Acetylcholine release form. Acetylcholine is an important neurotransmitter in the brain. Irreversibly active substances

Neurotransmitters play an important role in the proper functioning of the human nervous system. One of these substances is acetylcholine, an organic molecule, the presence of which is characteristic of the brain of various mammals, birds and, of course, humans. What role does the neurotransmitter acetylcholine play in the human body, why is it so important, and are there ways to increase the level of acetylcholine in the body.

What is the neurotransmitter acetylcholine and what are its functions?

The chemical formula of the neurotransmitter acetylcholine is CH3COO (CH2) 2N + (CH3). This organic molecule plays a role in the functioning of the central and peripheral nervous system. The site of acetylcholine synthesis is the axons of nerve cells, the substances necessary for the formation of acetylcholine: acetyl coenzyme A and choline (vitamin B4). Acetylcholinesterase (an enzyme) is responsible for the balance of this mediator, which is capable of breaking down excess acetylcholine into choline and acetate.

Functions of acetylcholine

  • improving cognitive abilities;
  • improvement of neuromuscular communication.

Scientists have found that the neurotransmitter acetylcholine not only helps improve memory and promote learning, it also helps the brain distinguish between old and new memories - it helps us remember what was yesterday and what was five years ago.

In the membrane of muscle cells there are H-cholinoresetters, which are sensitive to acetylcholine. When acetylcholine binds to this type of receptor, sodium ions are released into muscle cells, causing the muscles to contract. As for the effect of acetylcholine on the heart muscle, it differs from the effect on smooth muscle - the heart rate decreases.

Deficiency of the neurotransmitter acetylcholine: causes and methods of replacement

With a decrease in the level of the neurotransmitter acetylcholine, a deficiency of acetylcholine is observed.

Symptoms deficit acetylcholine:

  • inability to listen;
  • inability to concentrate;
  • inability to memorize and recall information (memory impairment);
  • slow processing of information;
  • fatty liver metamorphosis;

When the level of acetylcholine in the body is normalized, and this happens through proper nutrition, inflammation is suppressed and the connection between muscles and nerves improves.

At risk of lowering the level of the neurotransmitter acetylcholine are:

  • marathon runners and athletes who perform endurance exercises;
  • people who abuse alcohol;
  • vegetarians;
  • people whose diet is not balanced.

The main factor contributing to the decrease or increase in acetylcholine in the body is a balanced diet.

How to increase the level of the neurotransmitter acetylcholine in the body?

There are three main ways to increase the level of the neurotransmitter acetylcholine in the body:

  • nutrition;
  • regular physical activity;
  • intellectual training.

Foods rich in choline (vitamin B4) - liver (chicken, beef, etc.), eggs, milk and dairy products, turkey, green leafy vegetables. It is better to replace coffee with tea.

With a shortage of raw materials for the production of the neurotransmitter acetylcholine, the brain begins to "eat itself", so carefully monitor your diet.

THIS IS A DESCRIPTION OF THE CHARACTER OF THE "UNHAPPY" PERSON

Its 2 main problems:

1) chronic lack of satisfaction of needs,

2) the inability to direct his anger outside, restraining it, and with it restraining all warm feelings, make him more and more desperate every year: no matter what he undertakes, it does not get better, on the contrary, it only gets worse. The reason - he does a lot, but not that.

If nothing is done, then, over time, either the person will "burn out at work", loading himself more and more - to complete exhaustion; or his own self will be emptied and impoverished, an unbearable self-hatred will appear, a refusal to take care of oneself, in the long run - even from self-hygiene.

The person becomes like a house from which the bailiffs have taken the furniture.

Against the background of hopelessness, despair and exhaustion, there is no strength, energy, even for thinking.

Complete loss of the ability to love. He wants to live, but begins to die: sleep is disturbed, metabolism ...

It is difficult to understand what he lacks precisely because we are not talking about being deprived of possession of someone or something. On the contrary, he has the possession of deprivation, and he is unable to understand what he is deprived of. Lost is his own I. It is unbearably painful and empty for him: and he cannot even put it into words.

If you recognize yourself in the description and want to change something, you urgently need to learn two things:

1. Memorize the following text and repeat it all the time until you learn to use the results of these new beliefs:

  • I am entitled to needs. I am, and I am me.
  • I have the right to need and satisfy needs.
  • I have the right to ask for satisfaction, the right to pursue what I need.
  • I have the right to crave love and love others.
  • I have the right to a decent life organization.
  • I have the right to complain.
  • I have a right to regret and sympathy.
  • ... by birthright.
  • I might get rejected. I can be alone.
  • I will take care of myself anyway.

I would like to draw the attention of my readers to the fact that the task of “learning the text” is not an end in itself. Self-training by itself will not give any lasting results. It is important to live each phrase, to feel it, to find confirmation of it in life. It is important that a person wants to believe that the world can be arranged somehow differently, and not just the way he used to imagine it. That it depends on him, on his ideas about the world and about himself in this world, how he will live this life. And these phrases are just an excuse for thinking, thinking and searching for their own, new "truths."

2. Learn to direct aggression at the person to whom it is actually addressed.

… Then there will be an opportunity to experience and express warm feelings to people. Realize that anger is not destructive and can be presented.

WANT TO FIND OUT WHAT A PERSON IS NOT ENOUGH TO BECOME HAPPY?

FOR K ALWAYS "NEGATIVE EMOTION" LIES A NEED OR DESIRE, THE SATISFACTION OF WHICH IS THE KEY TO CHANGES IN LIFE ...

TO SEARCH THESE TREASURES, I INVITE YOU FOR MY CONSULTATION:

You can sign up for a consultation at this link:

Psychosomatic diseases (so it will be more correct) are those disorders in our body, which are based on psychological reasons. psychological reasons are our reactions to traumatic (complex) life events, our thoughts, feelings, emotions that do not find a timely, correct expression for a particular person.

Mental defenses are triggered, we forget about this event after a while, and sometimes instantly, but the body and the unconscious part of the psyche remember everything and send us signals in the form of disorders and diseases

Sometimes the call can be to respond to some events from the past, to bring “buried” feelings out, or a symptom simply symbolizes what we forbid ourselves.

You can sign up for a consultation at this link:

The negative impact of stress on the human body, and especially distress, is colossal. Stress and the likelihood of developing disease are closely related. Suffice it to say that stress can reduce immunity by about 70%. Obviously, such a decrease in immunity can result in anything. And it’s also good if it’s just colds, but if cancer or asthma, the treatment of which is already extremely difficult?

The mechanism of action of acetylcholine

Cholinergic receptors (acetylcholine receptors) are transmembrane receptors whose ligand is acetylcholine.

Acetylcholine serves as a neurotransmitter in both pre- and postganglionic synapses of the parasympathetic system and in preganglionic sympathetic synapses, in a number of postganglionic sympathetic synapses, neuromuscular synapses (somatic nervous system), as well as in some parts of the central nervous system. Nerve fibers that release acetylcholine from their endings are called cholinergic.

Acetylcholine synthesis occurs in the cytoplasm of nerve endings; its reserves are stored in the form of bubbles in presynaptic terminals. The emergence of a presynaptic action potential leads to the release of the contents of several hundred vesicles into the synaptic cleft. Acetylcholine released from these vesicles binds to specific receptors on the postsynaptic membrane, which increases its permeability to sodium, potassium and calcium ions and leads to the appearance of an excitatory postsynaptic potential. The action of acetylcholine is limited by its hydrolysis by the enzyme acetylcholinesterase.

From a pharmacological point of view, specific cholinergic receptors are divided into nicotinic (H-receptors) and muscarinic (M-receptors).

The acetylcholine nicotinic receptor is also an ion channel, i.e. belongs to the channel-forming receptor, while the acetylcholine muscarinic receptor belongs to the class of serpentine receptors that transmit signals through heterotrimeric G - proteins.

The cholinergic receptors of the autonomic ganglia and internal organs differ.

N-cholinergic receptors (sensitive to nicotine) are located on postganglionic neurons and cells of the adrenal medulla, and M-cholinergic receptors (sensitive to the alkaloid muscarin) are located on the internal organs. The former are blocked by ganglion blockers, the latter by atropine.

M-cholinergic receptors are divided into several subtypes:

M1-cholinergic receptors are located in the central nervous system and, possibly, on the neurons of the parasympathetic ganglia;

M2-cholinergic receptors - on smooth and cardiac muscles and cells of the glandular epithelium.

M3-cholinergic receptors are located on smooth muscles and glands.

Bethanechol serves as a selective stimulant of M2-cholinergic receptors. An example of a selective blocker of M1-cholinergic receptors is pirenzepine. This drug dramatically suppresses the production of HCl in the stomach.

Stimulation of M2-cholinergic receptors through the Gi-protein leads to inhibition of adenylate cyclase, and stimulation of M2-cholinergic receptors through the Gq-protein leads to the activation of phospholipase C and the formation of IF3 and DAG (Fig. 70.5).

Stimulation of M3-cholinergic receptors also leads to the activation of phospholipase C. Atropine serves as a blocker of these receptors.

Other subtypes of M-cholinergic receptors have been identified by the methods of molecular biology, but they are still insufficiently studied.

Acetylcholine (acetylcholine, Ach) [lat. acetum - vinegar, Greek. chole - bile and lat. -in (e) - suffix denoting "similar"] - acetic ester of choline (see Choline), a neurotransmitter that transmits nervous excitement through the synaptic cleft in the parasympathetic nervous system; synthesized in tissues with the participation of choline acetylase, hydrolyzed by the enzyme acetylcholinesterase. A. is also found in the composition of some plant poisons. First isolated from ergot in 1914 by G. Dale. For establishing the role of A. in the transmission of a nerve impulse, he, together with O. Levy, received the Nobel Prize for 1936.

Acetylcholine acts through cholinergic nerve endings, myoneural end plates, and other cholinergic receptors. Being in the protein-lipoid complex (precursor), acetylcholine is released during electrical and nervous excitement. Studies by Palay in 1956 using electron microscopy showed the accumulation of liquid droplets in the pores of the synapse, some of which burst during the passage of a nerve impulse. It is believed that the secreted fluid is acetylcholine (theory of pinocytosis). Released in the cholinergic substances of the heart, acetylcholine acts on adjacent cell membranes. According to modern views, a mebrana at rest carries a certain electric charge due to the redistribution of the K ion. The concentration of potassium at rest is much higher inside the cell than outside. For sodium, on the contrary, the concentration outside the cell is high, and inside it is low. The concentration of sodium ions inside the cell remains constant due to its active removal from the cell during a process called the "sodium pump". Potassium, on the other hand, penetrates the cell surface, leaving a more massive anion inside it, so the outer surface of the cell receives an excess of positive charges, the inner one - negative. The more potassium cations are released from the cell, the higher is the charge of its membrane, and vice versa - when the release of potassium slows down, the potential of the membrane decreases. Direct measurements of the resting potential showed that it is approximately 90 mV in the myocardium of the ventricles and atria, and 70 mV in the sinus node. If, for any reason, the potential of the membrane drops to 50 mV, the properties of the membrane change dramatically and it passes a significant amount of sodium ions into the cell. Then positive ions prevail inside the cell and the membrane potential changes its sign. Recharging (depolarization) of the membrane causes an electrical action potential. After the contraction, the concentrations of potassium and sodium are restored, characteristic of the state of rest (repolarization).

It was found that cholinergic (parasympathomimetic, parasympatotropic, trophotropic) reactions occur when acetylcholine (or other choline compounds) acts on cholinergic receptors, subcellular formations, cells, tissues, organs or the body as a whole. In addition to its main (cholinergic) action, acetylcholine causes the release of potassium bound by proteins, increases or decreases the permeability of biological membranes, takes part in the regulation of the selective permeability of erythrocytes, changes the activity of individual respiratory enzymes, affects the activity of cathepsins, the renewability of the phosphate group in phospholipids, and metabolism of macroergic phosphorus compounds, increases the resistance of individual tissues and the body as a whole to hypoxia. Koshtoyants suggested that, carrying out a mediator effect, acetylcholine enters the circle of tissue biochemical transformations.

The normal mechanism of automatism in the heart is based on a spontaneous decrease in the potential of the sinus node to -50 mV (generator potential). This occurs in the sinus node through a special metabolic process based on a decrease in the potassium permeability of the mebrane. Acetylcholine, on the other hand, specifically increases the K membrane permeability of the sinus node, thereby increasing the K output and preventing the development of the generator potential. Therefore, the heart rate drops. If the concentration of acetylcholine is increased even more, then the generator potential develops so slowly that the membranes of the sinus node lose their ability to develop an action potential (membrane accommodation). Cardiac arrest sets in. An increase in potassium permeability under the influence of acetylcholine causes a faster process of restoring the resting potential of the membrane (repolarization). The administered acetylcholine is not always distributed evenly by the blood. Therefore, in the atrium, this process of accelerated repolarization can also proceed unevenly, which, with the preserved excitation of the sinus node, manifests itself as atrial flutter and atrial fibrillation. The ventricles of the heart, devoid of cholinergic endings, remain insensitive to acetylcholine. The activation of the second order automatism centers (His bundle) is associated with the property of Purkinje fibers to develop spontaneous depolarization in the same way as it happens in the sinus node.

The non-mediatorial action of acetylcholine in the whole organism is one of the least studied and most controversial sections of the humoral-hormonal regulation of functions. It has been established that cholinergic (parasympathomimetic, parasympatotropic, trophotropic) reactions occur when acetylcholine (or other choline compounds) acts on cholinergic receptors, subcellular formations, cells, tissues, organs or the body as a whole. In addition to its main (cholinergic) action, acetylcholine causes the release of potassium bound by proteins, increases or decreases the permeability of biological membranes, takes part in the regulation of the selective permeability of erythrocytes, changes the activity of individual respiratory enzymes, affects the activity of cathepsins, the renewability of the phosphate group in phospholipids, on metabolism of high-energy phosphorus compounds, increases the resistance of individual tissues and the body as a whole to hypoxia. Koshtoyants suggested that, carrying out a mediator effect, acetylcholine enters the circle of tissue biochemical transformations. And inhibition of the action of acetylcholine is to some extent functionally equivalent to an increase in the concentration of dopamine.

Biochemical effect acetylcholine is that its attachment to the receptor opens a channel for the passage of Na and K ions through the cell membrane, which leads to membrane depolarization. Blocking the action of acetylcholine is fraught with serious problems, up to and including death. This is precisely the biochemical action of neurotoxins. Shown below are the structures of the two most potent neurotoxins, histrionicotoxin and D-tubocurarine chloride. Like acetylcholine, the D-tubocurarine molecule contains ammonium fragments. It blocks the site of attachment of acetylcholine to the receptor, excludes the transmission of a nerve signal, and prevents the transfer of ions across the membrane. A situation called paralysis of the living system is created.

The effect of acetylcholine on the heart.

Cholinergic mechanisms. On the outer membrane of cardiomyocytes, mainly muscarinic-sensitive (M-) cholinergic receptors are presented. The presence of nicotine-sensitive (N-) cholinergic receptors in the myocardium has also been proven, but their significance in parasympathetic effects on the heart is less clear. The density of muscarinic receptors in the myocardium depends on the concentration of muscarinic agonists in the tissue fluid. Excitation of muscarinic receptors inhibits the activity of pacemaker cells of the sinus node and at the same time increases the excitability of atrial cardiomyocytes. These two processes can lead to the occurrence of atrial extrasystoles in the event of an increase in the tone of the vagus nerve, for example, at night during sleep. Thus, the excitation of M-cholinergic receptors causes a decrease in the frequency and strength of atrial contractions, but increases their excitability.

Acetylcholine inhibits conductivity in the atrioventricular node. This is due to the fact that under the influence of acetylcholine, hyperpolarization of the cells of the atrioventricular node occurs due to an increase in the outgoing potassium current. Thus, the excitation of muscarinic cholinergic receptors has an opposite effect on the heart compared to the activation of B-adrenergic receptors. At the same time, the heart rate decreases, the conductivity and contractility of the myocardium, as well as the consumption of oxygen by the myocardium, are inhibited. The excitability of the atria in response to the use of acetylcholine increases, while the excitability of the ventricles, on the contrary, decreases.

Acetylcholine is one of the most important neurotransmitters in the brain. The most prominent role of acetylcholine is in neuromuscular transmission, where it is an excitatory transmitter. It is known that acetylcholine can have both exciting and inhibitory effects. This depends on the nature of the ion channel that it regulates when interacting with the corresponding receptor.

The neurotransmitter acetylcholine is released from vesicles at presynaptic nerve terminals and binds to both nicotinic receptors and muscarinic receptors on the cell surface. These two types of acetycholine receptors differ significantly in both structure and function.

Acetylcholine - acetic ester of choline, is a mediator in neuromuscular junctions, in presynaptic endings of motor neurons on Renshaw cells, in the sympathetic division of the autonomic nervous system - in all ganglionic synapses, in the synapses of the adrenal medulla and in the post-ganglionic glandular synapses; in the parasympathetic division of the autonomic nervous system - also in the synapses of all ganglia and in the postganglionic synapses of the effector organs. In the central nervous system, acetylcholine was found in fractions of many parts of the brain, sometimes in significant quantities, but no central cholinergic synapses were found.

Acetylcholine is synthesized in nerve endings from choline, which is delivered there via an as yet unknown transport mechanism. Half of the received choline is formed as a result of hydrolysis of previously released acetylcholine, and the rest, apparently, comes from blood plasma. The enzyme choline acetyltransferase is formed in the soma of the neuron and is transported along the axon to the presynaptic nerve endings in about 10 days. The mechanism of entry of synthesized acetylcholine into synaptic vesicles is still unknown.

Apparently, only a small part (15-20%) of the reserve of acetylcholine, which is stored in the vesicles, constitutes a fraction of the immediately available mediator, ready for release - spontaneously or under the influence of an action potential.

The deposited faction can only be mobilized after a certain delay. This is confirmed, firstly, by the fact that the newly synthesized acetylcholine is released approximately twice as fast as the previously present, and secondly, at nonphysiologically high frequencies of stimulation, the amount of acetylcholine released in response to one impulse drops to such a level at which the amount of acetylcholine released every minute remains constant. After blockade of choline uptake by hemicholinium, not all of the acetylcholine is released from the nerve endings. Therefore, there must be a third, stationary fraction, which may not be contained in synaptic vesicles. Apparently, there can be an exchange between these three factions. The histological correlates of these fractions have not yet been clarified, but it is assumed that the vesicles located near the synaptic cleft constitute a fraction of the immediately available transmitter, while the remaining vesicles correspond to the deposited fraction or part of it.

On the postsynaptic membrane, acetylcholine binds to specific macromolecules called receptors. These receptors are probably a lipoprotein with a molecular weight of about 300,000. Acetylcholine receptors are located only on the outer surface of the postsynaptic membrane and are absent in adjacent postsynaptic regions. Their density is about 10,000 per 1 sq. microns.

Acetylcholine serves as a mediator of all preganglionic neurons, postganglionic parasympathetic neurons, postganglionic sympathetic neurons that innervate the merocrine sweat glands, and somatic nerves. It is formed in nerve endings from acetyl-CoA and choline by the action of choline acetyltransferase. In turn, choline is actively captured by presynaptic endings from the extracellular fluid. In the nerve endings, acetylcholine is stored in synaptic vesicles and is released in response to the entry of an action potential and entry of divalent calcium ions. Acetylcholine is one of the most important neurotransmitters in the brain.

If the end plate is exposed to acetylcholine for several hundred milliseconds, then the membrane, depolarized at the beginning, gradually repolarizes, despite the constant presence of acetylcholine, that is, the postsynaptic receptors are inactivated. The reasons and mechanism of this process have not yet been studied.

Usually, the action of acetylcholine on the postsynaptic membrane lasts only 1-2 ms, because part of the acetylcholine diffuses from the end plate region, and part is hydrolyzed by the enzyme acetylcholinesterase (i.e., it is split into ineffective components choline and acetic acid). Acetylcholinesterase is present in large quantities in the end plate (the so-called specific or true cholinesterase), however, cholinesterases are also present in erythrocytes (also specific) and in blood plasma (nonspecific, i.e. they break down other choline esters). Therefore, acetylcholine, which diffuses from the end-plate region into the surrounding intercellular space and enters the bloodstream, is also broken down into choline and acetic acid. Most of the choline from the blood goes back to the presynaptic endings.

The action of acetylcholine on the postsynaptic membrane of postganglionic neurons can be reproduced by nicotine, and on the effector organs by muscarin (fly agaric toxin). In this regard, a hypothesis arose about the presence of two types of macromolecular acetylcholine receptors, and its action on these receptors is called nicotine-like or muscarinic. The nicotone-like action is blocked by bases, and the muscarinic-like action is blocked by atropine.

Substances that act on cells of effector organs in the same way as cholinergic postganglionic parasympathetic neurons are called parasympathomimetic, and substances that weaken the effect of acetylcholine are called parasympatholytic.

Bibliography

cholinergic receptor acetylcholine neuron

1. Kharkevich D.A. Pharmacology. M .: GEOTAR-MED, 2004

2. Zeimal E.V., Shelkovnikov S.A. - Muscarinic cholinergic receptors

3. Sergeev P.V., Galenko-Yaroshevsky P.A., Shimanovsky N.L., Essays on biochemical pharmacology, M., 1996.

4. Hugo F. Neurochemistry, M, "World", 1990

5. Sergeev P.V., Shimanovsky N.L., V.I. Petrov, Receptors, Moscow - Volgograd, 1999

Good day to all! What do we know about the brain and intellectual ability? Quite frankly, little, but what we know for sure is that there is a neurotransmitter that improves cognitive performance. If Darwin's theory is correct, then he, with each generation will be produced in greater quantities, if a person does not degrade. The interest is that its level can be increased already now, moreover, you can “play” with acetylcholine so that it develops first one and then another property of the brain. It will not make you happier, more energetic or calmer, but it will help you to become a more intelligent Human than it was before, it will speed up the learning process, all other things being equal.

Acetylcholine is one of the first discovered, it happened in the first half of the 20th century.

What is acetylcholine made for?

He is responsible for intellectual abilities, as well as for neuromuscular communication, not only biceps, triceps, but also the autonomic nervous system, that is, for the muscles of the organs.

Large dosages of acetylcholine "slow down" the body, "small" ones speed it up.

Begins to be more actively developed in a situation of obtaining new data or reproducing old ones.

Where and how is it produced

Acetylcholine is synthesized in axons, nerve terminals, this is the area where the end of one neuron adjoins another, from 2 substances:

Then the acetylcholine in the neuron is packed into a kind of balls, containers, called vesicles, in the amount of about 10,000 molecules. And it goes to the end of the neuron in the presynaptic end. There, the vesicles merge with the cell membrane, and their contents fly out of the neuron into the synaptic cleft. Imagine an iron mesh, which is often pulled up instead of fences in small towns, and a small bag of water. We throw this bag into the net, it breaks, remains on the net, and the water flies on. The principle is similar: acetylcholine in vesicles, balls is directed to the end of the neuron, there the ball "breaks" inside, and the acetylcholine flew by.

Acetylcholine is either retained in the synaptic cleft, or enters another neuron, or returns back to the first. If it comes back, it is collected again in packages and on the fence)

How does it get into the second neuron?

Each neurotransmitter tends to its own receptor on the surface of the 2nd neuron. Receptors are like doors, each door needs its own key, its own neurotransmitter. Acetylcholine has 2 types of keys, with which it opens 2 types of doors to another neuron: nicotinic and muscarinic.

Interesting moment : The enzyme Acetylcholinesterase is responsible for the balance of acetylcholine in the synaptic cleft. When you gorge on some nootropic pills, acetylcholine rises, if its amount gets crazy, then this enzyme turns on. It breaks down "excess" acetylcholine into choline and acetate.

In patients with Alzheimer's (poor memory), this enzyme works at an increased speed; drugs with temporary inhibition of the enzyme acetylcholinesterase show good results in their treatment. Inhibition means inhibition of the reaction, that is, drugs that inhibit the work of an enzyme that destroys acetylcholine, roughly speaking, make you smarter. BUT!!! There is a huge BUT! Irreversible inhibition of this enzyme increases the concentration of acetylcholine too much, this is not good.

It causes convulsions, paralysis, even death. Irreversible acetylcholinesterase inhibitors are the majority of nerve gases. There is so much neurotransmitter that all muscles literally freeze, in a contracted position. If, for example, the bronchi are strongly narrowed, the person will suffocate. Well, now you know how paralyzing gases work.

Pros of acetylcholine:

- Improves the cognitive abilities of the brain, makes it smarter.

- Improves memory, helps in old age.

- Improves neuromuscular communication. It is useful in sports, due to the faster adaptation of the body to stress. It will indirectly force you to lift more weight or run a distance faster, through a quick adaptation to existing conditions.

- Acetylcholine is not stimulated by any drugs, but rather suppressed, there is no reason for abuse. To the greatest extent, acetylcholine is suppressed by hallucinogens. This is logical, for the occurrence of delirium, a dull brain is required.

- In general, a useful neurotransmitter for everyday quiet life. Helps to plan, less impulsive decisions and mistakes. Corresponds to the proverb "measure 7 times, cut once."

Cons of acetylcholine:

- Harmful in stressful situations where you need to act.

- It inhibits the body when there is a lot of it. Look at the scientists, 90% calm and serene like boas. A dragon will fly by - they will not budge. But scientists are smart - you can't argue.

Amendment: people are different and the "sets" of neurotransmitters are different, if a person has a lot of acetylcholine and a lot of glutamate, then he will be faster and more decisive than someone else's. And the intellectual potential will change slightly.

Acetylcholine Reducing Supplements

Outcome:

Good luck!

The (endogenous) acetylcholine formed in the body plays an important role in vital processes: it contributes to the transmission of nervous excitement in the central nervous system, autonomic ganglia, and the endings of the parasympathetic (motor) nerves. Acetylcholine is a chemical transmitter (neurotransmitter) of nervous excitement; the endings of the nerve fibers for which it serves as a mediator are called cholinergic, and the receptors that interact with it are called cholinergic receptors. Cholinergic receptors are complex protein molecules (nucleoproteins) of tetrameric structure, localized on the outer side of the postsynaptic (plasma) membrane. By nature, they are heterogeneous. Cholinergic receptors located in the region of postganglionic cholinergic nerves (heart, smooth muscles, glands) are designated as m-cholinergic receptors (muscarinic-sensitive), and those located in the region of ganglionic synapses and in somatic neuromuscular synapses - as n-cholinergic receptors (nicotine-sensitive) (C. . Anichkov). This division is associated with the peculiarities of the reactions arising from the interaction of acetylcholine with these biochemical systems, muscarinic (lowering blood pressure, bradycardia, increased secretion of the salivary, lacrimal, gastric and other exogenous glands, constriction of the pupils, etc.) in the first case and nicotine-like ( contraction of skeletal muscles, etc.) in the second. M- and n-cholinergic receptors are localized in different organs and systems of the body, including the central nervous system. In recent years, muscarinic receptors have begun to be divided into a number of subgroups (m1, m2, m3, m4, m5). The localization and role of m1 and m2 receptors has been most studied at present. Acetylcholine does not have a strictly selective effect on various cholinergic receptors. To one degree or another, it affects m- and n-cholinergic receptors and subgroups of m-cholinergic receptors. The peripheral muscarinic action of acetylcholine is manifested in the slowing down of heart contractions, expansion of peripheral blood vessels and a decrease in blood pressure, activation of gastric and intestinal peristalsis, contraction of the muscles of the bronchi, uterus, gall and urinary bladder, increased secretion of the digestive, bronchial, sweat and lacrimal glands ( miosis). The latter effect is associated with increased contraction of the circular muscle of the iris, which is innervated by postganglionic cholinergic fibers of the oculomotor nerve (n. Oculomotorius). At the same time, as a result of contraction of the ciliary muscle and relaxation of the ciliary girdle zinn ligament, a spasm of accommodation occurs. Pupil constriction caused by the action of acetylcholine is usually accompanied by a decrease in intraocular pressure. This effect is partly explained by the dilatation of the pupil with constriction and flattening of the iris of the Schlemm's canal (venous sinus of the sclera) and fountain spaces (the space of the iris-corneal angle), which improves the outflow of fluid from the interior of the eye. It is possible, however, that other mechanisms are also involved in the decrease in intraocular pressure. Due to their ability to reduce intraocular pressure, substances that act like acetylcholine (cholinomimetics, anticholinesterase drugs) are widely used to treat glaucoma1. The peripheral nicotine-like action of acetylcholine is associated with its participation in the transmission of nerve impulses from the preganglionic fibers to the postganglionic fibers in the vegetative nodes, as well as from the motor nerves to the striated muscles. In small doses, it is a physiological transmitter of nervous excitement, in large doses it can cause persistent depolarization in the area of ​​synapses and block the transmission of excitation. Acetylcholine also plays an important role as a mediator in the central nervous system. It participates in the transmission of impulses in different parts of the brain, while in small concentrations it facilitates, and in large concentrations it inhibits synaptic transmission. Changes in the metabolism of acetylcholine can lead to impaired brain function. Some of its central antagonists are psychotropic drugs. An overdose of acetylcholine antagonists can cause disorders of higher nervous activity (hallucinogenic effect, etc.). For use in medical practice and experimental research, acetylcholine chloride (Acetylcholini chloridum) is produced.

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    ✪ Acetylcholine, IQ 160

    ✪ Chemistry of thought

    ✪ Lecture 5. Acetylcholine (Acch), Nicotinic and muscarinic receptors. Nicotine addiction.

    ✪ Stimulants: Superman for 1 day!

    ✪ Citicholine / CDP-Choline / Ceraxon: When You Need to Repair Your Brain

    Subtitles

Properties

Physical

Colorless crystals or white crystalline mass. Blurs in the air. Let's easily dissolve in water and alcohol. When boiled and stored for a long time, solutions decompose.

Medical

The physiological cholinomimetic effect of acetylcholine is due to its stimulation of the terminal membranes of M- and N-cholinergic receptors.

The peripheral muscarinic action of acetylcholine is manifested in the slowing down of heart contractions, expansion of peripheral blood vessels and lowering blood pressure, increased peristalsis of the stomach and intestines, contraction of the muscles of the bronchi, uterus, gallbladder and urinary bladder, increased secretion of the digestive, bronchial, sweat and miosis. The miotic effect is associated with increased contraction of the circular muscle of the iris, which is innervated by postganglionic cholinergic fibers of the oculomotor nerve. At the same time, as a result of contraction of the ciliary muscle and relaxation of the ciliary girdle zinn ligament, a spasm of accommodation occurs.

The constriction of the pupil, caused by the action of acetylcholine, is usually accompanied by a decrease in intraocular pressure. This effect is partially explained by the fact that when the pupil narrows and the iris is flattened, the Schlemm canal (venous sinus of the sclera) and fountain spaces (spaces of the iris-corneal angle) expand, which ensures a better outflow of fluid from the interior of the eye. It is possible that other mechanisms are also involved in lowering intraocular pressure. Due to the ability to reduce intraocular pressure, substances that act like acetylcholine (cholinomimetics, anticholinesterase drugs) are widely used for the treatment of glaucoma. It should be borne in mind that when these drugs are injected into the conjunctival sac, they are absorbed into the bloodstream and, having a resorptive effect, can cause side effects characteristic of these drugs. It should also be borne in mind that prolonged (over a number of years) use of miotic substances can sometimes lead to the development of persistent (irreversible) miosis, the formation of posterior petechiae and other complications, and prolonged use of anticholinesterase drugs as miotics can contribute to the development of cataracts.

Acetylcholine also plays an important role as a mediator of the central nervous system. It is involved in the transmission of impulses in different parts of the brain, while small concentrations facilitate, and large ones inhibit synaptic transmission. Changes in the metabolism of acetylcholine lead to gross dysfunction of the brain. Its lack largely determines the clinical picture of such a dangerous neurodegenerative disease as Alzheimer's disease. Some centrally acting antagonists of acetylcholine (see Amisil) are psychotropic drugs (see also Atropine). An overdose of acetylcholine antagonists can cause disorders of higher nervous activity (have a hallucinogenic effect, etc.). The anticholinesterase effect of a number of poisons is based precisely on the ability to cause the accumulation of acetylcholine in synaptic clefts, overexcitation of cholinergic systems and more or less rapid death (chlorophos, karbofos, sarin, soman) (Burnazyan, "Toxicology for students of medical universities", Kharkevich DI, " Pharmacology for students of the medical faculty ").

Application

General application

Acetylcholine chloride (lat. Acetylcholini chloridum). As a drug, acetylcholine chloride is not widely used.

Treatment

When taken orally, acetylcholine is very rapidly hydrolyzed and is not absorbed from the mucous membranes of the gastrointestinal tract. When administered parenterally, it has a quick, sharp and short-lived effect (like adrenaline). Like other quaternary compounds, acetylcholine poorly penetrates from the vascular bed through the blood-brain barrier and does not significantly affect the central nervous system when administered intravenously. Sometimes in the experiment, acetylcholine is used as a vasodilator for spasms of peripheral vessels (endarteritis, intermittent claudication, trophic disorders in the stumps, etc.), for spasms of the retinal arteries. In rare cases, acetylcholine was administered for intestinal and bladder atony. Acetylcholine has also been used occasionally to facilitate X-ray diagnosis of esophageal achalasia.

Application form

Since the 1980s, acetylcholine has not been used as a medicine in practical medicine (M. D. Mashkovsky, "Medicines", volume 1), since there are a large number of synthetic cholinomimetics with a longer and more targeted action. It was administered subcutaneously and intramuscularly at a dose (for adults) of 0.05 g or 0.1 g. Injections, if necessary, were repeated 2-3 times a day. During the injection, it was necessary to make sure that the needle did not enter the vein. Intravenous administration of cholinomimetics is not allowed due to the possibility of a sharp decrease in blood pressure and cardiac arrest.

Dangers of use in treatment

When using acetylcholine, it should be borne in mind that it causes a narrowing Participation in life processes

The (endogenous) acetylcholine formed in the body plays an important role in vital processes: it takes part in the transmission of nervous excitement in the central nervous system, vegetative nodes, the endings of the parasympathetic and motor nerves. Acetylcholine is associated with memory functions. Decreased acetylcholine in Alzheimer's disease leads to impaired memory in patients. Acetylcholine plays an important role in falling asleep and waking up. Awakening occurs with an increase in the activity of cholinergic neurons in the basal nuclei of the forebrain and (nucleoprotein) located on the outer side of the postsynaptic membrane. In this case, the cholinergic receptor of postganglionic cholinergic nerves (heart, smooth muscles, glands) is designated as m-cholinergic receptors (muscarinic-sensitive), and located in the region of ganglionic synapses and in somatic neuromuscular synapses - as n-cholinergic receptors (nicotine-sensitive). This division is associated with the peculiarities of the reactions arising from the interaction of acetylcholine with these biochemical systems: muscarinic in the first case and nicotine-like in the second; m- and n-cholinergic receptors are also found in different parts of the central nervous system.

According to modern data, muscarinic receptors are divided into M1-, M2- and M3-receptors, which are distributed differently in organs and are heterogeneous in physiological significance (see Atropine, Pirenzepin).

Acetylcholine does not have a strict selective effect on the types of cholinergic receptors. To one degree or another, it acts on m- and n-cholinergic receptors and on subgroups of m-cholinergic receptors. The peripheral nicotine-like action of acetylcholine is associated with its participation in the transmission of nerve impulses from the preganglionic fibers to the postganglionic fibers in the vegetative nodes, as well as from the motor nerves to the striated muscles. In small doses, it is a physiological transmitter of nervous excitement; in large doses, it can cause persistent depolarization in the area of ​​synapses and block the transmission of excitation.

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