed level for conservation of a homeostasis. At a chronic drunkenness of change in an exchange a piperidic acid are adaptive reaction of an organism against depressive influence of alcohol: activity glutamatdekarboksilazy grows, but the maintenance a piperidic acid, is especial in a cerebellum, decreases, that, probably, promotes development of tolerance of nervous frames to alcohol.

The sharp arrest of introduction of ethanol breaks the established metabolism of a brain at an alcoholism. For depressing subitaneous activization of function activity of the nervous cells caused by putting off of depressive action of ethanol, the piperidic acid, salvaging which sharply drops as a result of decrease of activity aminobutirat-aminotransferazy starts to be used again.

the Exchange of a serotonin in a brain at an intoxication ethanol.

the Acute drunkenness.Parameters of the maintenance of a serotonin in a brain at an acute venenating with the ethanol, submitted in works of different authors, sidetelstvujut about appearance of various effects.

Single-pass introduction of ethanol results in downstroke of the maintenance of a serotonin on 40 % in a brainstem. Appreciable downstroke of the maintenance of a serotonin in hvostatom a nucleus, lateralnoj subtalamic range and reticular formation of a brain is found out after single-pass introduction of ethanol.

On other data, single-pass introduction of ethanol enlarges the maintenance of a serotonin within 24 hours and reduces the maintenance 5-оксииндолуксусной acids in a tissue of a brain. Thus allocation of a serotonin in subcellular fractions variates: the maintenance of a serotonin in 2 times is enlarged in supernatante and almost in 2,7 times decreases in a fraction of nerve terminations.

The maintenance of a serotonin in a brain at an acute intoxication ethanol reflects balance between his synthesis and remission from reserve forms in serotoninergicheskih neurones. Ethanol variates an exchange of a serotonin in nervous cells (from an oxidative path with formation 5-ОИУК to the reduction with production 5-окситриптофола).

the Chronic drunkenness.In hvostatom a nucleus, lateralnoj subtalamic range and reticular formation of a brain under influence of chronic introduction of ethanol oxidation of a serotonin without rising a level 5-окситриптофола strengthens. Rate of an exchange at a chronic alcoholization dropped in experiment on rats at samok on 84 %, at on 74 %.

Tolerance and dependence on ethanol can be connected to decrease of synthesis of a serotonin in a tissue of a brain as a result of blockage serotoninergicheskih neurones at chronic action of alcohol.

On other data, chronic reception of ethanol does not render influence on synthesis of a serotonin in a brain. Apparently, originating of tolerance to alcohol and formation of physical dependence on him are not connected to changes in an exchange of a serotonin and with activity serotoninergicheskih pathes, but it is impossible to exclude an opportunity of alterations in a metabolism of a serotonin in separate regions of a brain in connection with his unequal allocation in different on the function significance kompartmentah.

It agrees the given T.G.Naumovoj, chronic reception of ethanol invokes augmentation of the maintenance of a serotonin in a brain.

Most likely, entering of a significant amount of ethanol promotes intensifying of a secretion kortikosteroidnyh Hormonums paranephroses which in turn stimulate activity triptofangidrokslazy in a brain. Conformity between augmentation of Corticosteronum in a blood plasma and augmentation of activity triptofangidroksilazy which is controlled by pituitary body - adrenal system, confirms the assumption, that the augmentation of a biosynthesis of a serotonin grows out his influences on biochemical processes in a pituitary body and paranephroses. On the other hand, have found, that ethanol inhibits metamorphosis of a tryptophan into a serotonin, probably, owing to not competitive inhibition triptofangidroksilazy. It is possible, that reacting serotoninergicheskoj systems on chronic introduction of ethanol is connected to adaptable changes of activity triptofangidroksilazy.

Influence of ethanol on an exchange of Noradrenalinum and Dofaminum.

Analysis of an exchange of biogenic amines allows to estimate a state of sympaticoadrenal system which changes reflect as infringement of fixed interrelations during an exchange of catecholamins, and originating of adaptive reactions to choronomic influences. Introduction of alcohol in dependence on his dose invokes the stressful, nonspecific reactions of an organism intimately connected to change of a level of biogenic amines in a CNS. The chronic drunkenness promotes formation of compensator processes which cause a becoming of the conforming balancing of the mechanisms providing function activity of a CNS.

The state of an exchange of biogenic amines correlates with stages of flow of an alcoholism. The state of an alcoholic abstinence is accompanied by the increased concentration in a blood of Noradrenalinum and a high egestion with urine of an epinephrine, Noradrenalinum and Dofaminum. It specifies the increased tone of sympaticoadrenal system to what downstroke of a level of a serotonin in a blood and urine testifies. Apparently, these changes are connected to compensator reactions by means of which the organism aspires to reduce a habitual homeostasis and to keep an optimum level of adrenergic reaction. Escaping of a state of an abstinence is accompanied by falloff of an egestion with urine of an epinephrine, Noradrenalinum and Dofaminum that testifies to achievement of a new level of a balancing of function activity of both departments of vegetative nervous system. In I.P.Anohinoj's opinion, acute influence of alcohol on adrenergic frames of a brain promotes release of Noradrenalinum in the departments concerning to aktivirujushchej to system of a brain. Long reception of alcohol causes falling tone of these frames of a CNS as a result of depressing activity Dofaminum - v-gidroksilazy and downstrokes of a level of Noradrenalinum. The compensator augmentation of synthesis of biogenic amines in a CNS invokes in turn necessity of their destruction that is reached by augmentation of a dose of alcohol. With exhaustion of functionalities of adrenergic frames of a brain at chronic introduction of alcohol the distortion of their activity that coincides with a stage of downstroke of tolerance to ethanol and psychopathologic changes of the person shows. Thus, unbalance between disintegration and synthesis of biogenic amines at an alcoholism promotes formation of "vicious circle" when escalating doses of alcohol are demanded for destruction of exuberant amount of synthesized catecholamins. The opportunity of participation of Noradrenalinum and Dofaminum in nejrohimicheskih the reactions connected to formation of an alcoholism is not excluded, as a result of blockage by alcohol of process of absorption of catecholamins in neurones and changes of a permeability of membranes of nervous cells.

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Keywords: alcohol, a nervous tissue, a CNS, nervous system, ethanol, alcohol, a histology, the abstract, the report, alkogolizm, a destruction of neurones, infringement of a microstructure of neurocytes at influence of alcohol, radioprotektornoe action of ethanol

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