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Pharmacological group acetylcholine. Use during pregnancy and breastfeeding

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Properties

Physical

Colorless crystals or white crystalline mass. Dissolves in the air. Easily soluble in water and alcohol. When boiled and stored for a long time, the 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-like effect of acetylcholine manifests itself in a slowdown of heart contractions, expansion of peripheral blood vessels and a decrease in blood pressure, increased peristalsis of the stomach and intestines, contraction of the muscles of the bronchi, uterus, gall and bladder, increased secretion of the digestive, bronchial, sweat and lacrimal glands, miosis. The miotic effect is associated with increased contraction of the orbicularis iris muscle, 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 zonular ligament of the ciliary girdle, a spasm of accommodation occurs.

Constriction of the pupil caused by the action of acetylcholine is usually accompanied by a decrease in intraocular pressure. This effect is partly explained by the fact that when the pupil narrows and the iris flattens, Schlemm’s canal (venous sinus of the sclera) and fountain spaces (spaces of the iridocorneal angle) expand, which ensures better outflow of fluid from internal environments eyes. It is possible that other mechanisms are also involved in the decrease in 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 introduced into the conjunctival sac, they are absorbed into the blood and, having a resorptive effect, can cause symptoms characteristic of these drugs. side effects. It should also be borne in mind that long-term (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 long-term use as miotics, anticholinesterase drugs may promote the development of cataracts.

Acetylcholine also plays an important role as a central nervous system neurotransmitter. It is involved in the transmission of impulses in different parts of the brain, with small concentrations facilitating, and large concentrations inhibiting synaptic transmission. Changes in acetylcholine metabolism lead to severe disruption of brain function. Its deficiency largely determines the clinical picture of such a dangerous neurodegenerative disease as Alzheimer's disease [ ] . Some centrally acting acetylcholine antagonists (see Amizil) 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 medical university students,” Kharkevich D.I., “ Pharmacology for students of the Faculty of Medicine").

Application

General Application

For use in medical practice and acetylcholine chloride (lat. Acetylcholini chloridum). As a medicine acetylcholine chloride wide application does not have.

Treatment

When taken orally, acetylcholine is hydrolyzed very quickly and is not absorbed from the mucous membranes of the gastrointestinal tract. When administered parenterally, it has a quick, sharp and short-lasting effect (like adrenaline). Like other quaternary compounds, acetylcholine penetrates poorly from the vascular bed through the blood-brain barrier and does not have a significant effect on the central nervous system when administered intravenously. Sometimes in experiments, acetylcholine is used as a vasodilator for spasms of peripheral vessels (endarteritis, intermittent claudication, trophic disorders in the stumps, etc.), and for spasms of the retinal arteries. IN in rare cases acetylcholine was administered for intestinal and bladder atony. Acetylcholine has also sometimes been used to relieve X-ray diagnostics achalasia of the esophagus.

Form of application

Since the 1980s, acetylcholine has been used as a drug in practical medicine not used (M. D. Mashkovsky, “ Medicines", volume 1), since there are a large number of synthetic cholinomimetics with a longer and more targeted effect. It was prescribed 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. When injecting, you had to make sure that the needle did not enter a vein. Intravenous administration Cholinomimetics are not allowed due to the possibility sharp decline blood pressure and cardiac arrest.

Danger of use during treatment

When using acetylcholine, it should be taken into account that it causes a narrowing Participation in life processes

Acetylcholine formed in the body (endogenous) plays important role in life processes: it takes part in the transmission nervous excitement in the central nervous system, autonomic nodes, endings of parasympathetic and motor nerves. Acetylcholine is associated with memory functions. A decrease in acetylcholine in Alzheimer's disease leads to memory impairment 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), localized on outside postsynaptic membrane. In this case, the cholinergic receptor of postganglionic cholinergic nerves (heart, smooth muscles, glands) are designated as m-cholinergic receptors (muscarinic-sensitive), and those located in the area of ganglion synapses and in somatic neuromuscular synapses are designated as n-cholinergic receptors (nicotine-sensitive). This division is associated with the characteristics of the reactions that occur when acetylcholine interacts with these biochemical systems: muscarinic-like in the first case and nicotine-like in the second; m- and n-cholinergic receptors are also located in different parts of the central nervous system.

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

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 effect of acetylcholine is associated with its participation in the transmission nerve impulses from preganglionic fibers to postganglionic fibers in the autonomic ganglia, as well as from motor nerves to striated muscles. In small doses it is a physiological transmitter of nervous excitation; in large doses it can cause persistent depolarization in the area of synapses and block the transmission of excitation.

Acetylcholine chloride is a drug from the group of m- and n-cholinomimetics; it has a stimulating effect on m- and n-cholinergic receptors.

What is the effect of Acetylcholine chloride?

The M-cholinomimetic effect will manifest itself as bradycardia, the tone will increase, as well as the contractile activity of the muscles of the bronchi, bladder, gastrointestinal tract, as well as the ciliary muscle of the eye. In addition, the secretion of the salivary, lacrimal glands, bronchi, stomach, and intestines will increase. The sphincters of the bladder and gastrointestinal tract will relax under the influence of this drug.

The N-cholinomimetic effect of the drug Acetylcholine chloride is associated with the participation of the substance acetylcholine in the transmission of nerve impulses to postganglionic autonomic nodes and to striated muscles. In small doses, this drug is considered a transmitter of nervous excitation, and in large doses it leads to persistent depolarization in the area of synapses, which leads to blocking the transmission of excitation.

The drug Acetylcholine chloride takes part directly in the transmission of nerve impulses in many parts of the brain, while in high concentrations it inhibits synaptic transmission, and in small concentrations it facilitates.

What are the indications for use of Acetylcholine chloride?

I will list some conditions in which the use of the drug Acetylcholine chloride is indicated:

The patient has endarteritis;
For intermittent claudication, this is also used medicinal product;
Its use is also shown for trophic disorders in the stumps;
The remedy is also effective in the presence of spasms of the retinal arteries;
It is used for intestinal atony, as well as for decreased bladder tone.

In addition, the drug Acetylcholine chloride is used to relieve x-ray examination if there is such pathological process as achalasia of the esophagus.

What are the contraindications for use of the drug Acetylcholine chloride?

Among the contraindications of Acetylcholine chloride, the instructions for use list the following conditions:

This product should not be used when bronchial asthma;
In the presence of angina, Acetylcholine chloride is also contraindicated;
It is not used for severe atherosclerotic processes in the human body;
The drug is not prescribed for epilepsy;
During lactation;
When bleeding from digestive tract;
With hyperkinesis;
Its use is contraindicated in all trimesters of pregnancy.

If the patient has any inflammatory processes, localized in abdominal cavity to surgical intervention, in this case Acetylcholine is also contraindicated.

What is the use and dosage of Acetylcholine chloride?

This drug is used parenterally, namely, it is administered subcutaneously or intramuscularly, and the dosage can be 50-100 mg, the frequency of use should not exceed three times during the day. Maximum doses Acetylcholine chloride is as follows: single dose - 100 mg, and daily amount no more than 300 mg.

At simultaneous use with anticholinesterase drugs, the cholinomimetic effect of acetylcholine chloride is noticeably enhanced.

At joint use m-anticholinergic agents, neuroleptics (clozapine, phenothiazine, chlorprothixene), as well as tricyclic antidepressants, reduce the effect of acetylcholine chloride. It should be noted that this drug is not used during breastfeeding, as well as during pregnancy.

What kind of medicine is Acetylcholine chloride? side effects?

When using Acetylcholine chloride, it is possible that side effects may occur, for example, from digestive system there may be nausea, vomiting, the patient will complain of pain in the abdomen, in addition loose stool, signs of salivation are noted.

From the outside cardiovascular system Side effects may also occur, in particular bradycardia, and the patient may complain of low blood pressure.

Other side effects may also occur and will appear increased sweating, add rhinorrhea, bronchospasm is possible, in addition, a person may experience frequent urination.

From the outside nervous system noted headache In addition, accommodation is disrupted and lacrimation occurs. With obvious manifestation side effects It is recommended to consult your doctor.

Special instructions

Currently, the use of Acetylcholine Chloride is limited in terms of systemic use, but it is included in combination drugs for local use in ophthalmic surgery, in order to create a rapid constriction of the pupil, the so-called miosis.

Preparations containing acetylcholine chloride (analogs)

Acetylcholine chloride is contained in the drug of the same name, it is produced in dosage form, which is represented by a fine powder, it is necessary to prepare a medicinal solution from it, which is intended for intramuscular injection, as well as for subcutaneous injections. It must be used before the expiration date indicated on the package.

This drug is often used in ophthalmology, for example, for surgical intervention on the anterior chamber of the eye, in particular, to remove existing cataracts, for iridectomy, as well as for keratoplasty. As a result of the use of Acetylcholine chloride, pupil constriction is ensured for some time.

Conclusion

Before using the drug, you must consult with your doctor.

Acetylcholine is a neurotransmitter considered to be a natural factor that modulates wakefulness and sleep. Its precursor is choline, which penetrates from the intercellular space into the internal space nerve cells.

Acetylcholine is the main messenger of the cholinergic system, also known as parasympathetic system, which is a subsystem of the autonomic nervous system responsible for the rest of the body and improves digestion. Acetylcholine is not used in medicine.

Acetylcholine is a so-called neurohormone. This is the first neurotransmitter discovered. This breakthrough occurred in 1914. The discoverer of acetylcholine was the English physiologist Henry Dale. Austrian pharmacologist Otto Lowy made a significant contribution to the study of this neurotransmitter and its popularization. The discoveries of both researchers were awarded the Nobel Prize in 1936.

Acetylcholine (ACh) is a neurotransmitter (i.e. chemical substance, whose molecules are responsible for the process of signal transmission between neurons through synapses and neuronal cells). It is located in a neuron, in a small vesicle surrounded by a membrane. Acetylcholine is a lipophobic compound and does not penetrate the blood-brain barrier well. The state of excitation caused by acetylcholine is the result of an action on peripheral receptors.

Acetylcholine acts simultaneously on two types of autonomic receptors:

M (muscarinic) - located in various tissues, such as smooth muscles, brain structures, endocrine glands, myocardium;
N (nicotine) - located in the ganglia of the autonomic nervous system and neuromuscular junctions.

Once it enters the bloodstream, it stimulates the entire system with a predominance of stimulating symptoms common system. The effects of acetylcholine are short-lived, non-specific and overly toxic. Therefore, it is not currently medicinal.

How is acetylcholine formed?

Acetylcholine (C7H16NO2) is an ester acetic acid(CH3COOH) and choline (C5H14NO +), which is formed by choline acetyltransferase. Choline is delivered to the central nervous system along with the blood, from where it is transferred to nerve cells through active transport.

Acetylcholine can be stored in synaptic vesicles. This neurotransmitter, due to depolarization of the cell membrane (electronegativity reduces the electrical potential of the cell membrane), is released into the synaptic space.

Acetylcholine is degraded in the central nervous system by enzymes with hydrolytic properties, the so-called cholinesterases. Catabolism ( general reaction, leading to degradation of complex chemical compounds into simpler molecules) acetylcholine, this is associated with acetylcholinesterase (AChE - an enzyme that breaks down acetylcholine to choline and the acetic acid residue) and butyrylcholinesterase (BuChE - an enzyme that catalyzes the reaction of acetylcholine + H2O → choline + carboxylic acid anion), which are responsible for the hydrolysis reaction (a double exchange reaction that takes place between water and a substance dissolved in it) in neuromuscular junctions. This is the result of the action of acetylcholinesterase and butyrylcholinesterase, which is reabsorbed into nerve cells as a result of the active functioning of the choline transporter.

The effect of acetylcholine on the human body

Acetylcholine shows, among others, effects on the body such as:

decrease in level blood pressure,
dilation of blood vessels,
reducing the force of myocardial contraction,
stimulation of glandular secretion,
compressing the airways,
releasing heart rate,
miosis,
contraction of smooth muscles of the intestines, bronchi, bladder,
causing contraction of striated muscles,
affecting memory processes, the ability to concentrate, the learning process,
maintaining a state of wakefulness,
providing communication between different areas of the central nervous system,
stimulation of peristalsis in the gastrointestinal tract.

Acetylcholine deficiency leads to inhibition of nerve impulse transmission, resulting in muscle paralysis. His low level means problems with memory and information processing. Acetylcholine preparations are available, the use of which has a positive effect on cognition, mood and behavior and delays the onset of neuropsychiatric changes. In addition, they prevent the formation of senile plaques. Increased concentration of acetylcholine in forebrain leads to improved cognitive function and slowdown of neurodegenerative changes. This prevents Alzheimer's disease or myasthenia gravis. A rare condition of excess acetylcholine in the body.

It is also possible to be allergic to acetylcholine, which is responsible for cholinergic urticaria. The disease mainly affects young people. The development of symptoms occurs as a result of irritation of affective cholinergic fibers. This occurs during excessive exertion or consumption of hot food. Skin changes in the form of small blisters surrounded by a red border are accompanied by itching. Cholinergic nettle disappears after the use of antihistamines, sedatives and medications against excessive sweating.

Acetylcholine- one of the most important neurotransmitters, it carries out neuromuscular transmission and is the main one in the parasympathetic nervous system. Destroyed by enzyme - acetylcholinesterase.

It is used as medicinal substance and in pharmacological research.

Medicine

Peripheral muscarinic-like action (muscarine is the one in fly agaric):

– slow heart rate

– spasm of accommodation

Demotion blood pressure

– dilation of peripheral blood vessels

– contraction of the muscles of the bronchi, gall and bladder, uterus

– increased peristalsis of the stomach, intestines,

– increased secretion of the digestive, sweat, bronchial, lacrimal glands, miosis.

Constriction of the pupil is associated with a decrease in intraocular pressure.

Acetylcholine plays an important role as a mediator of the central nervous system (transmission of impulses in parts of the brain, small concentrations facilitate, and large concentrations inhibit synaptic transmission).

Changes in acetylcholine metabolism can lead to impaired brain function. The deficiency largely determines the picture of the disease - Alzheimer's disease.

Some centrally acting antagonists are psychotropic drugs. An overdose of antagonists can have a hallucinogenic effect.

Why is it needed?

Formed in the body, it takes part in the transmission of nervous excitation to the central nervous system, autonomic nodes, and the endings of parasympathetic and motor nerves.

Acetylcholine associated with memory functions. The decline in Alzheimer's disease leads to memory loss.

Acetylcholine plays an important role in waking up and falling asleep. Awakening occurs when the activity of cholinergic neurons increases.

Physiological properties

In small doses it is a physiological transmitter of nervous excitation, and in large doses it can block the transmission of excitation.

This neurotransmitter is affected by smoking and consumption of fly agarics.

Acetylcholine is not the most famous substance, but it plays an important role in processes such as memory and learning. Let's lift the curtain on one of the most underrated neurotransmitters in our nervous system.

First among equals

Figure 1. Otto Löwy's classic experiment in identifying chemical mediators of nerve impulse transmission (1921). Objects - isolated and immersed in saline solution hearts of two frogs (donor and recipient). Description is given in the text. Figure from en.wikipedia.org, adapted.

In popular scientific literature of a medical and neurophysiological nature, three neurotransmitters are most often discussed: dopamine, serotonin and norepinephrine. This is largely due to the fact that normal and disease states associated with changes in the levels of these neurotransmitters are easier to understand and arouse more interest among readers. I have already written about these substances, now it’s time to pay attention to another mediator.

We'll talk about acetylcholine, and this will be symbolic, considering that he was first open neurotransmitter. At the beginning of the 20th century, there was a debate among scientists about how a signal is transmitted from one nerve cell to another. Some believed that electric charge Having run along one nerve fiber, it is transmitted to another along some thinner “wires”. Their opponents argued that there are substances that carry a signal from one nerve cell to another. In principle, both sides turned out to be right: there are chemical and electrical synapses. However, supporters of the second hypothesis turned out to be “to the right” - chemical synapses predominate in the human body.

To understand the peculiarities of signal transmission from one cell to another, physiologist Otto Löwy conducted simple but elegant experiments (Fig. 1). He stimulated electric shock the vagus nerve of the frog, which led to a decrease in heart rate*. Then Löwy collected the liquid around this heart and applied it to the heart of another frog - and it also slowed down. This proved the existence of a certain substance that transmits a signal from one nerve cell to another. Löwy named the mysterious substance vagusstoff("substance vagus nerve"). Now we know it under the name acetylcholine. The issue of chemical synaptic transmission was also dealt with by the Briton Henry Dale, who discovered acetylcholine even before Loewy. In 1936, both scientists received the Nobel Prize in Physiology or Medicine "for their discoveries concerning the chemical transmission of nerve impulses."

* - About how our heart contracts - about automatism, conducting pacemakers and even funny channels - read in the review " » . - Ed.

Acetylcholine (Figure 2) is produced in nerve cells from choline and acetyl coenzyme A (acetyl-CoA). The enzyme acetylcholinesterase, located in the synaptic cleft, is responsible for the destruction of acetylcholine; We will talk about this enzyme in detail later. The structure of the acetylcholinergic system of the brain is similar to the structure of other neurotransmitter systems (Fig. 3). There are a number of structures in the brainstem that release acetylcholine, which travels along axons to the basal ganglia of the brain. It has its own acetylcholine neurons, whose processes diverge widely throughout the cortex and penetrate the hippocampus.

Figure 3. The acetylcholine system of the brain. We see that in the deep parts of the brain there are clusters of nerve cells (in the forebrain and brainstem), which send their processes to various departments cortex and subcortical areas. At the terminal points, acetylcholine is released from neuron endings. The local effects of a neurotransmitter vary depending on the type of receptor and its location. MS - medial septal nucleus, DB - diagonal ligament of Broca, nBM - basal magnocellular nucleus (Meitner's nucleus); PPT - pedunculopontine tegmental nucleus, LDT - lateral dorsal tegmental nucleus (both nuclei are in the reticular formation of the brainstem). Drawing from, adapted.

Acetylcholine receptors are divided into two groups - muscarinic And nicotine. Stimulation of muscarinic receptors leads to changes in cell metabolism through the G-protein system* ( metabotropic receptors), and the effect on nicotine - to change membrane potential (ionotropic receptors). This occurs because nicotinic receptors bind to sodium channels on the surface of cells. Receptor expression varies among different areas nervous system (Fig. 4).

* - The spatial structures of several representatives of the huge family of GPCR receptors - membrane receptors acting through activation of the G protein - are clearly described in the articles: “ Receptors in active form" (about active form rhodopsin), " Structures of GPCR receptors “in the piggy bank”"(about dopamine and chemokine receptors), " Mood transmitter receptor"(about two serotonin receptors). - Ed.

Figure 4. Distribution of muscarinic and nicotinic receptors in the human brain. Drawing from the website, adapted.

Mediator of memory and learning

The acetylcholine system of the brain is directly related to such a phenomenon as synaptic plasticity- the ability of a synapse to increase or decrease the release of a neurotransmitter in response to an increase or decrease in its activity. Synaptic plasticity is important process For memory and learning, so scientists sought to detect it in the part of the brain responsible for these functions - the hippocampus. Large quantity acetylcholine neurons send their processes to the hippocampus, and there they influence the release of neurotransmitters from other nerve cells. The method for carrying out this process is quite simple: on the body of the neuron and its presynaptic part there are various nicotinic receptors (mainly α 7 - and β 2 -types). Their activation will lead to the fact that the passage of the signal through the innervated cell will be simplified, and it will be more likely to pass on to the next neuron. The greatest influence of this kind is experienced by GABAergic neurons - nerve cells whose neurotransmitter is γ-aminobutyric acid.

GABAergic neurons are important part system that generates electrical rhythms in our brain. These rhythms can be recorded and studied using an electroencephalogram, a widely available research method in neurophysiology. Rhythms of different frequencies are designated by Greek letters: 8–14 Hz is the alpha rhythm, 14–30 Hz is the beta rhythm, and so on. The use of acetylcholine receptor stimulants causes theta (0.4–14 Hz) and gamma (30–80 Hz) rhythms to appear in the brain. These rhythms typically accompany active cognitive activity. Stimulation of postsynaptic muscarinic acetylcholine receptors located on neurons of the hippocampus (memory center) and prefrontal cortex (center complex shapes behavior), leads to the excitation of these cells and the generation of the rhythms mentioned above. They accompany various cognitive activities - for example, building a temporal sequence of events.

The hippocampus and prefrontal cortex play an important role in learning. From the point of view of reflexes, any learning occurs in two ways. Let's say you are an experimenter, and the object of your experiment is a mouse. In the first case, the light in its cage turns on (the conditioned stimulus), and the rodent receives a piece of cheese (the unconditioned stimulus) before the light goes out. The emerging reflex can be called detainees. In the second case, the light also turns on, but the mouse receives the treat some time after the light turns off. This type of reflex is called trace. Reflexes of the second type depend on the awareness of stimuli more than reflexes of the first type. Suppression of the activity of the acetylcholinergic system leads to the fact that animals do not develop trace reflexes, although no problems arise with delayed ones.

When comparing the secretion of acetylcholine in the brain of rats that developed both types of reflexes, interesting data were obtained. Rats that successfully mastered the temporal relationship between a conditioned and an unconditioned stimulus showed a significant increase in acetylcholine levels in the medial prefrontal cortex (Fig. 5) compared to the hippocampus. The difference in acetylcholine levels was especially significant in rats that had developed the trace reflex. Those rodents that failed both tasks showed approximately equal levels of the neurotransmitter in the brain regions studied (Fig. 6). Based on this we can conclude that The prefrontal cortex plays a major role in learning directly, and the hippocampus stores acquired knowledge.

Figure 5. Acetylcholine release in the hippocampus (HPC) and prefrontal cortex (PFC) of rats during successful reflex acquisition. The maximum level of acetylcholine is observed in the prefrontal cortex during the development of the trace reflex. Drawing from .

Figure 6. Acetylcholine release in the hippocampus (HPC) and prefrontal cortex (PFC) of rats after learning failure. Almost the same acetylcholine content is recorded in the two zones, regardless of the reflex. Drawing from.

Attention receptors

Figure 7. Diversity of acetylcholine receptors (nAChRs) in the layers of the prefrontal cortex. Drawing from .

For learning, not only intelligence or memory capacity is important, but also attention. Without attention, even the most successful student will fail. Acetylcholine is also involved in processes that regulate attention.

Attention - focused perception or thinking about a problem - is accompanied by increased activity in the prefrontal cortex. Acetylcholine fibers are sent to the frontal cortex from deep sections brain Due to the fact that we often need a quick switch of attention, it is logical that nicotinic (ionotropic) acetylcholine receptors are involved in the regulation of attention, rather than muscarinic ones, which cause slower and predominantly structural changes in neurons. Damage to acetylcholine structures in the deep parts of the brain reduces the activity of the medial prefrontal cortex and impairs attention. Moreover, the interaction of deep acetylcholine structures with the prefrontal cortex is not limited to ascending signals. Neurons in the frontal cortex also send their signals to underlying regions, which allows for the creation of a self-regulating system for maintaining attention. Attention is maintained due to the effect of acetylcholine on presynaptic and postsynaptic receptors (Fig. 7).

When talking about nicotinic receptors and attention, the question arises about improving cognitive functions through smoking, that is, introducing an additional dose of nicotine, albeit in the form cigarette smoke. The situation here is quite clear, and the results do not give smokers an extra argument in favor of their addiction. Nicotine coming from outside disrupts normal development brain, which can lead to attention disorders(on for many years) . If we compare smokers and non-smokers, the former have worse attention indicators than their opponents. Improved attention in smokers occurs when smoking a cigarette after a long period of abstinence, when Bad mood and cognitive problems go up in smoke.

Medicine for memory

If normally the acetylcholinergic system of our brain is responsible for memory, attention and learning, then diseases in which this type of transmission in our brain is disrupted should be manifested by corresponding symptoms: memory loss, decreased attention and the ability to learn new things. Here we must immediately make a reservation that during normal aging, the vast majority of people experience a decrease in both the ability to remember new things and mental alertness in general. If these impairments are so severe that they interfere with the older person's ability to carry out daily activities and meet their daily needs (care for themselves), then doctors may suspect dementia. If you want to learn more about dementia, I recommend starting by reading WHO newsletter dedicated to this pathology.

Strictly speaking, dementia is not separate disease, but a syndrome that occurs in a number of diseases. One of the most common diseases that leads to dementia is Alzheimer's disease. It is believed that in Alzheimer's disease, a pathological protein β-amyloid accumulates in nerve cells, which disrupts the activity of nerve cells, which ultimately leads to their death. In addition to this theory, there are a number of others that have their own evidence. It is likely that in Alzheimer's disease, different processes occur in the brain cells of different patients, but they lead to similar symptoms. However, β-amyloid is interesting because it can inhibit the effect acetylcholine produces on the cell through nicotinic receptors. If we can intensify acetylcholinergic transmission, then we can reduce the manifestations of the disease and prolong the independent life of a person with dementia.

Drugs used for dementia include inhibitors of acetylcholinesterase (AChE), an enzyme that breaks down acetylcholine in the synaptic cleft. The use of AChE inhibitors leads to an increase in the content of acetylcholine in the interneuronal space and improved signal transmission. Research into the effectiveness of AChE inhibitors in Alzheimer's disease has determined that they can reduce symptoms of the disease and slow its progression. The three most commonly used drugs from this group are rivastigmine, galantamine and donepezil- comparable in effectiveness and safety. There is also a small but successful experience of using AChE inhibitors in the treatment musical hallucinations in older people.

With the help of acetylcholine, our brain learns and focuses attention on different objects and phenomena of the surrounding world. Our memory “works” on acetylcholine, and its deficiency can be compensated with the help of medications. I hope you enjoyed your introduction to acetylcholine.

Literature

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Metronome: how to control the discharges? ;
Receptors in active form;
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