Transmission of nerve impulses. Mechanism of neuromuscular transmission

A person acts as a kind of coordinator in our body. It transmits commands from the brain to muscles, organs, tissues and processes signals coming from them. A nerve impulse is used as a kind of data carrier. What is he? At what speed does it work? These, as well as a number of other questions, can be answered in this article.

What is a nerve impulse?

This is the name for the excitation wave that spreads along the fibers as a response to irritation of neurons. Thanks to this mechanism, information is transmitted from various receptors to the central nervous system. And from it, in turn, to different organs (muscles and glands). But what does this process represent at the physiological level? The mechanism of nerve impulse transmission is that neuron membranes can change their electrochemical potential. And the process that interests us occurs in the area of ​​synapses. The speed of the nerve impulse can vary from 3 to 12 meters per second. We will talk about it in more detail, as well as about the factors that influence it.

Study of structure and work

The passage of a nerve impulse was first demonstrated by German scientists E. Hering and G. Helmholtz using the example of a frog. It was then established that the bioelectric signal propagates at the previously indicated speed. In general, this is possible thanks to a special construction. In some ways, they resemble an electric cable. So, if we draw parallels with it, then the conductors are the axons, and the insulators are their myelin sheaths (they are a Schwann cell membrane, which is wound in several layers). Moreover, the speed of the nerve impulse depends primarily on the diameter of the fibers. The second most important factor is the quality of electrical insulation. By the way, the body uses lipoprotein myelin as a material, which has dielectric properties. All other things being equal, the larger its layer, the faster nerve impulses will travel. Even at the moment it cannot be said that this system has been fully explored. Much that relates to nerves and impulses still remains a mystery and a subject of research.

Features of structure and functioning

If we talk about the path of the nerve impulse, it should be noted that the fiber is not covered along its entire length. The design features are such that the current situation can best be compared with the creation of insulating ceramic couplings that are tightly strung on the rod of an electrical cable (albeit in this case on an axon). As a result, there are small non-insulated electrical areas from which ionic current can easily flow out of the axon into the environment (or vice versa). This irritates the membrane. As a result, generation is caused in areas that are not isolated. This process is called the interception of Ranvier. The presence of such a mechanism allows the nerve impulse to spread much faster. Let's talk about this with examples. Thus, the speed of nerve impulse conduction in a thick myelinated fiber, the diameter of which varies between 10-20 microns, is 70-120 meters per second. Whereas for those who have a suboptimal structure, this figure is 60 times less!

Where are they created?

Nerve impulses originate in neurons. The ability to create such “messages” is one of their main properties. A nerve impulse ensures rapid propagation of similar signals along axons over a long distance. Therefore, this is the body’s most important means for exchanging information within it. Data on irritation are transmitted by changing their frequency. A complex system of periodicals operates here, which can count hundreds of nerve impulses in one second. Computer electronics works on a somewhat similar principle, although much more complicated. So, when nerve impulses arise in neurons, they are encoded in a certain way, and only then are transmitted. In this case, information is grouped into special “packs”, which have different numbers and patterns. All this, put together, forms the basis for the rhythmic electrical activity of our brain, which can be recorded using an electroencephalogram.

Cell types

Speaking about the sequence of passage of a nerve impulse, we cannot ignore the neurons through which electrical signals are transmitted. So, thanks to them, different parts of our body exchange information. Depending on their structure and functionality, three types are distinguished:

1. Receptor (sensitive). They encode and transform into nerve impulses all temperature, chemical, sound, mechanical and light stimuli.
2. Insert (also called conductor or closure). They serve to process and switch impulses. The largest number of them are found in the human brain and spinal cord.
3. Effector (motor). They receive commands from the central nervous system to perform certain actions (in bright sunshine, close your eyes with your hand, and so on).

Each neuron has a cell body and a process. The path of a nerve impulse through the body begins with the last one. There are two types of shoots:

1. Dendrites. They are entrusted with the function of perceiving irritation from the receptors located on them.
2. Axons. Thanks to them, nerve impulses are transmitted from cells to the working organ.

Speaking about the conduction of nerve impulses by cells, it is difficult not to talk about one interesting point. So, when they are at rest, then, let's say, the sodium-potassium pump is engaged in moving ions in such a way as to achieve the effect of fresh water inside and salty outside. Due to the resulting imbalance, potential differences across the membrane can be observed up to 70 millivolts. For comparison, this is 5% of the usual ones. But as soon as the state of the cell changes, the resulting equilibrium is disrupted, and the ions begin to change places. This happens when the path of a nerve impulse passes through it. Due to the active action of ions, this action is also called an action potential. When it reaches a certain point, reverse processes begin and the cell reaches a state of rest.

About the action potential

Speaking about the transformation of a nerve impulse and its propagation, it should be noted that it could amount to measly millimeters per second. Then signals from the hand to the brain would take minutes, which is clearly not good. This is where the previously discussed myelin sheath plays its role in enhancing the action potential. And all its “passes” are placed in such a way that they only have a positive effect on the speed of signal transmission. So, when an impulse reaches the end of the main part of one axon body, it is transmitted either to the next cell or (if we talk about the brain) to numerous branches of neurons. In the latter cases, a slightly different principle works.

How does everything work in the brain?

Let's talk about what transmission sequence of nerve impulses works in the most important parts of our central nervous system. Here, neurons are separated from their neighbors by small gaps called synapses. The action potential cannot pass through them, so it looks for another way to get to the next nerve cell. At the end of each process there are small sacs called presynaptic vesicles. Each of them contains special compounds - neurotransmitters. When an action potential arrives at them, molecules are released from the sacs. They cross the synapse and attach to special molecular receptors that are located on the membrane. In this case, the equilibrium is disturbed and, probably, a new action potential appears. This is not yet known for certain; neurophysiologists are still studying the issue to this day.

The work of neurotransmitters

When they transmit nerve impulses, there are several options for what will happen to them:

1. They will diffuse.
2. Will undergo chemical breakdown.
3. They will return back to their bubbles (this is called recapture).

At the end of the 20th century, an amazing discovery was made. Scientists have learned that drugs that affect neurotransmitters (as well as their release and reuptake) can radically change a person's mental state. For example, a number of antidepressants like Prozac block the reuptake of serotonin. There are some reasons to believe that a deficiency in the brain neurotransmitter dopamine is to blame for Parkinson's disease.

Now researchers who study the borderline states of the human psyche are trying to figure out how all this affects the human mind. Well, for now we do not have an answer to such a fundamental question: what causes a neuron to create an action potential? For now, the mechanism for “launching” this cell is a secret to us. Particularly interesting from the point of view of this riddle is the work of neurons in the main brain.

In short, they can work with thousands of neurotransmitters sent by their neighbors. The details regarding the processing and integration of this type of impulses are almost unknown to us. Although many research groups are working on this. At the moment, we have learned that all received impulses are integrated, and the neuron makes a decision whether it is necessary to maintain the action potential and transmit them further. The functioning of the human brain is based on this fundamental process. Well, then it is not surprising that we do not know the answer to this riddle.

Some theoretical features

In the article, "nerve impulse" and "action potential" were used as synonyms. In theory this is true, although in some cases it is necessary to take into account some features. So, if you go into detail, the action potential is only part of the nerve impulse. With a detailed examination of scientific books, you can find out that this is only the name for a change in the charge of the membrane from positive to negative, and vice versa. Whereas a nerve impulse is understood as a complex structural-electrochemical process. It spreads across the neuron membrane as a traveling wave of change. The action potential is just the electrical component of a nerve impulse. It characterizes the changes that occur with the charge of a local area of ​​the membrane.

Where are nerve impulses created?

Where do they start their journey? The answer to this question can be given by any student who has diligently studied the physiology of arousal. There are four options:

1. Receptor end of the dendrite. If it exists (which is not a fact), then it is possible that there is an adequate stimulus, which will first create a generator potential, and then a nerve impulse. Pain receptors work in a similar way.
2. Membrane of the excitatory synapse. As a rule, this is only possible in the presence of severe irritation or their summation.
3. Dendritic trigger zone. In this case, local excitatory postsynaptic potentials are formed as a response to the stimulus. If the first node of Ranvier is myelinated, then they are summed up on it. Due to the presence of a section of membrane there that has increased sensitivity, a nerve impulse arises here.
4. Axon hillock. This is the name given to the place where the axon begins. The mound is the most frequent one to create impulses on a neuron. In all other places that were considered earlier, their occurrence is much less likely. This is due to the fact that here the membrane has increased sensitivity, as well as decreased sensitivity. Therefore, when the summation of numerous excitatory postsynaptic potentials begins, the hillock reacts to them first.

Example of propagating excitation

Talking in medical terms may cause misunderstanding of certain points. To eliminate this, it is worth briefly going through the knowledge presented. Let's take a fire as an example.

Remember the news reports from last summer (you can also hear this again soon). The fire is spreading! At the same time, trees and bushes that burn remain in their places. But the fire front is moving further and further from the place where the fire was located. The nervous system works in a similar way.

It is often necessary to calm the excitation of the nervous system that has begun. But this is not so easy to do, as in the case of fire. To do this, artificial interference is made in the functioning of the neuron (for therapeutic purposes) or various physiological means are used. This can be compared to pouring water on a fire.

A synapse is a structural and functional formation that ensures the transition of excitation or inhibition from the end of a nerve fiber to the innervating cell.

Synapse structure:

1) presynaptic membrane (electrogenic membrane in the axon terminal, forms a synapse on the muscle cell);

2) postsynaptic membrane (electrogenic membrane of the innervated cell on which the synapse is formed);

3) synaptic cleft (the space between the presynaptic and postsynaptic membrane, filled with liquid, which in composition resembles blood plasma).

There are several classifications of synapses.

1. By localization:

1) central synapses;

2) peripheral synapses.

Central synapses lie within the central nervous system and are also found in the ganglia of the autonomic nervous system.

There are several types of peripheral synapses:

1) myoneural;

2) neuroepithelial.

2. Functional classification of synapses:

1) excitatory synapses;

2) inhibitory synapses.

3. According to the mechanisms of excitation transmission in synapses:

1) chemical;

2) electric.

The transfer of excitation is carried out using mediators. There are several types of chemical synapses:

1) cholinergic. They transmit excitation using acetylcholine;

2) adrenergic. They transmit excitation with the help of three catecholamines;

3) dopaminergic. They transmit excitement using dopamine;

4) histaminergic. They transmit excitation with the help of histamine;

5) GABAergic. In them, excitation is transmitted with the help of gamma-aminobutyric acid, i.e., the process of inhibition develops.

Synapses have a number of physiological properties:

1) valve property of synapses, i.e. the ability to transmit excitation in only one direction from the presynaptic membrane to the postsynaptic;

2) the property of synaptic delay, associated with the fact that the rate of excitation transmission decreases;

3) the property of potentiation (each subsequent impulse will be carried out with a smaller postsynaptic delay);

4) low lability of the synapse (100–150 impulses per second).

When the presynaptic terminal is depolarized, voltage-sensitive calcium channels open, calcium ions enter the presynaptic terminal and trigger the fusion of synaptic vesicles with the membrane. As a result, the transmitter enters the synaptic cleft and attaches to receptor proteins of the postsynaptic membrane, which are divided into metabotropic and ionotropic. The former are associated with the G protein and trigger a cascade of intracellular signal transduction reactions. The latter are associated with ion channels, which open when a neurotransmitter binds to them, which leads to a change in membrane potential. The mediator acts for a very short time, after which it is destroyed by a specific enzyme. For example, in cholinergic synapses, the enzyme that destroys the transmitter in the synaptic cleft is acetylcholinesterase. At the same time, part of the transmitter can move with the help of carrier proteins across the postsynaptic membrane (direct uptake) and in the opposite direction through the presynaptic membrane (reverse uptake). In some cases, the mediator is also absorbed by neighboring neuroglial cells.

Two release mechanisms have been discovered: 1 vesicle connects to the membrane, and small molecules exit from it into the synaptic cleft, while large molecules remain in the vesicle. The second mechanism is presumably faster than the first, with the help of it synaptic transmission occurs when the content of calcium ions in the synaptic plaque is high.

The concept of the nerve center. Features of the conduction of excitation through nerve centers (unilateral conduction, slow conduction, summation of excitation, transformation and assimilation of rhythm).

The nerve center is a complex combination, an “ensemble” of neurons, coordinatedly involved in the regulation of a certain function or in the implementation of a reflex act. The cells of the nerve center are interconnected by synaptic contacts and are distinguished by a huge variety and complexity of external and internal connections. In accordance with the function performed, sensitive centers, centers of vegetative functions, motor centers, etc. are distinguished. Various nerve centers are characterized by a certain topography within the central nervous system.

in a physiological sense, the nerve center is a functional association of groups of nerve elements for the purpose of performing complex reflex acts.

Nerve centers consist of many neurons interconnected by an even greater number of synaptic connections. This abundance of synapses is determined by the basic properties of nerve centers: one-sided conduction of excitation, slowing of excitation conduction, summation of excitations, assimilation and transformation of the rhythm of excitations, trace processes and easy fatigue.

The one-sidedness of excitation in nerve centers is due to the fact that at synapses nerve impulses pass only in one direction - from the synaptic ending of the axon of one neuron through the synaptic cleft to the cell body and dendrites of other neurons.
The slowing down of the movement of nerve impulses is due to the fact that the “telegraphic”, i.e. electrical, method of transmitting nerve impulses at synapses is replaced by a chemical or transmitter method, the speed of which is a thousand times slower. The time of this so-called synaptic delay of impulses consists of the time of arrival of the impulse at the synaptic terminal, the time of diffusion of the transmitter into the synaptic cleft and its movement to the postsynaptic membrane, the time of change in the ionic permeability of the membrane and the occurrence of an action potential, i.e., a nerve impulse.
In reality, hundreds and thousands of neurons are involved in the implementation of any human reaction, and the total delay time of nerve impulses, called the central conduction time, increases to hundreds or more milliseconds. For example, the driver’s reaction time from the moment the traffic light turns red until the start of his response will be at least 200 ms.
Thus, the more synapses along the path of nerve impulses, the longer the time passes from the onset of stimulation to the onset of a response. This time is called reaction time or reflex latency time.
In children, the central delay time is longer; it also increases with various influences on the human body. When the driver is tired, it can exceed 1000 ms, which in dangerous situations leads to slow reactions and road accidents.
The summation of excitations was discovered by I.M. Sechenov in 1863. Currently, a distinction is made between spatial and temporal summation of nerve impulses. The first is observed when several impulses are simultaneously received by one neuron, each of which individually is a subthreshold stimulus and does not cause excitation of the neuron. In total, the nerve impulses reach the required strength and cause the appearance of an action potential.
Temporary summation occurs when a series of impulses arrive at the postsynaptic membrane of a neuron, which individually do not cause excitation of the neuron. The sum of these impulses reaches the threshold value of irritation and causes an action potential.
The phenomenon of summation can be observed, for example, with simultaneous subthreshold stimulation of several receptor zones of the skin or with rhythmic subthreshold stimulation of the same receptors. In both cases, subthreshold stimulation will cause a reflex response.
The assimilation and transformation of the rhythm of excitations in nerve centers were studied by the famous Russian and Soviet scientist A. A. Ukhtomsky (1875-1942) and his students. The essence of assimilation of the rhythm of excitations lies in the ability of neurons to “tune” to the rhythm of incoming stimuli, which is of great importance for optimizing the interaction of various nerve centers when organizing human behavioral acts. On the other hand, neurons are able to transform (change) the rhythmic stimuli coming to them into their own rhythm.
After the cessation of the stimulus, the activity of the neurons that make up the nerve centers does not stop. The time of this aftereffect, or trace processes, varies greatly among different neurons and depending on the nature of the stimuli. It is assumed that the aftereffect phenomenon is important in understanding the mechanisms of memory. A short aftereffect of up to 1 hour is probably associated with short-term memory mechanisms, while longer traces, stored in neurons for many years and of great importance in the learning of children and adolescents, are associated with long-term memory mechanisms.
Finally, the last feature of the nerve centers - their rapid fatigue - is also associated to a large extent with the “activity of the synapses. There is evidence that prolonged stimulation leads to a gradual depletion of the reserves of mediators in the synapses, to a decrease in the sensitivity of the postsynaptic membrane to them. As a result, reflex responses begin to weaken and eventually stop completely.

Akunets Ilya, 1st year, Anatomy.

2. Scheme of the structure of the neuromuscular synapse:

1 - nerve fiber;
2 - myelin sheath;
3 - Schwann cell;
4 - nerve ending;
5 - presynaptic membrane;
6 - synaptic vesicles;
7 - mitochondria;
8 - muscle fiber;
9 - postsynaptic membrane;
10 - synaptic cleft;
11 - core;
12 - myofibrils

3. Definition:

Synapses are special structural
education through which occurs
transfer of excitation from the nervous
conductor to the innervated organ or to
another nerve cell.

4.

Excitation through synaptic contacts
can be transmitted not only to other nerve
cells, but also on nerve fibers.
The excitation impulse causes neurosecretion
chemical mediator (intermediary) in
synaptic cleft. Such mediators
are acetylcholine, adrenaline, norepinephrine
and, less commonly, other substances, e.g.
aminobutyric acid! Influenced
transmitter postsynaptic membrane
depolarizes, transmitting excitation, or
hyperpolarizes, forming inhibitory
process.

5. Acetylcholine

Acetylcholine increases permeability
postsynaptic membrane for Na+ ions.
Negative postsynaptic is generated
potential, which, gradually increasing,
creates a wave of excitement. In between
separate excitation impulses,
arriving at the presynaptic membrane,
acetylcholine is broken down by an enzyme
cholinesterase.

6.

Mediators of inhibitory synapses, released in
synaptic cleft, interact with
postsynaptic membrane, cause
increasing its permeability for K+ ions and
inactivate sodium permeability.
Inhibitory postsynaptic is generated
potential. Examples of inhibitory mediators
are glycine, γ-aminobutyric acid.

7.

Excitation conduction slows down at synapses
- synaptic delay. It is 0.2 - 0.5 ms.
Due to its structural features, the synapse can conduct
excitation in only one direction - from presynaptic to
postsynaptic membrane. Therefore, despite
possibility of bilateral conduction of nerve impulses in
nerve conductor, in the nerve-synapse system excitation
transmitted in one direction only. Exception
is a bilateral conduction of excitation with so
called ephaptic (direct, mediatorless)
transmission of nerve impulses from neuron to neuron.

Synaptic transmission of nerve impulses. Electrical and chemical transmission of nerve impulses

English РусскийRules

Properties of chemical synapses

1. One-way conductivity is one of the most important properties of a chemical synapse. Asymmetry - morphological and functional - is a prerequisite for the existence of one-way conduction.

2. The presence of a synaptic delay: in order for a transmitter to be released in the presynaptic area in response to the generation of an AP and a change in the postsynaptic potential (VISI or IPSP) to occur, a certain time is required (synaptic delay). On average it is 0.2–0.5 ms.

3. Thanks to the synaptic process, the nerve cell that controls a given postsynaptic element (effector) can have an excitatory effect or, conversely, an inhibitory effect (this is determined by a specific synapse).

4. There is a negative feedback phenomenon in synapses - an antidromic effect. The point is that a transmitter released into the synaptic cleft can regulate the release of the next portion of the transmitter from the same presynaptic element by acting on specific receptors of the presynaptic membrane.

5. The efficiency of transmission at a synapse depends on the interval of signals passing through the synapse. If this interval is reduced for some time (the supply of an impulse along the axon is increased), then to each subsequent AP the response of the postsynaitic membrane (the magnitude of the EPSP or IPSP) will increase (up to a certain limit). This phenomenon facilitates transmission at the synapse and enhances the response of the postsynaptic element (control object) to the next stimulus; it is called “relief” or “potentiation”.

Question No. 41. Transmission of a nerve impulse through a synapse

It is based on the accumulation of calcium inside the presynapse. If the signal repetition rate through the synapse is very high, then due to the fact that the transmitter does not have time to be destroyed or removed from the synaptic cleft, persistent depolarization or cathodic depression occurs - a decrease in the efficiency of synaptic transmission. This phenomenon is called depression. If many impulses pass through the synapse, then ultimately the postsynaptic membrane can reduce the response to the release of the next portion of the transmitter. This is called the phenomenon of dsepsitization - loss of sensitivity. To a certain extent, deseisitization is similar to the process of refractoriness (loss of excitability). Synapses are subject to a process of fatigue. It is possible that fatigue (a temporary drop in the functionality of the synapse) is based on: a) depletion of transmitter reserves, b) difficulty in releasing the transmitter, c) the phenomenon of desensitization. Thus, fatigue is an integral indicator.

The brain has a number of mediators that cause neuron excitation: norepinephrine (produced by adrenergic neurons), dopamine (dopaminergic neurons), serotonin, peptides (peptidergic), glutamic acid, aspartic acid, etc. In all these cases, the released transmitter interacts with a specific receptor, as a result of which the permeability to sodium, potassium or chlorine ions changes, and ultimately depolarization (EPSP) develops. If it reaches a critical level of depolarization, then AP (neuron excitation) occurs.

Inhibitory synapses are formed by special inhibitory neurons (more precisely, their axons). The mediator can be glycine, gamma-aminobutyric acid (GABA) and a number of other substances. Typically, glycine is produced at synapses through which postsynaptic inhibition occurs. When glycine as a mediator interacts with glycine receptors of a neuron, hyperpolarization of the neuron (IPSP) occurs and, as a consequence, a decrease in the excitability of the neuron up to its complete refractoriness. As a result, the excitatory influences exerted through other axons become ineffective or ineffective. The neuron shuts down completely.

16)Temperament

Excitation in nerve and muscle fibers is carried out using electrical impulses propagating along the surface membrane. Transfer of excitation from one excitable formation to another, for example, from a nerve fiber to a muscle fiber or from one nerve cell to another, is based on a completely different mechanism.

11. Structure of the synapse. Mediators. Synaptic transmission of nerve impulses.

It is carried out as a result of the release by the nerve endings of highly active chemical compounds called mediators (transmitters) of the nerve impulse.

The assumption that in transfer of excitation V neuromuscular compounds involve some chemical agents, it was first stated by A.F. Samoilov in 1924. Later it was shown that when the motor nerve is irritated at its endings in the skeletal muscle, acetylcholine is released. G. Dale found that acetylcholine, supplied to the area of ​​the neuromuscular junction, depolarizes the muscle fiber membrane and, at a sufficiently high concentration, causes spreading excitation and contraction of the muscle.

Currently, Samoilov’s hypothesis about the chemical mechanism of excitation transmission in the neuromuscular junction is shared by the vast majority of researchers.

A synapse is an intercellular contact designed to transmit a nerve impulse between neurons.

To transmit an impulse from one neuron to another, there are intermembrane contacts - synapses.

Dendrites can be long, and the axon can be branched, but the difference is in the direction of the impulse path: in the dendrite - towards the body of the neuron, in the axon - away from the body.

There are 3 types of synapses:

1. Electrical synapses. The synaptic cleft is very narrow; special molecular complexes, connexons, pass through it, with a cavity inside through which the cytoplasms of two neurons contact. Electrical synapses are very fast and reliable, but they conduct impulses with equal intensity in both directions and are difficult to regulate. They are used primarily to transmit nerve impulses to muscles, such as the flight muscles of insects.

2. Chemical synapses. There are no contacts between the membranes. A neurotransmitter is formed in the neuron body - neurotransmitters in synaptic vesicles. There are special proteins on the vesicles and on the membrane. When an impulse approaches the synapse, it changes the conformation of the proteins, and they acquire a high affinity for each other, the vesicles are attracted to the membrane, merge with it and splash their contents out into the synaptic cleft. The neurotransmitter diffuses in the intercellular fluid, reaches the postsynaptic membrane and interacts with it, leading to a partial change in the membrane potential. The signal in this case is electrical in nature, and the transmission is chemical. The chemical synapse fires in one direction and is subject to powerful regulation, that is, it has high plasticity, but at the same time it is slow.

3. Mixed synapses. Such synapses include both principles discussed, but they have been little studied.

2 levels of perception:

— Whether the impulse will be formed or not.

— If the signal is sufficient, then the frequency of formation of the nerve impulse is important.

A single transmission may not be enough; the next neuron will be excited only if there are many signals - the principle of temporal summation of impulses - if there are many impulses, then they are summed. The arrival of a signal from one impulse may not be enough; the next neuron is excited only when an impulse is simultaneously received from 2 or more neurons - this is spatial summation. Sometimes the transmission of an impulse does not lead to excitation of the next neuron, but to inhibition. If there are two types of synapses: ↓ and ┴, then the neuron responds only if ↓ transmits a signal and ┴ does not. ┴-synapse allows you to choose the most optimal response option. The woman slowly puts the full hot pan in its place, rather than throwing it away.

In the brain, 95% of synapses are chemical.

Chemical transmission of nerve impulses

The process of transmitting an impulse through a chemical synapse is much slower than transmitting an impulse through a neuron, which means it is beneficial to have as few synapses as possible. The lack of specialization of neurons would lead to automation of reactions. The regulatory function of the nervous system is secondary, since the nervous system was originally designed to respond to the body's external environment. At the moment, only chemical compounds have been studied in detail. synapses. Therefore, let us consider the transfer of impulse using their example. We remember that chem. synapses transmit impulses using neurotransmitters. They are found in the presynaptic membrane in small synaptic vesicles. These vesicles accumulate here during rest, and they are also surrounded by a membrane, which has a special protein complex that is sensitive to the concentration of Ca + ions. When a signal occurs is enriched with Ca 2+ ions, and the bubble acquires a certain affinity for the cell membrane. It merges with it, and the neurotransmitters go into syn. gap. There he interacts. with proteins of the postsynaptic membrane, which trigger the corresponding cascade processes, and neurotransmitters return back to the presynaptic membrane.

⇐ Previous32333435363738394041Next ⇒

Date of publication: 2015-02-28; Read: 631 | Page copyright infringement

Studopedia.org - Studopedia.Org - 2014-2018 (0.001 s)…

Finding the meaning/interpretation of words

The section is very easy to use. Just enter the desired word in the field provided, and we will give you a list of its meanings.

Transmission of a nerve impulse through a synapse

I would like to note that our site provides data from various sources - encyclopedic, explanatory, word-formation dictionaries. Here you can also see examples of the use of the word you entered.

efaps in the crossword dictionary

Dictionary of medical terms

ephaps (Greek ephapsis touch, from ep- + hapsis touch, contact)

an area of ​​close contact between two neurons, in which it is possible to transfer excitation from one cell to another without the participation of mediators.

Transliteration: efaps
Back to front reads: spafe
Ephaps consists of 5 letters

words rhyming with efaps, words from word "efaps", words starting with "e", words starting with "ef", words starting with "efa", words starting with "efap", words ending with "s", words ending with "ps" ", words ending with "aps", words ending with "faps", words containing "f", words containing "fa", words containing "fap",

The details of the structure and operation of chemical synapses may differ, but the general principle of operation is the same:

1) when the AP reaches the axon terminal, a portion is released into the synaptic cleft through the presynaptic membrane mediator(chemical substance - intermediary). In this case, the following principles are observed: a) one neuron - one type of transmitter, b) one impulse - one portion of the transmitter, c) no matter how many terminals (end branches) the axon forms, the portion of the transmitter in each synapse remains unchanged.

2) The mediator acts on receptor-dependent channels of the postsynaptic membrane, causing local excitation (or inhibition). An excitatory (EPSP) or inhibitory (IPSP - hyperpolarization leading to inhibition) postsynaptic potential occurs.

3) When (if) the EPSP value reaches the level of PorP, then AP develops in those parts of the membrane where φ-dependent channels are located.

4) The transmitter is removed from the synaptic cleft.

Let us dwell in more detail on neuromuscular and interneuron synapses.

A) Neuromuscular (myoneural) junction.

Skeletal muscles are innervated by motor neurons. Each motor fiber in a muscle branches and innervates a group of muscle fibers. The terminal branches of nerve fibers (1-1.5 µm in diameter) are devoid of a myelin sheath and have an expanded flask shape. The presynaptic ending contains many submicroscopic formations - synaptic vesicles (vesicles) with a transmitter with a diameter of about 50 nm.

Presynaptic axon terminals form synaptic connections with a specialized region of the sarcolemma - motor endplate. The latter forms depressions and folds that increase the surface area of ​​the postsynaptic membrane.

The width of the synaptic cleft is greater than in other synapses and is 50-100 nm. This ensures the dispersion of the transmitter along the postsynaptic membrane.

Mediator - acetylcholine. When the membrane of the nerve ending is depolarized under the influence of PD, synaptic vesicles are exocytosed into the synaptic cleft.

Acetylcholine is released in portions of 4 * 10 4 molecules, which corresponds to the contents of several bubbles. One nerve impulse causes the synchronous release of 100-200 portions of the transmitter in less than 1 ms. In total, acetylcholine reserves at the end are enough for 2500-5000 impulses. (to contents)

Acetylcholine molecules diffuse through the gap and reach the outside of the postsynaptic membrane, where they bind to specific receptors. The number of receptors is approximately 13,000 per 1 µm 2; they are absent in other areas of the muscle membrane. An excitatory postsynaptic potential (EPSP) occurs (in this case, the end plate potential - EPP). The time from the appearance of a nerve impulse at the presynaptic terminal to the occurrence of an EPSP is called the synaptic delay. It is 0.2-0.5 ms.

For every impulse from a motor neuron, an action potential always occurs in the muscle. This is due to the fact that the presynaptic terminal releases a certain number of portions of the transmitter and the EPSP always reaches a threshold value. PD travels deep into the muscle fiber through the T-tube system (see the topic “muscle tissue”).

The transmitter has fulfilled its function and must be removed from the synaptic cleft. This function is performed by an enzyme localized here, acetylcholinesterase, which hydrolyzes acetylcholine to acetate and choline. The membrane is repolarized. This process goes very quickly: all acetylcholine released into the gap is broken down in 20 ms.

The resulting breakdown products - acetate and choline - are mostly transported back to the presynaptic endings, where they are used in the resynthesis of acetylcholine with the participation of the enzyme choline acetyltransferase

Botulinum toxin, even in trace amounts, blocks the release of acetylcholine at synapses and causes muscle paralysis. Curare poison, by binding to receptor proteins, interferes with the action of acetylcholine and suppresses EPSP.

b) Chemical interneuron synapses.

Peculiarities:

1) the synaptic cleft is narrower than in the neuromuscular junction - about 20 nm;

2) in contrast to the end plate potential (EPP) of muscles, the excitatory potential (EPSP) arising in a neuron upon depolarization of a single synaptic plaque is insufficient (1-2 mV) for a threshold change in membrane potential (from -70–80 to -50 mV) . In this regard, AP occurs on a postsynaptic neuron only with the simultaneous activation of several synapses - spatial summation, or with repeated discharges in one synapse - temporal summation (see below “integration of neural connections”).

3) The generation of a propagating action potential in neurons does not occur at the junction with the postsynaptic membrane, as in the neuromuscular junction, but at the membrane of the axon hillock.

4) Chemical interneuron synapses can be not only excitatory, but also inhibitory.

The differences are due to the nature of the transmitter and the specifics of the postsynaptic cell. The transmitter can either depolarize the postsynaptic membrane or hyperpolarize it. In the first case, the permeability of the membrane for Na + ions increases, and an EPSP occurs; in the second case, permeability increases only for K + and C1 - and an inhibitory postsynaptic potential (IPSP) is generated.

Exciting mediators are acetylcholine(at the endings of motor neurons and parasympathetic nerve fibers), norepinephrine(in the endings of the sympathetic nerves, in a number of parts of the brain), dopamine(in the subcortical ganglia of the brain).

Inhibitory mediators – gamma-aminobutyric acid and glycine.

In addition, although each neuron releases the same transmitter at all its synaptic terminals, it can bind to different receptors on the postsynaptic membrane and cause different effects.

Braking occurring at neuromuscular or neuroglandular junctions is called peripheral, and implemented in the structures of the central nervous system - central. The phenomenon of central inhibition was discovered in 1862 by I.M. Sechenov. The further development of the theory of inhibition was made by N. E.

Synapse structure. Mediators. Synaptic transmission of nerve impulses.

Vvedensky, C. Sherrington, A. A. Ukhtomsky and others.

Currently, inhibition is considered as an independent active nervous process caused by excitation and manifested in the weakening or suppression of other excitation.

In contrast to excitation, which manifests itself in two forms - local (local) potential and action potential, inhibition develops only in the form of a local process and is always associated with the action of specific inhibitory neurons and inhibitory transmitters.

In interneuron synapses, two types of inhibition are distinguished - postsynaptic And presynaptic.

Postsynaptic inhibition occurs due to a decrease in the excitability of the soma and dendrites of the neuron.

This decrease is based on hyperpolarization of the membrane of the receptive neuron by inhibitory neurons. This type of inhibition appears to predominate in the central nervous system of vertebrates.

Presynaptic inhibition occurs when the release of transmitter from presynaptic nerve endings in contact with a given cell decreases or stops. This phenomenon is based on hyperpolarization of the presynaptic fiber membrane by the inhibitory transmitter of special interneurons. This process is localized, therefore, not on the neuron body, but on the axon terminals. Presynaptic inhibition is characteristic mainly of somatic and autonomic afferent neurons (i.e., characteristic of peripheral inhibition). It is usually longer in duration than postsynaptic inhibition.

Postsynaptic inhibition (left). Presynaptic inhibition (right).

Since the endings of both excitatory and inhibitory neurons can branch on the body and dendrites of one nerve cell (for example, a motor neuron), the cell’s response to incoming impulses is integrative. That is, the occurrence of a nerve impulse depends on the value of the total potential formed as a result of the addition of all emerging EPSPs and IPSPs. Thus, the basis of interneuron connections is the interaction of the processes of excitation and inhibition.

⇐ Previous6789101112131415Next ⇒

Date of publication: 2015-07-22; Read: 443 | Page copyright infringement

Studopedia.org - Studopedia.Org - 2014-2018 (0.002 s)…

Stimulation of receptors causes the transformation of the influencing energy of the stimulus into nerve impulses, the transmission of which in the nervous system is carried out using synapses.

Functional structures of the cell membrane. The cell membrane (cell membrane) is a thin lipoprotein plate, the lipid content is about 40%, the protein content is 60%. Schematically, a cell membrane can be represented as follows: the membrane consists of a double layer of phospholipid molecules, covered on the inside with a layer of protein molecules, and on the outside with a layer of complex carbohydrate molecules. The cell membrane contains very thin tubules - ion channels, having selectivity. There are channels that allow only one ion to pass through (sodium, potassium, calcium, chlorine) or several.

Resting potential and action potential. At rest in the protoplasm of a nerve cell, the concentration of potassium ions is more than 30 times higher than the concentration of these ions in the external solution. The membrane is practically impermeable to sodium, while potassium passes through it. The diffusion of potassium ions from the protoplasm into the outer liquid is very high, which gives the outer membrane a positive charge and the inner one a negative charge. Thus, the concentration of potassium ions is the main factor that forms and determines the value resting potential(PP).

When a cell is exposed to irritation, the permeability of the membrane for sodium ions increases sharply and becomes approximately 10 times greater than the permeability for potassium ions. Therefore, the flow of positively charged potassium ions from the protoplasm into the external solution decreases, and the flow of positively charged sodium ions from the external solution into the protoplasm of the cell increases. It leads to recharging membranes, the outer surface becomes charged electronegatively, and the inner surface becomes positively charged ( depolarization phase).

The increase in membrane permeability to sodium ions lasts for a very short time. Following this, reduction processes occur in the cell, leading to the fact that the permeability for sodium ions again decreases, and its permeability for potassium ions increases. And as a result of these two processes, the outer membrane again acquires a positive charge, and the inner membrane acquires a negative charge ( repolarization phase).

An instantaneous increase in permeability for sodium ions and their penetration into the cell is sufficient to change the sign of the membrane potential and occurs action potential (AP), which propagates along the axon at a fairly high speed, the duration of the AP is usually 1-3 ms.

Synaptic transmission of information. The place where excitation is transferred from one neuron to another is called synapse(translated from Greek - contact). A synapse consists of the membranes of two neighboring neurons ( presynaptic and postsynaptic membranes) and the space between them, which is called synaptic cleft.

There are axo-somatic synapses, formed by the membranes of the axon and the body (soma) of another neuron, axo-dendritic, consisting of the membrane of the axon and the dendrites of another neuron, axo-axonal, in which the axon approaches the axon of another neuron. The synapse between axons and muscle fibers is called neuromuscular plate.

The nerve impulse along the axon reaches the end of the axon and causes the opening of calcium channels on the presynaptic membrane. Here, on the presynaptic membrane are vesicles(bubbles) that contain biologically active substances - mediators.

The opening of calcium channels leads to depolarization on the presynaptic membrane. Calcium binds with proteins that form the membrane of the vesicles in which the mediator is stored. Then the vesicles burst and all the contents enter the synaptic cleft. Next, the mediator molecules bind to special protein molecules ( receptors), which are located on the membrane of another neuron - on the postsynaptic membrane.

When transmitter molecules bind to receptors, channels for sodium and potassium ions open on the postsynaptic membrane, causing a change in potential (depolarization) on it. This potential is called - postsynaptic potential (PSP). Depending on the nature of the open ion channels, excitatory (EPSP) or inhibitory (IPSP) postsynaptic potentials arise

Thus, the excitation (AP) of a neuron at the synapse turns from an electrical impulse into a chemical impulse (release of a transmitter from the vesicles).

The time between the onset of presynaptic depolarization and the postsynaptic response is 0.5 ms, this is synaptic delay.

Main mediators: acetylcholine, monoamines (serotonin, histamine), catecholamines (dopamine, norepinephrine, adrenaline), amino acids (glutamate, glycine, aspartate, gamma-aminobutyric acid - GABA, alanine), peptides, vasopressin, oxytocin, adenosine, ATP, etc.

Spinal cord

Spinal cord, in appearance it is a long, cylindrical strand, flattened from front to back. In this regard, the transverse diameter of the spinal cord is larger than the anteroposterior one.

The spinal cord is located in the spinal canal and at the level of the lower edge of the foramen magnum passes into the brain. In this place, roots emerge from the spinal cord (its upper border), forming the right and left spinal nerves. The lower border of the spinal cord corresponds to the level of 1-11 lumbar vertebrae. Below this level, the apex of the conus medullaris of the spinal cord continues into a thin filum terminale. The filum terminale in its upper parts still contains nervous tissue and is a rudiment of the caudal end of the spinal cord. This part of the terminal filum, called the internal one, is surrounded by the roots of the lumbar and sacral spinal nerves and, together with them, is located in a blind-ending sac formed by the dura mater of the spinal cord. In an adult, the inner part of the filum terminale has a length of about 15 cm. Below the level of the 2nd sacral vertebra, the filum terminale is a connective tissue formation that is a continuation of all three membranes of the spinal cord and is called the outer part of the filum terminale. The length of this part is about 8 cm. It ends at the level of the body of the 2nd coccygeal vertebra, fused with its periosteum.

The length of the spinal cord in an adult is on average 43 cm (in men 45 cm, in women 41-42 cm), weight - about 34-38 g, which is approximately 2% of the mass of the brain.

In the cervical and lumbosacral regions of the spinal cord, two noticeable thickenings are found: the cervical thickening and the lumbosacral thickening. The formation of thickenings is explained by the fact that the upper and lower extremities are innervated from the cervical and lumbosacral parts of the spinal cord, respectively. In these sections of the spinal cord there is a greater number of nerve cells and fibers compared to other sections. In the lower parts of the spinal cord gradually narrows and forms the conus medullaris.

On the anterior surface of the spinal cord, the anterior median fissure is visible, which protrudes into the tissue of the spinal cord deeper than the posterior median beard. These grooves are the boundaries that divide the spinal cord into two symmetrical halves. In the depths of the posterior median sulcus there is a glial posterior median septum penetrating almost the entire thickness of the white matter. This septum extends to the posterior surface of the gray matter of the spinal cord.

On the anterior surface of the spinal cord, on each side of the anterior fissure, runs the anterolateral beard. It is the site of exit from the spinal cord of the anterior (motor) roots of the spinal nerves and the boundary on the surface of the spinal cord between the anterior and lateral cords. On the posterior surface of each half of the spinal cord there is a posterolateral groove, the site of penetration of the posterior sensory roots of the spinal nerves into the spinal cord. This groove serves as the boundary between the lateral and posterior funiculi.

The anterior cortex consists of processes of motor (motor) nerve cells located in the anterior horn of the gray matter of the spinal cord. The dorsal root is sensitive, represented by a collection of central processes of pseudounipolar cells penetrating into the spinal cord, the bodies of which form the spinal ganglion, which lies at the junction of the dorsal root with the anterior one. Throughout the entire length of the spinal cord, 31 pairs of roots emerge from each side. The anterior and posterior roots at the inner edge of the intervertebral foramen come together, merge with each other and form the spinal nerve. Thus, 31 pairs of spinal nerves are formed from the roots. The section of the spinal cord corresponding to two pairs of roots (two anterior and two posterior) is called a segmenton.

It is very important for a doctor to know the topographic relationships of the spinal cord segments with the spinal column (skeletotopy of the segments). The length of the spinal cord is significantly less than the length of the spinal column, therefore the serial number of any segment of the spinal cord and the level of its position, starting from the lower cervical region, do not correspond to the serial number of the vertebra of the same name. The position of the segments in relation to the vertebrae can be determined as follows. The upper cervical segments are located at the level of the vertebral bodies corresponding to their serial number. The lower cervical and upper thoracic segments lie one vertebra higher than the bodies of the corresponding vertebrae. In the middle thoracic region, this difference between the corresponding segment of the spinal cord and the vertebral body increases by 2 vertebrae, in the lower thoracic region - by 3. The lumbar segments of the spinal cord lie in the spinal canal at the level of the bodies of the 10th, 11th thoracic vertebrae, the sacral and coccygeal segments - by level of 12 thoracic and 1 lumbar vertebrae.

The spinal cord consists of nerve cells and fibers of gray matter, which in cross section looks like the letter B or a butterfly with outstretched wings. Beyond the periphery of the gray matter is white matter, formed only by nerve fibers.

The gray matter of the spinal cord contains a central canal. It is a remnant of the neural tube cavity and contains cerebrospinal fluid. The upper end of the canal communicates with the 9th ventricle, and the lower, slightly expanding, forms a blindly ending terminal ventricle. The walls of the central canal of the spinal cord are lined with ependyma, around which there is a central gelatinous (gray) substance. In an adult, the central canal becomes overgrown in various parts of the spinal cord, and sometimes throughout its entire length.

The gray matter along the spinal cord to the right and left of the central canal forms symmetrical gray columns. Anterior and posterior to the central canal of the spinal cord, these gray columns are connected to each other by thin plates of gray matter, called the anterior and posterior commissures.

In each column of gray matter, its front part is distinguished - the anterior column and its back part - the posterior column. Behind the level of the lower cervical, all thoracic and two upper lumbar segments of the spinal cord.

The gray matter on each side forms a lateral protrusion - a lateral column. In other parts of the spinal cord (above the 8th cervical and below the 2nd lumbar segments) there are no lateral columns.

Behind the cross section of the spinal cord, the columns of gray matter on each side have the appearance of horns. There is a wider anterior horn and a narrow posterior horn1, corresponding to the anterior and posterior columns. The lateral horn corresponds to the lateral intermediate column (autonomous) of gray matter.

The anterior horns contain large nerve root cells - motor (efferent) neurons. These neurons form 5 nuclei: two lateral (anterolateral and posterolateral), two medial (anteromedial and posteromedial) and a central nucleus. The posterior horns of the spinal cord are represented predominantly by smaller cells. The dorsal, or sensitive, roots contain central processes of pseudounipolar cells located in the spinal (sensitive) nodes.

The gray matter of the dorsal horns of the spinal cord is heterogeneous. The bulk of the nerve cells of the dorsal horn form its own nucleus. In the white matter immediately adjacent to the apex of the posterior horn of the gray matter, a border zone is distinguished. Anterior to the latter in the gray matter is a spongy zone, which received its name due to the presence in this section of a large-loop glial network containing nerve cells. A gelatinous substance consisting of small nerve cells is secreted even more anteriorly. The processes of nerve cells of the jellylike substance, the spongy zone and tuft cells diffusely scattered throughout the gray matter communicate with several neighboring segments. As a rule, they end in synapses with neurons located in the anterior horns of their segment, as well as above and below the segments. Directing from the posterior horns of the gray matter to the anterior horns, the processes of these cells are located along the periphery of the gray matter, forming a narrow border of white matter near it. These bundles of nerve fibers are called the anterior, lateral and posterior intrinsic bundles. The cells of all nuclei of the dorsal horns of the gray matter are, as a rule, intercalary (intermediate, or conductor) neurons. Neurites extending from the nerve cells, the totality of which makes up the central and thoracic nuclei of the dorsal horns, are directed in the white matter of the spinal cord to the brain.

The intermediate zone of gray matter of the spinal cord is located between the anterior and posterior horns. Here, from the 8th cervical to the 2nd lumbar segment, there is a protrusion of gray matter - the lateral horn.

In the medial part of the base of the lateral horn, a difficult nucleus consisting of large nerve cells is noticeable, well outlined by a layer of white matter. This nucleus extends along the entire posterior column of gray matter in the form of a cellular cord (Clark's nucleus). The largest diameter of this nucleus is at the level from 11 thoracic to 1 lumbar segment. The lateral horns contain the centers of the sympathetic part of the autonomic nervous system in the form of several groups of small nerve cells united in the lateral intermediate (gray) substance. The axons of these cells pass through the anterior horn and exit the spinal cord as part of the ventral roots.

In the intermediate zone there is a central intermediate (gray) substance, the cell processes of which participate in the formation of the spinocerebellar tract. At the level of the cervical segments of the spinal cord, between the anterior and posterior horns, and at the level of the upper thoracic segments, between the lateral and posterior horns, a reticular formation is located in the white matter adjacent to the gray matter. The reticular formation here looks like thin bars of gray matter intersecting in different directions and consists of nerve cells with a large number of processes.

The gray matter of the spinal cord with the posterior and anterior roots of the spinal nerves and its own bundles of white matter bordering the gray matter forms its own, or segmental, apparatus of the spinal cord. The main purpose of the segmental apparatus, as the phylogenetically oldest part of the spinal cord, is to carry out innate reactions (reflexes) in response to stimulation (internal or external). I. P. Pavlov defined this type of activity of the segmental apparatus of the spinal cord with the term “unconditioned reflexes.”

White matter, as noted, is localized outward from the gray matter. The grooves of the spinal cord divide the white matter into three cords symmetrically located on the right and left. The anterior cord is located between the anterior median fissure and the anterior lateral groove. In the white matter posterior to the anterior median fissure, the anterior white commissure is distinguished, which connects the anterior cords of the right and left sides. The posterior funiculus is located between the posterior median and posterior lateral grooves. The lateral funiculus is the area of ​​white matter between the anterior and posterior lateral sulci.

The magnitude of the force impulse acting on a body is equal to the change in the amount of motion (impulse) of this body.

QUESTION 1. Transfer by a notary of statements of individuals and legal entities.

QUESTION 4. Transfer of inherited property into trust management

The basic unit of the nervous system is the neuron. A neuron is a nerve cell whose function is to distribute and interpret information.

An elementary manifestation of activity is excitation that occurs as a result of a change in the polarity of the nerve cell membrane. In fact, nervous activity is the result of processes occurring at synapses - at the points of contact of two neurons, where the transfer of excitation from one cell to another occurs. Transmission is carried out using chemical compounds - neurotransmitters. At the moment of excitation, a significant number of molecules are released into the synaptic cleft (the space separating the membranes of contacting cells), diffuse through it and bind to receptors on the surface of cells. The latter means the perception of the signal.

The specificity of the interaction of neurotransmitters in receptors is determined by the structure of both receptors and ligands. The basis of the action of most chemicals on the central nervous system is their ability to change the process of synaptic transmission of excitation. Most often, these substances act as agonists (activators), they increase the functional activity of receptors, or antagonists (blockers). At the synapses of neuromuscular junctions, the main transmitter is chloroacetylcholine. If the nerve nodes are located near the spinal cord, the transmitter is norepinephrine.

At most excited synapses in the mammalian brain, the neurotransmitter released is L-glutamic acid (1-aminopropane-1,3-dicarboxylic acid).

This is one of the mediators belonging to the class of excitatory amino acids, and γ‑aminobutyric acid (GABA), like glycine, is an inhibitory mediator of the central nervous system. The most important physiological functions of γ-aminobutyric acid are the regulation of brain excitability and participation in the formation of behavioral reactions, for example, the suppression of an aggressive state.

γ-Aminobutyric acid is formed in the body by decarboxylation of L-glutamic acid under the action of the enzyme glutamate decarboxylase.

The main pathway of metabolic transformation of γ-aminobutyric acid in nervous tissue is transamination with the participation of α-ketoglutaric acid. The catalyst in this case is the enzyme GABA-T (GABA transamylase). Transamination results in glutamic acid, a metabolic precursor of γ-aminobutyric acid, and succinic semialdehyde, which then becomes GHB (γ-hydroxybutyric acid), which is an antihypoxic agent.

It is this process of inactivation of γ-aminobutyric acid that has become the target for research aimed at the accumulation of mediators in brain tissue to enhance its neuroinhibitory activity.

It is believed that 70% of central synapses intended to stimulate the central nervous system use L-glutamic acid as a mediator, but its excessive accumulation leads to irreversible damage to neurons and severe pathologies such as Alzheimer's disease, stroke, etc.

Glutamate receptors are divided into two main types:

1. ionotropic (i Gly Rs)

2. metabotropic (m Gly Rs)

Ionotropic glutamate receptors form ion channels and directly transmit electrical signals from nerve cells by generating an ionic current.

Metabotropic glutamate receptors transmit an electrical signal not directly, but through a system of secondary messengers - molecules or ions, which ultimately cause changes in the configuration of proteins involved in specific cellular processes.

Ionotropic glutamate receptors– a family of glutamate receptors associated with ion channels. Includes two subtypes that differ in pharmacological and structural properties. The names of these subtypes are derived from the names of the most selective agonist ligands for each of the corresponding receptors. These are N-methyl-D-aspartic acid (NMDA), 2-amino-3-hydroxy-5-methylisoxazol-4-yl-propanoic acid (AMPA), kainic acid

Thus, two subtypes of ionotropic glutamate receptors are distinguished: NMDA and NMPA (kainate subtype).

NMDA is the most studied of all glutamate receptors. Studies of the action of compounds of various classes have shown the presence of several regulatory sites in it - this is an area of ​​​​special binding to ligands. The NMDA receptor has two amino acid sites: one for the specific binding of glutamic acid, the other for the specific binding of glycine, which are coagonists of glutamate. In other words, activation of both (glutamine and glycine) binding centers is necessary to open the ion channel. The channel associated with NMDA receptors is permeable to Na + , K + , Ca 2+ cations, and it is with an increase in the intracellular concentration of calcium ions that the death of nerve cells is associated with diseases accompanied by hyperexcitation of the NMDA receptor.

In the NMDA receptor channel there is a site for specific binding of divalent ions Mg 2+ and Zn 2+, which have an inhibitory effect on the processes of synaptic excitation of NMDA receptors. There are other allosteric modulatory sites on the NMDA receptor, e.g. those, interaction with which does not have a direct effect on the main transmitter transmission, but are capable of influencing the functioning of the receptor. These are:

1) Phencyclidine site. It is located in an ion channel, and the action of PCP is to selectively block the open ion channel.

2) A polyamine site located on the inner side of the postsynaptic membrane of a neuron and capable of binding some endogenous polyamines, for example, spermidine, spermine.

Let's consider the chemistry of compounds active in relation to NMDA receptors.