Resting membrane potential

At rest, there is a thin layer of positive charges on the outside of the plasma membrane, and negative charges on the inside. The difference between them is called resting membrane potential. If we assume the outer charge to be zero, then the charge difference between the outer and inner surfaces of most neurons turns out to be close to -65 mV, although it can vary from -40 to -80 mV in individual cells.

The occurrence of this charge difference is due to the unequal distribution of potassium, sodium and chlorine ions inside and outside the cell, as well as the greater permeability of the resting cell membrane only for potassium ions.

In excitable cells, the resting membrane potential (RMP) can vary greatly, and this ability is the basis for the occurrence of electrical signals. A decrease in the resting membrane potential, for example from -65 to -60 mV, is called depolarization , and an increase, for example, from -65 to -70 mV, – hyperpolarization .

If depolarization reaches a certain critical level, for example -55 mV, then the permeability of the membrane for sodium ions becomes maximum for a short time, they rush into the cell and, therefore, the transmembrane potential difference rapidly decreases to 0 and then becomes positive. This circumstance leads to the closure of sodium channels and the rapid release of potassium ions from the cell through channels intended only for them: as a result, the original value of the resting membrane potential is restored. These rapidly occurring changes in resting membrane potential are called action potential. The action potential is a driven electrical signal; it quickly spreads along the axon membrane to its very end, and does not change its amplitude anywhere.

Except action potentials in a nerve cell, due to changes in its membrane permeability, local or local signals may arise: receptor potential And postsynaptic potential. Their amplitude is much smaller than that of the action potential; in addition, it decreases significantly as the signal propagates. For this reason, local potentials cannot propagate across the membrane far from their point of origin.

The work of the sodium-potassium pump in the cell creates high concentration potassium ions, and in the cell membrane there are open channels for these ions. Potassium ions leaving the cell along a concentration gradient increase the number of positive charges on the outer surface of the membrane. There are many large-molecular organic anions in the cell, and therefore the membrane turns out to be negatively charged from the inside. All other ions can pass through the resting membrane in very small quantities, their channels are mostly closed. Consequently, the resting potential owes its origin mainly to the flow of potassium ions from the cell .

Electrical signals: input, combined, conductive and output

Neurons come into contact with certain target cells, and the cytoplasm of the contacting cells does not connect and a synaptic gap always remains between them.

Modern version neural theory connects certain parts nerve cell with the nature of the electrical signals arising in them. A typical neuron has four morphologically defined regions: dendrites, soma, axon, and presynaptic axon terminal. When a neuron is excited, four types of electrical signals appear in it sequentially: input, combined, conductive and output(Fig. 3.3). Each of these signals occurs only in a specific morphological region.

Input signals are either receptor, or postsynaptic potential. Receptor potential is formed in the endings of a sensitive neuron when a certain stimulus acts on them: stretching, pressure, light, a chemical substance, etc. The action of the stimulus causes the opening of certain ion channels in the membrane, and the subsequent flow of ions through these channels changes the initial value of the resting membrane potential; in most cases depolarization occurs. This depolarization is the receptor potential, its amplitude is proportional to the strength of the current stimulus.

The receptor potential can spread from the site of the stimulus along the membrane to a relatively short distance - the amplitude of the receptor potential decreases with distance from the site of the stimulus, and then the depolarizing shift will disappear altogether.

The second type of input signal is postsynaptic potential. It is formed on a postsynaptic cell after an excited presynaptic cell sends a neurotransmitter for it. Having reached the postsynaptic cell through diffusion, the mediator attaches to specific receptor proteins in its membrane, which causes the opening of ion channels. The resulting ion current through the postsynaptic membrane changes the initial value of the resting membrane potential - this shift is the postsynaptic potential.

In some synapses, such a shift represents depolarization and, if it reaches a critical level, the postsynaptic neuron is excited. In other synapses, a shift in the opposite direction occurs: the postsynaptic membrane is hyperpolarized: the value of the membrane potential becomes larger and it becomes more difficult to reduce it to a critical level of depolarization. It is difficult to excite such a cell; it is inhibited. Thus, the depolarizing postsynaptic potential is exciting, and hyperpolarizing – braking. Accordingly, the synapses themselves are divided into excitatory (causing depolarization) and inhibitory (causing hyperpolarization).

Regardless of what happens on the postsynaptic membrane: depolarization or hyperpolarization, the magnitude of postsynaptic potentials is always proportional to the number of transmitter molecules that acted, but usually their amplitude is small. Just like the receptor potential, they spread along the membrane over a very short distance, i.e. also relate to local potentials.

Thus, input signals are represented by two types of local potentials, receptor and postsynaptic, and these potentials arise in strictly defined areas of the neuron: either in sensory endings or in synapses. Sensory endings belong to sensory neurons, where the receptor potential arises under the influence of external stimuli. For interneurons, as well as for efferent neurons, only the postsynaptic potential can be the input signal.

Combined signal can occur only in a region of the membrane where there are a sufficient number of ion channels for sodium. In this regard, the ideal object is the axon hillock - the place where the axon departs from the cell body, since it is here that the density of channels for sodium is highest in the entire membrane. Such channels are potential-dependent, i.e. open only when the initial value of the resting potential reaches a critical level. The typical resting potential for the average neuron is approximately -65 mV, and the critical level of depolarization corresponds to approximately -55 mV. Therefore, if it is possible to depolarize the membrane of the axon hillock from -65 mV to -55 mV, then an action potential will arise there.

Input signals are capable of depolarizing the membrane, i.e. either postsynaptic potentials or receptor potentials. In the case of receptor potentials, the place of origin of the combined signal is the node of Ranvier closest to the sensitive endings, where depolarization to a critical level is most likely. Each sensory neuron has many endings, which are branches of one process. And, if in each of these endings, during the action of a stimulus, a very small amplitude receptor potential arises and spreads to the node of Ranvier with a decrease in amplitude, then it is only a small part of the total depolarizing shift. From each sensitive ending, these small receptor potentials move at the same time to the nearest node of Ranvier, and in the area of ​​the interception they are all summed up. If total amount If the depolarizing shift is sufficient, an action potential will arise at the interception.

Postsynaptic potentials arising on dendrites are as small as receptor potentials and also decrease as they propagate from the synapse to the axon hillock, where an action potential can arise. In addition, inhibitory hyperpolarizing synapses may be in the way of the propagation of postsynaptic potentials throughout the cell body, and therefore the possibility of depolarization of the axon hillock membrane by 10 mV seems unlikely. However, this result is regularly achieved as a result of the summation of many small postsynaptic potentials that arise simultaneously at numerous synapses formed by the dendrites of the neuron with the axon terminals of presynaptic cells.

Thus, the combined signal arises, as a rule, as a result of the summation of simultaneously formed numerous local potentials. This summation occurs in the place where there are especially many voltage-gated channels and therefore the critical level of depolarization is more easily achieved. In the case of integration of postsynaptic potentials, such a place is the axon hillock, and the summation of receptor potentials occurs in the node of Ranvier closest to the sensory endings (or the area of ​​​​the unmyelinated axon close to them). The area where the combined signal occurs is called integrative or trigger.

The accumulation of small depolarizing shifts is transformed with lightning speed in the integrative zone into an action potential, which is the maximum electrical potential of the cell and occurs according to the “all or nothing” principle. This rule must be understood in such a way that depolarization below a critical level does not bring any result, and when this level is reached, the maximum response is always revealed, regardless of the strength of the stimuli: there is no third option.

Conducting an action potential. The amplitude of the input signals is proportional to the strength of the stimulus or the amount of neurotransmitter released at the synapse - such signals are called gradual. Their duration is determined by the duration of the stimulus or the presence of the transmitter in the synaptic cleft. The amplitude and duration of the action potential do not depend on these factors: both of these parameters are entirely determined by the properties of the cell itself. Therefore, any combination of input signals, any variant of summation, under the single condition of depolarization of the membrane to a critical value, causes the same standard pattern of action potential in the trigger zone. It always has the maximum amplitude for a given cell and approximately the same duration, no matter how many times the conditions causing it are repeated.

Having arisen in the integrative zone, the action potential quickly spreads along the axon membrane. This occurs due to the appearance of a local electric current. Since the depolarized section of the membrane turns out to be differently charged than its neighbor, an electric current arises between the polarly charged sections of the membrane. Under the influence of this local current, the neighboring area is depolarized to a critical level, which causes the appearance of an action potential in it. In the case of a myelinated axon, such a neighboring section of the membrane is the node of Ranvier closest to the trigger zone, then the next one, and the action potential begins to “jump” from one node to another at a speed reaching 100 m/s.

Different neurons may differ from each other in many ways, but the action potentials arising in them are very difficult, often impossible, to distinguish. This is a highly stereotypical signal in a variety of cells: sensory, interneurons, motor. This stereotypy indicates that the action potential itself does not contain any information about the nature of the stimulus that generated it. The strength of the stimulus is indicated by the frequency of action potentials that occur, and specific receptors and well-ordered interneuron connections determine the nature of the stimulus.

Thus, the action potential generated in the trigger zone quickly spreads along the axon to its end. This movement is associated with the formation of local electrical currents, under the influence of which the action potential appears anew in the adjacent section of the axon. The parameters of the action potential when carried along the axon do not change at all, which allows information to be transmitted without distortion. If the axons of several neurons find themselves in a common bundle of fibers, then excitation propagates along each of them separately.

Output signal addressed to another cell or to several cells at the same time and in the vast majority of cases represents the release of a chemical intermediary - a mediator. In the presynaptic endings of the axon, the pre-stored transmitter is stored in synaptic vesicles, which accumulate in special areas - active zones. When the action potential reaches the presynaptic terminal, the contents of the synaptic vesicles are emptied into the synaptic cleft by exocytosis.

Chemical mediators of information transmission can be different substances: small molecules, such as acetylcholine or glutamate, or fairly large peptide molecules - all of them are specially synthesized in the neuron for signal transmission. Once in the synaptic cleft, the transmitter diffuses to the postsynaptic membrane and attaches to its receptors. As a result of the connection of receptors with the transmitter, the ion current through the channels of the postsynaptic membrane changes, and this leads to a change in the value of the resting potential of the postsynaptic cell, i.e. an input signal arises in it - in this case, a postsynaptic potential.

Thus, in almost every neuron, regardless of its size, shape and position in the neuron chain, four functional areas can be found: local receptive zone, integrative zone, signal conduction zone and output or secretory zone(Fig. 3.3).

Irritants

By nature, irritants are divided into:
physical (sound, light, temperature, vibration, osmotic pressure), electrical stimuli are of particular importance for biological systems;
chemical (ions, hormones, neurotransmitters, peptides, xenobiotics);
informational (voice commands, conventional signs, conditioned stimuli).

By biological significance irritants are divided into:
adequate - stimuli for the perception of which the biological system has special adaptations;
inadequate - irritants that do not correspond to the natural specialization of the receptor cells on which they act.

A stimulus causes arousal only if it is strong enough. Excitation threshold - the minimum strength of the stimulus sufficient to cause excitation of the cell. The expression “threshold of excitation” has several synonyms: threshold of irritation, threshold strength of stimulus, threshold of strength.

Excitation as an active reaction of a cell to a stimulus

Cell response to external influence(irritation) differs from the reaction of non-biological systems in the following features:
the energy for the cell reaction is not the energy of the stimulus, but the energy generated as a result of metabolism in the biological system itself;
the strength and form of the cell reaction is not determined by the strength and form of the external influence (if the strength of the stimulus is above the threshold).

In some specialized cells, the reaction to the stimulus is particularly intense. This intense reaction is called arousal. Excitation is an active reaction of specialized (excitable) cells to an external influence, manifested in the fact that the cell begins to perform its specific functions.

An excitable cell can be in two discrete states:
state of rest (readiness to respond to external influences, perform internal work);
state of excitement (active performance of specific functions, performance of external work).

There are 3 types of excitable cells in the body:
nerve cells (excitation is manifested by the generation of an electrical impulse);
- muscle cells (excitation is manifested by contraction);
secretory cells (excitation is manifested by the release of biologically active substances into the intercellular space).

Excitability is the ability of a cell to move from a resting state to an excitation state when exposed to a stimulus. Different cells have different excitability. The excitability of the same cell changes depending on its functional state.

Excitable cell at rest

The membrane of an excitable cell is polarized. This means that there is a constant potential difference between the inner and outer surface of the cell membrane, which is called membrane potential(MP). At rest, the MF value is –60…–90 mV ( inner side membrane is charged negatively relative to the outer one). The MP value of a cell at rest is called resting potential(PP). Cell MP can be measured by placing one electrode inside and the other outside the cell (Fig. 1 A) .

Decrease in MP relative to it normal level(PP) is called depolarization, and the increase is called hyperpolarization. Repolarization is understood as the restoration of the initial level of MP after its change (see Fig. 1 B).

Electrical and physiological manifestations of arousal

Let us consider various manifestations of excitation using the example of irritating a cell with an electric current (Fig. 2).

Under the action of weak (subthreshold) pulses of electric current, an electrotonic potential develops in the cell. Electrotonic potential(EP) – a shift in the cell membrane potential caused by the action of direct electric current . EP is a passive reaction of the cell to an electrical stimulus; the state of ion channels and ion transport do not change. EP does not manifest itself as a physiological reaction of the cell. Therefore, EP is not arousal.

Under the action of a stronger subthreshold current, a more prolonged shift of the MP occurs - a local response. Local response (LR) is an active reaction of the cell to an electrical stimulus, but the state of ion channels and ion transport changes slightly. LO does not manifest itself in a noticeable physiological reaction of the cell. LO is called local excitement , since this excitation does not spread across the membranes of excitable cells.

Under the influence of threshold and superthreshold current, the cell develops action potential(PD). AP is characterized by the fact that the cell MP value very quickly decreases to 0 (depolarization), and then the membrane potential acquires a positive value (+20...+30 mV), i.e., the inner side of the membrane is charged positively relative to the outer one. Then the MP value quickly returns to its original level. Strong depolarization of the cell membrane during AP leads to the development of physiological manifestations of excitation (contraction, secretion, etc.). PD is called spreading excitement, because, having arisen in one section of the membrane, it quickly spreads in all directions.

The mechanism of AP development is almost the same for all excitable cells. The mechanism for coupling electrical and physiological manifestations of excitation is different for different types excitable cells (coupling of excitation and contraction, coupling of excitation and secretion).

The structure of the cell membrane of an excitable cell

Four types of ions are involved in the mechanisms of development of excitation: K+, Na+, Ca++, Cl – (Ca++ ions are involved in the processes of excitation of some cells, for example cardiomyocytes, and Cl – ions are important for the development of inhibition). The cell membrane, which is a lipid bilayer, is impermeable to these ions. In the membrane, there are 2 types of specialized integral protein systems that ensure the transport of ions across the cell membrane: ion pumps and ion channels.

Ion pumps and transmembrane ion gradients

Ion pumps (pumps)– integral proteins that provide active transport of ions against a concentration gradient. The energy for transport is the energy of ATP hydrolysis. There are Na+ / K+ pump (pumps out Na+ from the cell in exchange for K+), Ca++ pump (pumps out Ca++ from the cell), Cl– pump (pumps out Cl– from the cell).

As a result of the operation of ion pumps, transmembrane ion gradients are created and maintained:
concentration of Na+, Ca++, Cl – inside the cell is lower than outside (in the intercellular fluid);
the concentration of K+ inside the cell is higher than outside.

Ion channels

Ion channels are integral proteins that provide passive transport of ions along a concentration gradient. The energy for transport is the difference in ion concentration on both sides of the membrane (transmembrane ion gradient).

Non-selective channels
allow all types of ions to pass through, but the permeability for K+ ions is significantly higher than for other ions;
are always open.

Selective channels have the following properties:
only one type of ion passes through; for each type of ion there is its own type of channel;
can be in one of 3 states: closed, activated, inactivated.

The selective permeability of the selective channel is ensured selective filter , which is formed by a ring of negatively charged oxygen atoms, which is located at the narrowest point of the channel.

Changing the channel state is ensured by the operation gate mechanism, which is represented by two protein molecules. These protein molecules, the so-called activation gate and inactivation gate, by changing their conformation, can block the ion channel.

In the resting state, the activation gate is closed, the inactivation gate is open (the channel is closed) (Fig. 3). When a signal acts on the gate system, the activation gate opens and ion transport through the channel begins (the channel is activated). With significant depolarization of the cell membrane, the inactivation gate closes and ion transport stops (the channel is inactivated). When the MP level is restored, the channel returns to its original (closed) state.

Depending on the signal that causes the activation gate to open, selective ion channels are divided into:
• chemosensitive channels – the signal for the opening of the activation gate is a change in the conformation of the receptor protein associated with the channel as a result of the attachment of a ligand to it;
• potential sensitive channels – the signal to open the activation gate is a decrease in MP (depolarization) of the cell membrane to a certain level, which is called critical level of depolarization (KUD).

Mechanism of resting potential formation

The resting membrane potential is formed mainly due to the release of K+ from the cell through non-selective ion channels. The leakage of positively charged ions from the cell leads to the fact that the inner surface of the cell membrane becomes negatively charged relative to the outer one.

The membrane potential resulting from K+ leakage is called the “equilibrium potassium potential” ( Ek). It can be calculated using the Nernst equation

Where R– universal gas constant,
T– temperature (Kelvin),
F– Faraday number,
[K+]nar – concentration of K+ ions outside the cell,
[K+] ext – concentration of K+ ions inside the cell.

PP is usually very close to Ek, but not exactly equal to it. This difference is explained by the fact that the following contribute to the formation of PP:

entry of Na+ and Cl– into the cell through non-selective ion channels; in this case, the entry of Cl– into the cell additionally hyperpolarizes the membrane, and the entry of Na+ additionally depolarizes it; the contribution of these ions to the formation of PP is small, since the permeability of non-selective channels for Cl– and Na+ is 2.5 and 25 times lower than for K+;

direct electrogenic effect of the Na+ /K+ ion pump, which occurs if the ion pump operates asymmetrically (the number of K+ ions transferred into the cell is not equal to the number of Na+ ions carried out of the cell).

Mechanism of action potential development

There are several phases in the action potential (Fig. 4):

depolarization phase;
phase of rapid repolarization;
slow repolarization phase (negative trace potential);
hyperpolarization phase (positive trace potential).

Depolarization phase. The development of AP is possible only under the influence of stimuli that cause depolarization of the cell membrane. When the cell membrane is depolarized to a critical depolarization level (CDL), an avalanche-like opening of voltage-sensitive Na+ channels occurs. Positively charged Na+ ions enter the cell along a concentration gradient (sodium current), as a result of which the membrane potential very quickly decreases to 0 and then becomes positive. The phenomenon of changing the sign of the membrane potential is called reversion membrane charge.

Fast and slow repolarization phase. As a result of membrane depolarization, voltage-sensitive K+ channels open. Positively charged K+ ions leave the cell along a concentration gradient (potassium current), which leads to restoration of the membrane potential. At the beginning of the phase, the intensity of the potassium current is high and repolarization occurs quickly; towards the end of the phase, the intensity of the potassium current decreases and repolarization slows down.

Hyperpolarization phase develops due to residual potassium current and due to the direct electrogenic effect of the activated Na+ / K+ pump.

Overshoot– the period of time during which the membrane potential has a positive value.

Threshold potential – the difference between the resting membrane potential and the critical level of depolarization. The magnitude of the threshold potential determines the excitability of the cell - the higher the threshold potential, the less excitability of the cell.

Changes in cell excitability during the development of excitation

If we take the level of excitability of a cell in a state of physiological rest as the norm, then during the development of the excitation cycle, its fluctuations can be observed. Depending on the level of excitability, the following cell states are distinguished (see Fig. 4).

Supernormal excitability ( exaltation ) – a state of a cell in which its excitability is higher than normal. Supernormal excitability is observed during the initial depolarization and during the slow repolarization phase. The increase in cell excitability in these AP phases is due to a decrease in the threshold potential compared to the norm.

Absolute refractoriness - a state of a cell in which its excitability drops to zero. No stimulus, even the strongest, can cause additional stimulation of the cell. During the depolarization phase, the cell is non-excitable, since all its Na+ channels are already in an open state.

Relative refractoriness – a state in which the excitability of the cell is significantly lower than normal; Only very strong stimuli can excite the cell. During the repolarization phase, the channels return to a closed state and cell excitability is gradually restored.

Subnormal excitability is characterized by a slight decrease in cell excitability below the normal level. This decrease in excitability occurs due to an increase in the threshold potential during the hyperpolarization phase.

Ion concentration inside and outside the cell

So, there are two facts that need to be considered in order to understand the mechanisms that maintain the resting membrane potential.

1 . The concentration of potassium ions in the cell is significantly higher than in the extracellular environment. 2 . The membrane at rest is selectively permeable to K +, and for Na + the permeability of the membrane at rest is insignificant. If we take the permeability for potassium to be 1, then the permeability for sodium at rest is only 0.04. Hence, there is a constant flow of K+ ions from the cytoplasm along a concentration gradient. Potassium current from the cytoplasm creates a relative deficiency of positive charges on the inner surface for anions cell membrane is impenetrable as a result, the cytoplasm of the cell becomes negatively charged in relation to the environment surrounding the cell. This potential difference between the cell and the extracellular space, the polarization of the cell, is called the resting membrane potential (RMP).

The question arises: why does the flow of potassium ions not continue until the concentrations of the ion outside and inside the cell are balanced? It should be remembered that this is a charged particle, therefore, its movement also depends on the charge of the membrane. The intracellular negative charge, which is created due to the flow of potassium ions from the cell, prevents new potassium ions from leaving the cell. The flow of potassium ions stops when the action of the electric field compensates for the movement of the ion along the concentration gradient. Consequently, for a given difference in ion concentrations on the membrane, the so-called EQUILIBRIUM POTENTIAL for potassium is formed. This potential (Ek) is equal to RT/nF *ln /, (n is the valency of the ion.) or

Ek=61.5 log/

The membrane potential (MP) largely depends on the equilibrium potential of potassium; however, some sodium ions still penetrate into the resting cell, as well as chlorine ions. Thus, the negative charge that the cell membrane has depends on the equilibrium potentials of sodium, potassium and chlorine and is described by the Nernst equation. The presence of this resting membrane potential is extremely important because it determines the cell's ability to excite - a specific response to a stimulus.

Cell excitation

IN excitement cells (transition from a resting to an active state) occurs when the permeability of ion channels for sodium and sometimes for calcium increases. The reason for the change in permeability may also be a change in the membrane potential - electrically excitable channels are activated, and the interaction of membrane receptors with biological active substance– receptor - controlled channels, and mechanical action. In any case, for the development of arousal it is necessary initial depolarization - a slight decrease in the negative charge of the membrane, caused by the action of a stimulus. An irritant can be any change in the parameters of the external or internal environment of the body: light, temperature, chemicals(impact on taste and olfactory receptors), stretching, pressure. Sodium rushes into the cell, an ion current occurs and the membrane potential decreases - depolarization membranes.

Table 4

Change in membrane potential upon cell excitation.

Please note that sodium enters the cell along a concentration gradient and an electrical gradient: the sodium concentration in the cell is 10 times lower than in the extracellular environment and the charge relative to the extracellular is negative. Potassium channels are also activated at the same time, but sodium (fast) channels are activated and inactivated within 1 - 1.5 milliseconds, and potassium channels longer.

Changes in membrane potential are usually depicted graphically. The top figure shows the initial depolarization of the membrane - the change in potential in response to the action of a stimulus. For each excitable cell there is a special level of membrane potential, upon reaching which the properties of sodium channels sharply change. This potential is called critical level of depolarization (KUD). When the membrane potential changes to KUD, fast, voltage-dependent sodium channels open, and a flow of sodium ions rushes into the cell. When positively charged ions enter the cell, the positive charge increases in the cytoplasm. As a result of this, the transmembrane potential difference decreases, the MP value decreases to 0, and then, as sodium continues to enter the cell, the membrane is recharged and the charge is reversed (overshoot) - now the surface becomes electronegative with respect to the cytoplasm - the membrane is completely DEPOLARIZED - middle picture. No further change in charge occurs because sodium channels are inactivated– more sodium cannot enter the cell, although the concentration gradient changes very slightly. If the stimulus has such a force that it depolarizes the membrane to CUD, this stimulus is called threshold; it causes excitation of the cell. The potential reversal point is a sign that the entire range of stimuli of any modality has been translated into the language of the nervous system - excitation impulses. Impulses or excitation potentials are called action potentials. Action potential (AP) is a rapid change in membrane potential in response to a stimulus of threshold strength. AP has standard amplitude and time parameters that do not depend on the strength of the stimulus - the “ALL OR NOTHING” rule. The next stage is the restoration of the resting membrane potential - repolarization(bottom figure) is mainly due to active ion transport. The most important process of active transport is the work of the Na/K pump, which pumps sodium ions out of the cell while simultaneously pumping potassium ions into the cell. The restoration of the membrane potential occurs due to the flow of potassium ions from the cell - potassium channels are activated and allow potassium ions to pass through until the equilibrium potassium potential is reached. This process is important because until the MPP is restored, the cell is not able to perceive a new impulse of excitation.

HYPERPOLARIZATION is a short-term increase in MP after its restoration, which is caused by an increase in membrane permeability for potassium and chlorine ions. Hyperpolarization occurs only after AP and is not typical for all cells. Let us once again try to graphically represent the phases of the action potential and the ionic processes underlying changes in membrane potential (Fig. 9). On the abscissa axis we plot the values ​​of the membrane potential in millivolts, on the ordinate axis we plot time in milliseconds.

1. Depolarization of the membrane to KUD - any sodium channels can open, sometimes calcium, both fast and slow, and voltage-gated and receptor-gated. It depends on the type of stimulus and the type of cells

2. Rapid entry of sodium into the cell - fast, voltage-dependent sodium channels open, and depolarization reaches the potential reversal point - the membrane is recharged, the sign of the charge changes to positive.

3. Restoration of the potassium concentration gradient - pump operation. Potassium channels are activated, potassium moves from the cell to the extracellular environment - repolarization, restoration of MPP begins

4. Trace depolarization, or negative trace potential - the membrane is still depolarized relative to the MPP.

5. Trace hyperpolarization. Potassium channels remain open and the additional potassium current hyperpolarizes the membrane. After this, the cell returns to its original level of MPP. The duration of the AP ranges from 1 to 3-4 ms for different cells.

Figure 9 Action potential phases

Pay attention to the three potential values, important and constant for each cell, its electrical characteristics.

1. MPP - electronegativity of the cell membrane at rest, providing the ability to excite - excitability. In the figure, MPP = -90 mV.

2. CUD - critical level of depolarization (or threshold for generation of membrane action potential) - this is the value of the membrane potential, upon reaching which they open fast, voltage-dependent sodium channels and the membrane is recharged due to the entry of positive sodium ions into the cell. The higher the electronegativity of the membrane, the more difficult it is to depolarize it to CUD, the less excitable such a cell is.

3. Potential reversal point (overshoot) - this value positive membrane potential, at which positively charged ions no longer penetrate the cell - short-term equilibrium sodium potential. In the figure + 30 mV. The total change in membrane potential from –90 to +30 will be 120 mV for a given cell, this value is the action potential. If this potential arises in a neuron, it will spread along the nerve fiber if muscle cells– will spread across the membrane muscle fiber and will lead to contraction, in the glandular to secretion - to the action of the cell. This is the specific response of the cell to the action of the stimulus, excitation.

When exposed to a stimulus subliminal strength incomplete depolarization occurs - LOCAL RESPONSE (LO). Incomplete or partial depolarization is a change in membrane charge that does not reach the critical level of depolarization (CLD).

": The resting potential is an important phenomenon in the life of all cells in the body, and it is important to know how it is formed. However, this is a complex dynamic process, difficult to comprehend in its entirety, especially for junior students (biological, medical and psychological specialties) and unprepared readers. However, when considered point by point, it is quite possible to understand its main details and stages. The work introduces the concept of the resting potential and highlights the main stages of its formation using figurative metaphors that help to understand and remember the molecular mechanisms of the formation of the resting potential.

Membrane transport structures - sodium-potassium pumps - create the prerequisites for the emergence of a resting potential. These prerequisites are the difference in ion concentration on the internal and outside cell membrane. The difference in sodium concentration and the difference in potassium concentration manifest itself separately. An attempt by potassium ions (K+) to equalize their concentration on both sides of the membrane leads to its leakage from the cell and the loss of positive electrical charges along with them, due to which the overall negative charge of the inner surface of the cell is significantly increased. This "potassium" negativity constitutes the majority of the resting potential (−60 mV on average), and a smaller portion (−10 mV) is the "exchange" negativity caused by the electrogenicity of the ion exchange pump itself.

Let's take a closer look.

Why do we need to know what resting potential is and how it arises?

Do you know what “animal electricity” is? Where do “biocurrents” come from in the body? How living cell, located in an aquatic environment, can turn into an “electric battery” and why does it not immediately discharge?

These questions can only be answered if we know how the cell creates its electrical potential difference (resting potential) across the membrane.

It is quite obvious that in order to understand how the nervous system works, it is necessary to first understand how its individual nerve cell, the neuron, works. The main thing that underlies the operation of a neuron is the movement of electrical charges through its membrane and, as a result, the appearance of electrical potentials on the membrane. We can say that the neuron, preparing for its nervous work, first stores energy in electrical form, and then uses it in the process of conducting and transmitting nervous excitation.

Thus, our very first step to studying the functioning of the nervous system is to understand how the electrical potential appears on the membrane of nerve cells. This is what we will do, and we will call this process formation of the resting potential.

Definition of the concept of “resting potential”

Normally, when a nerve cell is at physiological rest and ready to work, it has already experienced a redistribution of electrical charges between the inner and outer sides of the membrane. Due to this, an electric field arose, and an electric potential appeared on the membrane - resting membrane potential.

Thus, the membrane becomes polarized. This means that it has different electrical potentials on the outer and inner surfaces. The difference between these potentials is quite possible to register.

This can be verified if a microelectrode connected to a recording unit is inserted into the cell. As soon as the electrode gets inside the cell, it instantly acquires some constant electronegative potential with respect to the electrode located in the fluid surrounding the cell. The value of the intracellular electrical potential in nerve cells and fibers, for example, the giant nerve fibers of the squid, at rest is about −70 mV. This value is called the resting membrane potential (RMP). At all points of the axoplasm this potential is almost the same.

Nozdrachev A.D. and others. Beginnings of physiology.

A little more physics. Macroscopic physical bodies, as a rule, are electrically neutral, i.e. they contain both positive and negative charges in equal quantities. You can charge a body by creating an excess of charged particles of one type in it, for example, by friction against another body, in which an excess of charges of the opposite type is formed. Considering the presence of an elementary charge ( e), the total electric charge of any body can be represented as q= ±N× e, where N is an integer.

Resting potential- this is the difference in electrical potentials present on the inner and outer sides of the membrane when the cell is in a state of physiological rest. Its value is measured from inside the cell, it is negative and averages −70 mV (millivolts), although it can vary in different cells: from −35 mV to −90 mV.

It is important to consider that in nervous system Electrical charges are not represented by electrons, as in ordinary metal wires, but by ions - chemical particles that have an electrical charge. And in general in aqueous solutions It is not electrons, but ions that move in the form of electric current. Therefore everything electric currents in cells and their environment - this is ion currents.

So, the inside of the cell at rest is negatively charged, and the outside is positively charged. This is characteristic of all living cells, with the possible exception of red blood cells, which, on the contrary, are negatively charged on the outside. More specifically, it turns out that positive ions (Na + and K + cations) will predominate outside the cell around the cell, and negative ions (anions of organic acids that are not able to move freely through the membrane, like Na + and K +) will prevail inside.

Now we just have to explain how everything turned out this way. Although, of course, it is unpleasant to realize that all our cells except red blood cells only look positive on the outside, but on the inside they are negative.

The term “negativity,” which we will use to characterize the electrical potential inside the cell, will be useful to us to easily explain changes in the level of the resting potential. What is valuable about this term is that the following is intuitively clear: the greater the negativity inside the cell, the lower the negative side The potential is shifted from zero, and the lower the negativity, the closer the negative potential is to zero. This is much easier to understand than to understand every time what exactly the expression “potential increases” means - an increase in absolute value (or “modulo”) will mean a shift of the resting potential down from zero, and simply an “increase” means a shift in potential up to zero. The term "negativity" does not create similar problems of ambiguity of understanding.

The essence of the formation of the resting potential

Let's try to figure out where the electric charge of nerve cells comes from, although no one rubs them, as physicists do in their experiments with electric charges.

Here one of the logical traps awaits the researcher and student: the internal negativity of the cell does not arise due to the appearance of extra negative particles(anions), but, on the contrary, due to loss of a certain amount of positive particles(cations)!

So where do positively charged particles go from the cell? Let me remind you that these are sodium ions - Na + - and potassium - K + that have left the cell and accumulated outside.

The main secret of the appearance of negativity inside the cell

Let’s immediately reveal this secret and say that the cell loses some of its positive particles and becomes negatively charged due to two processes:

1. first, she exchanges “her” sodium for “foreign” potassium (yes, some positive ions for others, equally positive);
2. then these “replaced” positive potassium ions leak out of it, along with which they leak out of the cell positive charges.

We need to explain these two processes.

The first stage of creating internal negativity: exchange of Na + for K +

Proteins are constantly working in the membrane of a nerve cell. exchanger pumps(adenosine triphosphatases, or Na + /K + -ATPases) embedded in the membrane. They exchange the cell’s “own” sodium for external “foreign” potassium.

But when one positive charge (Na +) is exchanged for another of the same positive charge (K +), no deficiency of positive charges can arise in the cell! Right. But, nevertheless, due to this exchange, very few sodium ions remain in the cell, because almost all of them have gone outside. And at the same time, the cell is overflowing with potassium ions, which were pumped into it by molecular pumps. If we could taste the cytoplasm of the cell, we would notice that as a result of the work of the exchange pumps, it turned from salty to bitter-salty-sour, because the salty taste of sodium chloride was replaced by the complex taste of a rather concentrated solution of potassium chloride. In the cell, the potassium concentration reaches 0.4 mol/l. Solutions of potassium chloride in the range of 0.009–0.02 mol/l have a sweet taste, 0.03–0.04 - bitter, 0.05–0.1 - bitter-salty, and starting from 0.2 and above - a complex taste consisting of salty, bitter and sour.

The important thing here is that exchange of sodium for potassium - unequal. For every cell given three sodium ions she gets everything two potassium ions. This results in the loss of one positive charge with each ion exchange event. So already at this stage, due to unequal exchange, the cell loses more “pluses” than it receives in return. In electrical terms, this amounts to approximately −10 mV of negativity within the cell. (But remember that we still need to find an explanation for the remaining −60 mV!)

To make it easier to remember the operation of exchanger pumps, we can figuratively put it this way: “The cell loves potassium!” Therefore, the cell drags potassium towards itself, despite the fact that it is already full of it. And therefore, it exchanges it unprofitably for sodium, giving 3 sodium ions for 2 potassium ions. And therefore it spends ATP energy on this exchange. And how he spends it! Up to 70% of a neuron’s total energy expenditure can be spent on the operation of sodium-potassium pumps. (That's what love does, even if it's not real!)

By the way, it is interesting that the cell is not born with a ready-made resting potential. She still needs to create it. For example, during differentiation and fusion of myoblasts, their membrane potential changes from −10 to −70 mV, i.e. their membrane becomes more negative - polarized during the process of differentiation. And in experiments on multipotent mesenchymal stromal cells of human bone marrow, artificial depolarization, counteracting the resting potential and reducing cell negativity, even inhibited (depressed) cell differentiation.

Figuratively speaking, we can put it this way: By creating a resting potential, the cell is “charged with love.” This is love for two things:

1. the cell's love for potassium (therefore the cell forcibly drags it towards itself);
2. potassium's love for freedom (therefore potassium leaves the cell that has captured it).

We have already explained the mechanism of saturating the cell with potassium (this is the work of exchange pumps), and the mechanism of potassium leaving the cell will be explained below, when we move on to describing the second stage of creating intracellular negativity. So, the result of the activity of membrane ion exchanger pumps at the first stage of the formation of the resting potential is as follows:

1. Sodium (Na+) deficiency in the cell.
2. Excess potassium (K+) in the cell.
3. The appearance of a weak electric potential (−10 mV) on the membrane.

We can say this: at the first stage, membrane ion pumps create a difference in ion concentrations, or a concentration gradient (difference), between the intracellular and extracellular environment.

Second stage of creating negativity: leakage of K+ ions from the cell

So, what begins in the cell after its membrane sodium-potassium exchanger pumps work with ions?

Due to the resulting sodium deficiency inside the cell, this ion strives to rush inside: dissolved substances always strive to equalize their concentration throughout the entire volume of the solution. But sodium does this poorly, since sodium ion channels are usually closed and open only under certain conditions: under the influence of special substances (transmitters) or when the negativity in the cell decreases (membrane depolarization).

At the same time, there is an excess of potassium ions in the cell compared to the external environment - because the membrane pumps forcibly pumped it into the cell. And he, also trying to equalize his concentration inside and outside, strives, on the contrary, get out of the cage. And he succeeds!

Potassium ions K + leave the cell under the influence of a chemical gradient of their concentration on different sides of the membrane (the membrane is much more permeable to K + than to Na +) and carry away positive charges with them. Because of this, negativity grows inside the cell.

It is also important to understand that sodium and potassium ions do not seem to “notice” each other, they react only “to themselves.” Those. sodium reacts to the same sodium concentration, but “does not pay attention” to how much potassium is around. Conversely, potassium only responds to potassium concentrations and “ignores” sodium. It turns out that to understand the behavior of ions, it is necessary to separately consider the concentrations of sodium and potassium ions. Those. it is necessary to separately compare the concentration of sodium inside and outside the cell and separately - the concentration of potassium inside and outside the cell, but it makes no sense to compare sodium with potassium, as is sometimes done in textbooks.

According to the law of alignment chemical concentrations, which acts in solutions, sodium “wants” to enter the cell from the outside; it is also drawn there by electrical force (as we remember, the cytoplasm is negatively charged). He wants to, but he can’t, since the membrane in its normal state does not allow him to pass through it well. Sodium ion channels present in the membrane are normally closed. If, nevertheless, a little of it comes in, then the cell immediately exchanges it for external potassium using its sodium-potassium exchanger pumps. It turns out that sodium ions pass through the cell as if in transit and do not stay in it. Therefore, sodium in neurons is always in short supply.

But potassium can easily leave the cell to the outside! The cage is full of him, and she can’t hold him. It exits through special channels in the membrane - "potassium leak channels", which are normally open and release potassium.

K + -leakage channels are constantly open when normal values resting membrane potential and exhibit bursts of activity during shifts in membrane potential, which last several minutes and are observed at all potential values. An increase in K+ leakage currents leads to hyperpolarization of the membrane, while their suppression leads to depolarization. ...However, the existence of a channel mechanism responsible for leakage currents remained in question for a long time. Only now has it become clear that potassium leakage is a current through special potassium channels.

Zefirov A.L. and Sitdikova G.F. Ion channels of an excitable cell (structure, function, pathology).

From chemical to electrical

And now - once again the most important thing. We must consciously move away from movement chemical particles to the movement electric charges.

Potassium (K+) is positively charged, and therefore, when it leaves the cell, it carries out not only itself, but also a positive charge. Behind it, “minuses” - negative charges - stretch from inside the cell to the membrane. But they cannot leak through the membrane - unlike potassium ions - because... there are no suitable ion channels for them, and the membrane does not allow them to pass through. Remember about the −60 mV of negativity that remains unexplained by us? This is the very part of the resting membrane potential that is created by the leakage of potassium ions from the cell! And this is a large part of the resting potential.

There is even a special name for this component of the resting potential - concentration potential. Concentration potential - this is part of the resting potential created by the deficiency of positive charges inside the cell, formed due to the leakage of positive potassium ions from it.

Well, now a little physics, chemistry and mathematics for lovers of precision.

Electrical forces are related to chemical forces according to the Goldmann equation. Its special case is the simpler Nernst equation, the formula of which can be used to calculate the transmembrane diffusion potential difference based on different concentrations ions of the same type on different sides of the membrane. So, knowing the concentration of potassium ions outside and inside the cell, we can calculate the potassium equilibrium potential E K:

Where E k - equilibrium potential, R- gas constant, T- absolute temperature, F- Faraday's constant, K + ext and K + int - concentrations of K + ions outside and inside the cell, respectively. The formula shows that to calculate the potential, the concentrations of ions of the same type - K + - are compared with each other.

More precisely, the final value of the total diffusion potential, which is created by the leakage of several types of ions, is calculated using the Goldman-Hodgkin-Katz formula. It takes into account that the resting potential depends on three factors: (1) polarity electric charge each ion; (2) membrane permeability R for each ion; (3) [concentrations of the corresponding ions] inside (internal) and outside the membrane (external). For the squid axon membrane at rest, the conductance ratio R K: PNa :P Cl = 1: 0.04: 0.45.

Conclusion

So, the resting potential consists of two parts:

1. −10 mV, which are obtained from the “asymmetrical” operation of the membrane pump-exchanger (after all, it pumps more positive charges (Na +) out of the cell than it pumps back with potassium).
2. The second part is potassium leaking out of the cell all the time, carrying away positive charges. His main contribution is: −60 mV. In total, this gives the desired −70 mV.

Interestingly, potassium will stop leaving the cell (more precisely, its input and output are equalized) only at a cell negative level of −90 mV. In this case, the chemical and electrical forces that push potassium through the membrane are equal, but direct it in opposite directions. But this is hampered by sodium constantly leaking into the cell, which carries with it positive charges and reduces the negativity for which potassium “fights.” And as a result, the cell maintains an equilibrium state at a level of −70 mV.

Now the resting membrane potential is finally formed.

Scheme of operation of Na + /K + -ATPase clearly illustrates the “asymmetrical” exchange of Na + for K +: pumping out excess “plus” in each cycle of the enzyme leads to negative charging of the inner surface of the membrane. What this video doesn't say is that the ATPase is responsible for less than 20% of the resting potential (−10 mV): the remaining "negativity" (−60 mV) comes from K ions leaving the cell through "potassium leak channels" +, seeking to equalize their concentration inside and outside the cell.

Literature

1. Jacqueline Fischer-Lougheed, Jian-Hui Liu, Estelle Espinos, David Mordasini, Charles R. Bader, et. al.. (2001). Human Myoblast Fusion Requires Expression of Functional Inward Rectifier Kir2.1 Channels . J Cell Biol. 153 , 677-686;
2. Liu J.H., Bijlenga P., Fischer-Lougheed J. et al. (1998). Role of an inward rectifier K+ current and of hyperpolarization in human myoblast fusion. J. Physiol. 510 , 467–476;
3. Sarah Sundelacruz, Michael Levin, David L. Kaplan. (2008). Membrane Potential Controls Adipogenic and Osteogenic Differentiation of Mesenchymal Stem Cells. PLoS ONE. 3 , e3737;
4. Pavlovskaya M.V. and Mamykin A.I. Electrostatics. Dielectrics and conductors in an electric field. Direct Current / Electronic Manual general course physics. SPb: St. Petersburg State Electrotechnical University;
5. Nozdrachev A.D., Bazhenov Yu.I., Barannikova I.A., Batuev A.S. and others. The beginnings of physiology: Textbook for universities / Ed. acad. HELL. Nozdracheva. St. Petersburg: Lan, 2001. - 1088 pp.;
6. Makarov A.M. and Luneva L.A. Fundamentals of Electromagnetism / Physics in technical university. T. 3;
7. Zefirov A.L. and Sitdikova G.F. Ion channels of an excitable cell (structure, function, pathology). Kazan: Art Cafe, 2010. - 271 pp.;
8. Rodina T.G. Sensory analysis of food products. Textbook for university students. M.: Academy, 2004. - 208 pp.;
9. Kolman, J. and Rehm, K.-G. Visual biochemistry. M.: Mir, 2004. - 469 pp.;
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Resting membrane potential (MPP) or resting potential (PP) is the potential difference of a resting cell between the inner and outer sides of the membrane. The inner side of the cell membrane is negatively charged relative to the outer. Taking the potential of the external solution as zero, the MPP is written with a minus sign. Magnitude MPP depends on the type of tissue and varies from -9 to -100 mV. Therefore, in a state of rest the cell membrane polarized. A decrease in the MPP value is called depolarization, increase - hyperpolarization, restoring the original value MPP-repolarization membranes.

Basic provisions of the membrane theory of origin MPP boil down to the following. At rest, the cell membrane is highly permeable to K + ions (in some cells and for SG), less permeable to Na + and practically impermeable to intracellular proteins and other organic ions. K + ions diffuse out of the cell along a concentration gradient, and non-penetrating anions remain in the cytoplasm, providing the appearance of a potential difference across the membrane.

The resulting potential difference prevents the exit of K+ from the cell and at a certain value, an equilibrium occurs between the exit of K+ along the concentration gradient and the entry of these cations along the resulting electrical gradient. The membrane potential at which this equilibrium is achieved is called equilibrium potential. Its value can be calculated from the Nernst equation:

10 In nerve fibers, signals are transmitted by action potentials, which are rapid changes in membrane potential that propagate rapidly along the nerve fiber membrane. Each action potential begins with a rapid shift in the resting potential from a normal negative value to a positive value, then it returns almost as quickly to a negative potential. When a nerve signal is conducted, the action potential moves along the nerve fiber until it ends. The figure shows the changes that occur at the membrane during an action potential, with positive charges moving into the fiber at the beginning and positive charges returning outward at the end. The lower part of the figure graphically represents the successive changes in membrane potential over a period of several 1/10,000 sec, illustrating the explosive onset of the action potential and an almost equally rapid recovery. Rest stage. This stage is represented by the resting membrane potential, which precedes the action potential. The membrane is polarized during this stage due to the presence of a negative membrane potential of -90 mV. Depolarization phase. At this time, the membrane suddenly becomes highly permeable to sodium ions, allowing large numbers of positively charged sodium ions to diffuse into the axon. The normal polarized state of -90 mV is immediately neutralized by the incoming positively charged sodium ions, causing the potential to rapidly increase in the positive direction. This process is called depolarization. In large nerve fibers, a significant excess of incoming positive sodium ions usually causes the membrane potential to “jump” beyond the zero level, becoming slightly positive. In some smaller fibers, as in most neurons of the central nervous system, the potential reaches the zero level without “jumping” over it. Repolarization phase. Within a few fractions of a millisecond after a sharp increase in the permeability of the membrane to sodium ions, sodium channels begin to close and potassium channels begin to open. As a result, rapid outward diffusion of potassium ions restores the normal negative resting membrane potential. This process is called membrane repolarization. action potential To more fully understand the factors that cause depolarization and repolarization, it is necessary to study the characteristics of two other types of transport channels in the nerve fiber membrane: electrically gated sodium and potassium channels. Electrogated sodium and potassium channels. An electrically controlled sodium channel is a necessary participant in the processes of depolarization and repolarization during the development of an action potential in the nerve fiber membrane. The electrically gated potassium channel also plays important role in increasing the rate of membrane repolarization. Both types of electrically controlled channels exist in addition to the Na+/K+ pump and K*/Na+ leakage channels. Electrically controlled sodium channel. The top part of the figure shows an electrically driven sodium channel in three various states. This channel has two gates: one near the outer part of the channel, which is called the activation gate, the other - near the inner part of the channel, which is called the inactivation gate. The upper left part of the figure shows the resting state of this gate when the resting membrane potential is -90 mV. Under these conditions, the activation gate is closed and prevents sodium ions from entering the fiber. Sodium channel activation. When the resting membrane potential shifts towards less negative values, rising from -90 mV towards zero, at a certain level (usually between -70 and -50 mV) a sudden conformational change occurs in the activation gate, resulting in it moving into a completely open state . This state is called the activated state of the channel, in which sodium ions can freely enter the fiber through it; in this case, the sodium permeability of the membrane increases in the range from 500 to 5000 times. Inactivation of the sodium channel. The upper right part of the figure shows the third state of the sodium channel. The increase in potential that opens the activation gate closes the inactivation gate. However, the inactivation gate closes within a few tenths of a millisecond after the activation gate opens. This means that the conformational change that leads to the closing of the inactivation gate is a slower process than the conformational change that opens the activation gate. As a result, a few tenths of a millisecond after the opening of the sodium channel, the inactivation gate closes, and sodium ions can no longer penetrate into the fiber. From this moment, the membrane potential begins to return to the resting level, i.e. the repolarization process begins. There is another important characteristic of the sodium channel inactivation process: the inactivation gate does not re-open until the membrane potential returns to a value equal to or close to the level of the original resting potential. In this regard, re-opening of sodium channels is usually impossible without prior repolarization of the nerve fiber.

13The mechanism for conducting excitation along nerve fibers depends on their type. There are two types of nerve fibers: myelinated and unmyelinated. Metabolic processes in unmyelinated fibers do not provide rapid compensation for energy expenditure. The spread of excitation will occur with gradual attenuation - with decrement. Decremental behavior of excitation is characteristic of a low-organized nervous system. Excitation propagates due to small circular currents that arise into the fiber or into the surrounding liquid. A potential difference arises between excited and unexcited areas, which contributes to the emergence of circular currents. The current will spread from the “+” charge to the “-”. At the point where the circular current exits, the permeability of the plasma membrane for Na ions increases, resulting in depolarization of the membrane. A potential difference again arises between the newly excited area and the neighboring unexcited one, which leads to the emergence of circular currents. The excitation gradually covers neighboring areas of the axial cylinder and thus spreads to the end of the axon. In myelin fibers, due to the perfection of metabolism, excitation passes without fading, without decrement. Due to the large radius of the nerve fiber due to the myelin sheath, electric current can enter and exit the fiber only in the area of ​​interception. When stimulation is applied, depolarization occurs in the area of ​​interception A, the neighboring interception B is polarized at this time. Between the interceptions, a potential difference arises, and circular currents appear. Due to circular currents, other interceptions are excited, while the excitation spreads saltatory, jumpwise from one interception to another. There are three laws for the conduction of stimulation along a nerve fiber. Law of anatomical and physiological integrity. Conduction of impulses along a nerve fiber is possible only if its integrity is not compromised. Law of isolated conduction of excitation. There are a number of features of the spread of excitation in peripheral, pulpal and non-pulpate nerve fibers. In peripheral nerve fibers, excitation is transmitted only along the nerve fiber, but is not transmitted to neighboring ones, which are located in the same nerve trunk. In the pulpy nerve fibers, the myelin sheath plays the role of an insulator. Due to myelin, the resistivity increases and the electrical capacitance of the sheath decreases. In non-pulp nerve fibers, excitation is transmitted in isolation. The law of two-way conduction of excitation. The nerve fiber conducts nerve impulses in two directions - centripetal and centrifugal.

14 Synapses - this is a specialized structure that ensures the transmission of a nerve impulse from a nerve fiber to an effector cell - a muscle fiber, neuron or secretory cell.

Synapses– these are the junctions of the nerve process (axon) of one neuron with the body or process (dendrite, axon) of another nerve cell (intermittent contact between nerve cells).

All structures that provide signal transmission from one nerve structure to another - synapses .

Meaning– transmits nerve impulses from one neuron to another => ensures the transmission of excitation along the nerve fiber (signal propagation).

A large number of synapses provides a large area for information transfer.

Synapse structure:

1. Presynaptic membrane- belongs to the neuron from which the signal is transmitted.

2. Synaptic cleft, filled with liquid with a high content of Ca ions.

3. Postsynaptic membrane- belongs to the cells to which the signal is transmitted.

There is always a gap between neurons filled with interstitial fluid.

Depending on the density of the membranes, there are:

- symmetrical(with the same membrane density)

- asymmetrical(the density of one of the membranes is higher)

Presynaptic membrane covers the extension of the axon of the transmitting neuron.

Extension - synaptic button/synaptic plaque.

On the plaque - synaptic vesicles (vesicles).

On the inner side of the presynaptic membrane - protein/hexagonal lattice(necessary for the release of the mediator), which contains the protein - neurin . Filled with synaptic vesicles that contain mediator– a special substance involved in signal transmission.

The composition of the vesicle membrane includes - Stenin (protein).

Postsynaptic membrane covers the effector cell. Contains protein molecules that are selectively sensitive to the mediator of a given synapse, which ensures interaction.

These molecules are part of the channels of the postsynaptic membrane + enzymes (many) that can destroy the connection of the transmitter with the receptors.

Receptors of the postsynaptic membrane.

The postsynaptic membrane contains receptors that are related to the mediator of a given synapse.

Between them is snaptic fissure . It is filled with intercellular fluid, which has large number calcium. Possesses nearby structural features– contains protein molecules that are sensitive to the mediator that transmits signals.

15 Synaptic conduction delay

In order for the excitement to spread throughout reflex arc it takes a certain amount of time. This time consists of the following periods:

1. the period temporarily necessary for excitation of receptors (receptors) and for conducting excitation impulses along afferent fibers to the center;

2. the period of time required for the spread of excitation through the nerve centers;

3. the period of time required for the propagation of excitation along the efferent fibers to the working organ;

4. latent period of the working organ.

16 Inhibition plays an important role in the processing of information entering the central nervous system. This role is especially pronounced in presynaptic inhibition. It regulates the excitation process more precisely, since individual nerve fibers can be blocked by this inhibition. Hundreds and thousands of impulses can approach one excitatory neuron through different terminals. At the same time, the number of impulses reaching the neuron is determined by presynaptic inhibition. Inhibition of lateral pathways ensures the selection of significant signals from the background. Blockade of inhibition leads to widespread irradiation of excitation and convulsions, for example, when presynaptic inhibition is turned off by bicuculline.