General physiology of excitable tissues. Resting potential

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 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 cell itself biological system;
the strength and form of the cell reaction is not determined by the strength and form of 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 a state of excitation when exposed to a stimulus. Different cells have different excitability. The excitability of the same cell varies 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 surfaces cell membrane which is called membrane potential(MP). At rest, the MF value is –60…–90 mV (the inner side of the membrane is negatively charged relative to the outer). 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) .

A decrease in MP relative to its normal level (LP) is called depolarization, and an 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's consider various manifestations excitation using the example of irritating a cell with electric current (Fig. 2).

Under the action of weak (subthreshold) pulses of electric current, an electrotonic potential develops in the cell. Electrotonic potential(EP) – shift membrane potential cells 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 appear physiological reaction cells. 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 value of the cell MP very quickly decreases to 0 (depolarization), and then the membrane potential acquires positive value(+20…+30 mV), i.e. the inner side of the membrane is charged positively relative to the outer. 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 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 acting on gate system signal, the activation gate opens and the transport of ions 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 critical level depolarization (CUD), 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 nonexcitable because 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.

Resting membrane potential

At rest, on the outer side of the plasma membrane is located thin layer positive charges, and on inside– negative. 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 may individual cells vary from -40 to -80 mV.

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 will decrease a short time becomes maximum, they rush into the cell and, in connection with this, the transmembrane potential difference rapidly decreases to 0, and then acquires a positive value. 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 significantly 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 a high concentration of 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 .

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.

The modern version of neural theory connects certain parts of a nerve cell with the nature of the electrical signals that arise 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 acting, 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 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 quite a lot 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 the total amount of 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 in highest degree a 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).

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. In the resting state, 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 of 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 an 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 a large number of calcium. It has a number of structural features - it 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 by bicuculline is turned off.

The membrane of all living cells is polarized. The inner side of the membrane carries a negative charge compared to the intercellular space (Fig. 1). The amount of charge carried by the membrane is called membrane potential (MP). In no excitable tissues The MP is low and is about -40 mV. In excitable tissues it is high, about -60 - -100 mV and is called resting potential (RP).

The resting potential, like any membrane potential, is formed due to the selective permeability of the cell membrane. As is known, the plasmalemma consists of a lipid bilayer through which the movement of charged molecules is difficult. Proteins embedded in the membrane can selectively change the permeability of the membrane to different ions, depending on incoming stimuli. At the same time, potassium ions play a leading role in the formation of the resting potential; in addition to them, sodium and chloride ions are important.

Rice. 1. Concentrations and distribution of ions from the internal and outside membranes.

Most ions are distributed unevenly on the inside and outside of the cell (Fig. 1). Inside the cell, the concentration of potassium ions is higher, and sodium and chlorine ions are lower than outside. At rest, the membrane is permeable to potassium ions and practically impermeable to sodium and chlorine ions. Although potassium can freely leave the cell, its concentrations remain unchanged due to the negative charge on the inside of the membrane. Thus, potassium is acted upon by two forces that are in balance: osmotic (K + concentration gradient) and electrical (membrane charge), due to which the number of potassium ions entering the cell is equal to those leaving. The movement of potassium occurs through potassium leak channels, open at rest. The amount of membrane charge at which potassium ions are in equilibrium can be calculated using the Nernst equation:

Where E k is the equilibrium potential for K +; R - gas constant; T - absolute temperature; F - Faraday number; n - valence of K + (+1), [K + n] - [K + ext] - external and internal concentrations of K +.

If we substitute the values ​​from the table in Fig. 43, then we get the equilibrium potential value equal to approximately -95 mV. This value fits into the range of membrane potential of excitable cells. Differences in the PP of different cells (even excitable ones) can arise for three reasons:

• differences in intracellular and extracellular concentrations of potassium ions in different tissues (the table shows data for an average neuron);
• sodium-potassium ATPase can contribute to the charge value, since it removes 3 Na + from the cell in exchange for 2 K +;
• Despite the minimal permeability of the membrane to sodium and chlorine, these ions can still enter the cells, although 10 to 100 times worse than potassium.

To take into account the penetration of other ions into the cell, there is the Nernst-Goldmann equation:

Where Em - membrane potential; R- gas constant; T- absolute temperature; F- Faraday number; PK, PNa And P Cl - membrane permeability constants for K + Na + and Cl, respectively; [TO+ n ], , , , [Cl - n] and [Cl - ext] - concentrations of K +, Na + and Cl outside (n) and inside (in) the cell.