Resting cell membrane potential. Cell resting potential

This equation allows you to establish a more accurate PP value. Typically, the membrane is several mV less polarized than the equilibrium potential for K+.

Action potential (AP) may occur in excitable cells. If irritation is applied to a nerve or muscle above the excitation threshold, then the PP of the nerve or muscle will quickly decrease and for a short period of time (millisecond) a short-term recharge of the membrane will occur: its inner side will become positively charged relative to the outside, after which the PP will be restored. This short-term change in PP that occurs when a cell is excited is called an action potential.

The occurrence of PD is possible due to the fact that, unlike potassium ions, sodium ions are far from equilibrium. If we substitute sodium instead of potassium into the Nernst equation, we get an equilibrium potential of approximately +60 mV. During PD, there is a transient increase in Na + permeability. At the same time, sodium will begin to penetrate into the cell under the influence of two forces: along the concentration gradient and along the membrane charge, trying to adjust the membrane charge to its equilibrium potential. The movement of sodium is carried out by voltage dependent sodium channels, which open in response to a shift in membrane potential, after which they themselves are inactivated.

Rice. 2. Action potential nerve fiber(A) and changes in membrane conductivity for sodium and potassium ions (B).

In the recording, the AP appears as a short-term peak (Fig. 2), which has several phases.

1. Depolarization (rising phase) (Fig. 2) - increase in sodium permeability due to opening sodium channels. Sodium strives for its equilibrium potential, but does not reach it, since the channel has time to inactivate.
2. Repolarization is the return of charge to the resting potential value. In addition to potassium leak channels, voltage-gated potassium channels are connected here (activated by depolarization). At this time, potassium leaves the cell, returning to its equilibrium potential.
3. Hyperpolarization (not always) - occurs in cases where the equilibrium potassium potential exceeds the PP modulus. The return to PP occurs after the return to the equilibrium potential for K +.

During AP, the polarity of the membrane charge changes. The AP phase in which the membrane charge is positive is called overshoot(Fig. 2).

For the generation of AP, the system of activation and inactivation turns out to be very important. voltage-gated sodium channels(Fig. 3). These channels have two doors: activation (M-gate) and inactivation (H-gate). At rest, the M-gate is open and the H-gate is closed. During membrane depolarization, the M gate quickly opens and the H gate begins to close. The flow of sodium into the cell is possible while the M-gate is already open, and the H-gate has not yet closed. The entry of sodium leads to further depolarization of the cell, leading to the opening more channels and starting a chain of positive feedback. Membrane depolarization will continue until all voltage-gated sodium channels are inactivated, which occurs at the peak of AP. The minimum stimulus value leading to the occurrence of PD is called threshold. Thus, the resulting PD will obey the “all or nothing” law and its magnitude will not depend on the magnitude of the stimulus that caused the PD.

Thanks to the H-gate, inactivation of the channel occurs before the potential on the membrane reaches the equilibrium value for sodium. After sodium stops entering the cell, repolarization occurs due to potassium ions leaving the cell. Moreover, in this case, voltage-activated potassium channels are also connected to the leak channels. During repolarization, the M-gate in the fast sodium channel closes rapidly. The H-gate opens much more slowly and remains closed for some time after the charge returns to resting potential. This period is usually called refractory period.

Rice. 3. Operation of a voltage-gated sodium channel.

The concentration of ions inside the cell is restored by sodium-potassium ATPase, which, with the expenditure of energy in the form of ATP, pumps out 3 sodium ions from the cell and pumps in 2 potassium ions.

Along unmyelinated fiber or the action potential propagates continuously along the muscle membrane. The resulting action potential due to the electric field is capable of depolarizing the membrane of the neighboring area to a threshold value, as a result of which depolarization occurs in the neighboring area. The main role in the emergence of potential in a new section of the membrane is the previous section. In this case, at each site, immediately after the PD, a refractory period begins, due to which the PD spreads unidirectionally. All other things being equal, the propagation of an action potential along an unmyelinated axon occurs the faster, the larger the fiber diameter. In mammals, the speed is 1-4 m/s. Since invertebrate animals lack myelin, AP speeds in giant squid axons can reach 100 m/s.

Along myelinated fiber The action potential propagates spasmodically (saltatory conduction). Myelinated fibers are characterized by a concentration of voltage-gated ion channels only in the areas of nodes of Ranvier; here their density is 100 times greater than in the membranes of unmyelinated fibers. There are almost no voltage-gated channels in the area of ​​myelin couplings. The action potential that arises in one node of Ranvier, due to the electric field, depolarizes the membrane of neighboring nodes to a threshold value, which leads to the emergence of new action potentials in them, that is, the excitation passes spasmodically, from one node to another. If one node of Ranvier is damaged, the action potential excites the 2nd, 3rd, 4th, and even the 5th, since the electrical insulation created by the myelin sleeves reduces the dissipation of the electric field. Saltatory conduction increases the speed of AP conduction 15-20 times up to 120 m/s.

https://shishadrugs.com The work of neurons

The nervous system consists of neurons and glial cells. However, main role Neurons play a role in the conduction and transmission of nerve impulses. They receive information from many cells along dendrites, analyze it and transmit it or not transmit it to the next neuron.

The transmission of nerve impulses from one cell to another is carried out using synapses. There are two main types of synapses: electrical and chemical (Fig. 4). The task of any synapse is to transmit information from presynaptic membrane(axon membrane) on postsynaptic(membrane of a dendrite, another axon, muscle or other target organ). Most synapses in the nervous system are formed between the endings of axons and dendrites, which form dendritic spines in the area of ​​the synapse.

Advantage electrical synapse is that the signal from one cell to another passes without delay. In addition, such synapses do not get tired. To do this, the pre- and postsynaptic membranes are connected by cross bridges, through which ions from one cell can move to another. However, a significant disadvantage of such a system is the lack of unidirectional PD transmission. That is, it can be transmitted both from the presynaptic membrane to the postsynaptic membrane, and vice versa. Therefore, this design is quite rare and mainly in nervous system invertebrates.

Rice. 4. Scheme of the structure of chemical and electrical synapses.

Chemical synapse very common in nature. O is more complicated, since a system is needed to convert an electrical impulse into a chemical signal, then again into an electrical impulse. All this leads to the emergence synaptic delay, which can be 0.2-0.4 ms. In addition, stock depletion may occur chemical substance, which will lead to fatigue of the synapse. However, such a synapse ensures unidirectional transmission of action potentials, which is its main advantage.

Rice. 5. Scheme of operation (a) and electron micrograph (b) of a chemical synapse.

In the resting state, the axon terminal, or presynaptic terminal, contains membrane vesicles (vesicles) with a neurotransmitter. The surface of the vesicles is negatively charged to prevent binding to the membrane, and is coated with special proteins involved in the release of the vesicles. Each vial contains the same amount of a chemical called quantum neurotransmitter. Neurotransmitters are very diverse in chemical structure, however, most of them are produced right at the end. Therefore, it may contain systems for the synthesis of a chemical mediator, as well as the Golgi apparatus and mitochondria.

Postsynaptic membrane contains receptors to the neurotransmitter. Receptors can be in the form of ion channels that open upon contact with their ligand ( ionotropic), and membrane proteins that trigger an intracellular cascade of reactions ( metabotropic). One neurotransmitter can have several ionotropic and metabotropic receptors. At the same time, some of them can be exciting, and some can be inhibitory. Thus, the cell's response to a neurotransmitter will be determined by the type of receptor on its membrane, and different cells can react completely differently to the same chemical.

Between the pre- and postsynaptic membrane is located synaptic cleft, 10-15 nm wide.

When an AP arrives at the presynaptic terminal, voltage-activated calcium channels open on it and calcium ions enter the cell. Calcium binds to proteins on the surface of the vesicles, which leads to their transport to the presynaptic membrane, followed by membrane fusion. After such interaction, the neurotransmitter ends up in the synaptic cleft (Fig. 5) and can contact its receptor.

Ionotropic receptors are ligand-activated ion channels. This means that the channel opens only in the presence of a certain chemical. For different neurotransmitters, these can be sodium, calcium or chloride channels. The current of sodium and calcium causes depolarization of the membrane, which is why such receptors are called excitatory. The chloride current leads to hyperpolarization, which makes it difficult to generate AP. Therefore, such receptors are called inhibitory.

Metabotropic neurotransmitter receptors belong to the class of G protein-associated receptors (GPCRs). These proteins trigger various intracellular cascades of reactions, ultimately leading to either further transmission of excitation or inhibition.

After signal transmission, it is necessary to quickly remove the neurotransmitter from the synaptic cleft. To do this, either enzymes that break down the neurotransmitter are present in the gap, or transporters that pump the neurotransmitter into the cells can be located at the presynaptic terminal or neighboring glial cells. IN the latter case it can be reused.

Each neuron receives impulses from 100 to 100,000 synapses. A single depolarization on one dendrite will not lead to further signal transmission. A neuron can simultaneously receive many excitatory and inhibitory stimuli. All of them are summed up on the soma of the neuron. This summation is called spatial. Further, PD may or may not occur (depending on the received signals) in the area axon hillock. The axon hillock is the region of the axon adjacent to the soma and has a minimum threshold of action potential. Next, the impulse spreads along the axon, the end of which can branch strongly and form synapses with many cells. In addition to spatial, there is time summation. It occurs when frequently repeated impulses are received from one dendrite.

In addition to the classical synapses between axons and dendrites or their spines, there are also synapses that modulate transmission at other synapses (Fig. 6). These include axo-axonal synapses. Such synapses can enhance or inhibit synaptic transmission. That is, if an AP arrives at the end of the axon forming the axo-spine synapse, and at that time an inhibitory signal arrives at it via the axo-axonal synapse, the release of the neurotransmitter at the axo-spine synapse will not occur. Axo-dendritic synapses can change the conduction of AP membranes on the way from the spine to the cell soma. There are also axo-somatic synapses that can influence the summation of the signal in the soma region of the neuron.

Thus, there is a huge variety of different synapses, differing in the composition of neurotransmitters, receptors and their location. All this ensures a variety of reactions and plasticity of the nervous system.

Rice. 6. Diversity of synapses in the nervous system.

History of discovery

In 1902, Julius Bernstein hypothesized that cell membrane allows K+ ions into the cell, and they accumulate in the cytoplasm. The calculation of the resting potential value using the Nernst equation for the potassium electrode coincided satisfactorily with the measured potential between the muscle sarcoplasm and environment, which was about - 70 mV.

According to the theory of Yu. Bernstein, when a cell is excited, its membrane is damaged, and K + ions flow out of the cell along a concentration gradient until the membrane potential becomes zero. The membrane then restores its integrity and the potential returns to the resting potential level. This claim, which relates rather to the action potential, was refuted by Hodgkin and Huxley in 1939.

Bernstein's theory of the resting potential was confirmed by Kenneth Stewart Cole, sometimes erroneously spelled K.C. Cole, because of his nickname, Casey ("Kacy"). PP and PD are depicted in a famous illustration by Cole and Curtis, 1939. This drawing became the emblem of the Membrane Biophysics Group of the Biophysical Society (see illustration).

General provisions

In order for a potential difference to be maintained across the membrane, it is necessary that there be a certain difference in the concentration of various ions inside and outside the cell.

Ion concentrations in the cell skeletal muscle and in the extracellular environment

The resting potential for most neurons is on the order of −60 mV - −70 mV. Cells of non-excitable tissues also have a potential difference on the membrane, which is different for cells of different tissues and organisms.

Formation of the resting potential

The PP is formed in two stages.

First stage: the creation of slight (-10 mV) negativity inside the cell due to the unequal asymmetric exchange of Na + for K + in a ratio of 3: 2. As a result, more positive charges leave the cell with sodium than return to it with potassium. This feature of the sodium-potassium pump, which exchanges these ions through the membrane with the expenditure of ATP energy, ensures its electrogenicity.

The results of the activity of membrane ion exchanger pumps at the first stage of PP formation are as follows:

1. Deficiency of sodium ions (Na +) in the cell.

2. Excess potassium ions (K +) in the cell.

3. The appearance of a weak electric potential (-10 mV) on the membrane.

Second phase: creation of significant (-60 mV) negativity inside the cell due to the leakage of K + ions from it through the membrane. Potassium ions K+ leave the cell and take away positive charges from it, bringing the negative charge to -70 mV.

So, the resting membrane potential is a deficiency of positive electrical charges inside the cell, resulting from the leakage of positive potassium ions from it and the electrogenic action of the sodium-potassium pump.

see also

Notes

Links

Dudel J, Rüegg J, Schmidt R, et al. Human physiology: in 3 volumes. Per. from English / edited by R. Schmidt and G. Teus. - 3. - M.: Mir, 2007. - T. 1. - 323 with illustrations. With. - 1500 copies.

- ISBN 5-03-000575-3

Wikimedia Foundation. 2010. Any living cell covered with a semi-permeable membrane through which passive movement and active selective transport of positively and negatively charged ions occurs. Due to this transfer, there is a difference in electrical charges (potentials) between the outer and inner surfaces of the membrane - the membrane potential. There are three distinct manifestations of membrane potential: resting membrane potential, local potential, or local response.

, And action potential, then the membrane potential remains constant for a long time. The membrane potential of such a resting cell is called the resting membrane potential. For the outer surface of the cell membrane, the resting potential is always positive, and for the inner surface of the cell membrane it is always negative. It is customary to measure the resting potential on the inner surface of the membrane, because the ionic composition of the cell cytoplasm is more stable than intercellular fluid. The magnitude of the resting potential is relatively constant for each cell type. For striated muscle cells it ranges from –50 to –90 mV, and for nerve cells from –50 to –80 mV.

The causes of the resting potential are different concentrations of cations and anions outside and inside the cell, as well as selective permeability for them the cell membrane. Cytoplasm of resting nervous and muscle cell contains approximately 30–50 times more potassium cations, 5–15 times less sodium cations and 10–50 times less chlorine anions than extracellular fluid.

At rest, almost all sodium channels of the cell membrane are closed, and most potassium channels are open. Whenever potassium ions encounter an open channel, they pass through the membrane. Since there are much more potassium ions inside the cell, the osmotic force pushes them out of the cell. The released potassium cations increase the positive charge on the outer surface of the cell membrane. As a result of the release of potassium ions from the cell, their concentrations inside and outside the cell would soon be equalized. However, this is prevented by the electrical force of repulsion of positive potassium ions from the positively charged outer surface of the membrane.

The greater the positive charge on the outer surface of the membrane becomes, the more difficult it is for potassium ions to pass from the cytoplasm through the membrane. Potassium ions will leave the cell until the electrical repulsion force becomes equal strength osmotic pressure K + . At this level of potential on the membrane, the entrance and exit of potassium ions from the cell are in equilibrium, therefore the electric charge on the membrane at this moment is called potassium equilibrium potential. For neurons it is from –80 to –90 mV.

Since in a resting cell almost all sodium channels of the membrane are closed, Na + ions enter the cell along the concentration gradient in small quantities. They compensate for the loss of positive charge only to a very small extent. internal environment cells caused by the release of potassium ions, but cannot significantly compensate for this loss. Therefore, the penetration (leakage) of sodium ions into the cell leads to only a slight decrease in the membrane potential, as a result of which the resting membrane potential has a slightly lower value compared to the potassium equilibrium potential.

Thus, potassium cations leaving the cell together with an excess of sodium cations in extracellular fluid create a positive potential on the outer surface of the membrane of a resting cell.

At rest, the plasma membrane of the cell is highly permeable to chlorine anions. Chlorine anions, which are more abundant in the extracellular fluid, diffuse into the cell and carry with them a negative charge. Complete equalization of the concentrations of chlorine ions outside and inside the cell does not occur, because this is prevented by the force of electrical mutual repulsion of like charges. Created chlorine equilibrium potential, in which the entry of chlorine ions into the cell and their exit from it are in equilibrium.

The cell membrane is practically impermeable to large anions organic acids. Therefore, they remain in the cytoplasm and, together with incoming chlorine anions, provide a negative potential on the inner surface of the membrane of a resting nerve cell.

Essential The resting membrane potential is that it creates an electric field that acts on the macromolecules of the membrane and gives their charged groups a certain position in space. It is especially important that this electric field causes the activation gate of sodium channels to be closed and open state their inactivation gate (Fig. 61, A). This ensures that the cell is in a state of rest and is ready to be excited. Even a relatively small decrease in the resting membrane potential opens the activation “gate” of sodium channels, which removes the cell from the resting state and gives rise to excitation.

Between the outer surface of the cell and its cytoplasm at rest there is a potential difference of about 0.06-0.09 V, and the cell surface is charged electropositively with respect to the cytoplasm. This potential difference is called resting potential or membrane potential. Accurate measurement of the resting potential is only possible with the help of microelectrodes designed for intracellular current drainage, very powerful amplifiers and sensitive recording instruments - oscilloscopes.

The microelectrode (Fig. 67, 69) is a thin glass capillary, the tip of which has a diameter of about 1 micron. This capillary is filled saline solution, immerse a metal electrode in it and connect it to an amplifier and an oscilloscope (Fig. 68). As soon as the microelectrode pierces the membrane covering the cell, the oscilloscope beam is deflected down from its original position and established at a new level. This indicates the presence of a potential difference between the outer and inner surfaces of the cell membrane.

The origin of the resting potential is most fully explained by the so-called membrane-ion theory. According to this theory, all cells are covered with a membrane that is unequally permeable to different ions. In this regard, inside the cell in the cytoplasm there are 30-50 times more potassium ions, 8-10 times less sodium ions and 50 times less chlorine ions than on the surface. At rest, the cell membrane is more permeable to potassium ions than to sodium ions. The diffusion of positively charged potassium ions from the cytoplasm to the cell surface gives the outer surface of the membrane a positive charge.

Thus, the surface of the cell at rest carries a positive charge, while the inner side of the membrane turns out to be negatively charged due to chlorine ions, amino acids and other large organic anions that practically do not penetrate the membrane (Fig. 70).

Action potential

If the area of ​​the nerve or muscle fiber expose enough strong irritant, then excitation occurs in this area, manifested in a rapid oscillation of the membrane potential and called action potential.

The action potential can be recorded either using electrodes applied to outer surface fiber (extracellular lead), or a microelectrode inserted into the cytoplasm (intracellular lead).

With extracellular abduction, one can find that the surface of the excited area for a very short period, measured in thousandths of a second, becomes charged electronegatively with respect to the resting area.

The reason for the occurrence of an action potential is a change in the ionic permeability of the membrane. When irritated, the permeability of the cell membrane to sodium ions increases. Sodium ions tend to enter the cell because, firstly, they are positively charged and are drawn inward by electrostatic forces, and secondly, their concentration inside the cell is low. At rest, the cell membrane was poorly permeable to sodium ions. Irritation changed the permeability of the membrane, and the flow of positively charged sodium ions from external environment cells into the cytoplasm significantly exceeds the flow of potassium ions from the cell to the outside. As a result inner surface The membrane becomes positively charged, and the outer membrane becomes negatively charged due to the loss of positively charged sodium ions. At this moment the peak of the action potential is recorded.

The increase in membrane permeability for sodium ions continues very a short time. Following this, the cell appears recovery processes, leading to the fact that the permeability of the membrane for sodium ions again decreases, and for potassium ions increases. Since potassium ions are also positively charged, when they leave the cell, they restore the original relationship between the outside and inside the cell.

Accumulation of sodium ions inside the cell during repeated excitation does not occur because sodium ions are constantly evacuated from it due to the action of a special biochemical mechanism called the “sodium pump”. There is also evidence of active transport of potassium ions using the “sodium-potassium pump”.

Thus, according to the membrane-ion theory, the selective permeability of the cell membrane is of decisive importance in the origin of bioelectric phenomena, which determines the different ionic composition on the surface and inside the cell, and, consequently, the different charge of these surfaces. It should be noted that many provisions of the membrane-ion theory are still debatable and require further development.

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 sharp increase membrane permeability for 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, thanks 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, and 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. Nerve fiber conducts nerve impulses in two directions - centripetal and centripetal.

14 Synapses 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.