The performance of its main functions by a neuron - the generation, conduction and transmission of a nerve impulse - becomes possible primarily because the concentration of a number of ions inside and outside the cell differs significantly. The most important here are the ions K +, Na +, Ca2 +, Cl-. Potassium in the cell is 30-40 times more than outside, and sodium is about 10 times less. In addition, the cell contains much less chlorine and free calcium ions than the extracellular medium.

The difference in the concentration of sodium and potassium is created by a special biochemical mechanism called sodium potassium pump... It is a protein molecule built into the membrane of a neuron (Fig. 6) and carrying out active transport of ions. Using the energy of ATP (adenosine triphosphoric acid), such a pump exchanges sodium for potassium in a 3: 2 ratio. To transfer three sodium ions from the cell to the environment and two potassium ions in the opposite direction (i.e. against the concentration gradient), the energy of one molecule is required ATP.

When neurons mature, sodium-potassium pumps are incorporated into their membrane (up to 200 such molecules can be located per 1 μm2), after which potassium ions are pumped into the nerve cell and sodium ions are removed from it. As a result, the concentration of potassium ions in the cell increases, and sodium decreases. The speed of this process can be very high: up to 600 Na + ions per second. In real neurons, it is determined, first of all, by the availability of intracellular Na + and sharply increases with its penetration from the outside. In the absence of any of the two types of ions, the work of the pump stops, since it can only proceed as a process of exchange of intracellular Na + for extracellular K +.

Similar transport systems exist for Cl- and Ca2 + ions. In this case, chlorine ions are removed from the cytoplasm into the intercellular environment, and calcium ions are usually transported inside cellular organelles - mitochondria and channels of the endoplasmic reticulum.

To understand the processes occurring in a neuron, it is necessary to know that there are ion channels in the cell membrane, the number of which is given genetically. Ion channel Is a hole in a special protein molecule built into the membrane. A protein can change its conformation (spatial configuration), as a result of which the channel is in an open or closed state. There are three main types of such channels:

- constantly open;

- voltage-dependent (voltage-dependent, electrosensitive) - the channel opens and closes depending on the transmembrane potential difference, i.e. the potential difference between the outer and inner surfaces of the cytoplasmic membrane;

- chemically dependent (ligand-dependent, chemosensitive) - the channel opens depending on the effect on it of a substance specific to each channel.

Microelectrode technology is used to study electrical processes in a nerve cell. Microelectrodes allow recording electrical processes in one single neuron or nerve fiber. These are usually glass capillaries with a very thin tip, less than 1 μm in diameter, filled with an electrically conductive solution (for example, potassium chloride).

If two electrodes are installed on the cell surface, then no potential difference is recorded between them. But if one of the electrodes pierces the cytoplasmic membrane of a neuron (ie, the tip of the electrode is in the internal environment), the voltmeter will register a potential jump up to about -70 mV (Fig. 7). This potential was called membrane potential. It can be registered not only in neurons, but also in a less pronounced form in other cells of the body. But only in nerve, muscle and glandular cells the membrane potential can change in response to the stimulus. In this case, the membrane potential of the cell, which is not affected by any stimulus, is called resting potential(PP). In different nerve cells, the value of PP is different. It ranges from -50 to -100 mV. How does this PP arise?

The initial (before the development of PP) state of the neuron can be characterized as devoid of internal charge, i.e. the number of cations and anions in the cytoplasm of the cell is equal due to the presence of large organic anions, for which the neuron membrane is impenetrable. In reality, such a picture is observed in the early stages of embryonic development of nervous tissue. Then, as it matures, genes are turned on that trigger the synthesis constantly open K + -channels... After their incorporation into the membrane, K + ions are able, due to diffusion, to freely leave the cell (where there are many of them) into the intercellular environment (where there are much less of them).

But this does not lead to a balance of potassium concentrations inside and outside the cell, because the release of cations leads to the fact that more and more uncompensated negative charges remain in the cell. This causes the formation of an electric potential, which prevents the release of new positively charged ions. As a result, the release of potassium continues until the force of the concentration pressure of potassium, due to which it leaves the cell, and the action of the electric field, which prevents this, are balanced. As a result, a potential difference arises between the external and internal environment of the cell, or the equilibrium potassium potential, which is described the Nernst equation:

EK = (RT / F) (ln [K +] o / [K +] i),

where R is the gas constant, T is the absolute temperature, F is the Faraday number, [K +] o is the concentration of potassium ions in the external solution, [K +] i is the concentration of potassium ions in the cell.

The equation confirms the dependence, which can be derived even by logical reasoning - the greater the difference in the concentrations of potassium ions in the external and internal environment, the greater (in absolute value) PP.

Classic studies of PP were performed on giant squid axons. Their diameter is about 0.5 mm, so the entire contents of the axon (axoplasm) can be removed without any problems and the axon can be filled with a potassium solution, the concentration of which corresponds to its intracellular concentration. The axon itself was placed in a potassium solution with a concentration corresponding to the intercellular environment. After that, the PP was recorded, which turned out to be equal to -75 mV. The equilibrium potassium potential calculated by the Nernst equation for this case turned out to be very close to that obtained in the experiment.

But the PP in a squid axon filled with real axoplasm is approximately -60 mV . Where does the 15 mV difference come from? It turned out that not only potassium ions but also sodium ions participate in the creation of PP. The fact is that, in addition to potassium channels, and constantly open sodium channels... There are much fewer of them than potassium, but the membrane still allows a small amount of Na + ions into the cell, and therefore, in most neurons, the PP is –60– (–65) mV. The sodium current is also proportional to the difference in its concentrations inside and outside the cell - therefore, the smaller this difference, the higher the absolute value of the PP. The sodium current also depends on the PP itself. In addition, very few Cl- ions diffuse across the membrane. Therefore, when calculating the real PP, the Nernst equation is supplemented with data on the concentrations of sodium and chlorine ions inside and outside the cell. In this case, the calculated parameters turn out to be very close to the experimental ones, which confirms the correctness of the explanation of the origin of PP by the diffusion of ions through the membrane of the neuron.

Thus, the final level of the resting potential is determined by the interaction of a large number of factors, the main of which are the currents K +, Na + and the activity of the sodium-potassium pump. The final PP value is the result of the dynamic equilibrium of these processes. By acting on any of them, you can shift the level of PP and, accordingly, the level of excitability of the nerve cell.

As a result of the events described above, the membrane is constantly in a state of polarization - its inner side is charged negatively with respect to the outer one. The process of decreasing the potential difference (i.e., decreasing the PP in absolute value) is called depolarization, and increasing it (increasing the PP in absolute value) is called hyperpolarization.

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2-1. Resting membrane potential is:

1) the potential difference between the outer and inner surfaces of the cell membrane in a state of functional rest *

2) a characteristic feature of only excitable tissue cells

3) fast oscillation of the cell membrane charge with an amplitude of 90-120 mV

4) the potential difference between the excited and unexcited sections of the membrane

5) the potential difference between the damaged and undamaged sections of the membrane

2-2. In a state of physiological rest, the inner surface of the membrane of the excitable cell in relation to the outer surface is charged:

1) positive

2) as well as the outer surface of the membrane

3) negative *

4) has no charge

5) there is no right answer

2-3. A shift in the positive direction (decrease) of the resting membrane potential under the action of an irritant is called:

1) hyperpolarization

2) repolarization

3) exaltation

4) depolarization *

5) static polarization

2-4. A negative shift (increase) in the resting membrane potential is called:

1) depolarization

2) repolarization

3) hyperpolarization *

4) exaltation

5) reversion

2-5. The descending phase of the action potential (repolarization) is associated with an increase in membrane permeability for ions:

2) calcium

2-6. The concentration of ions inside the cell is higher than in the intercellular fluid:

3) calcium

2-7. An increase in potassium current during the development of an action potential causes:

1) rapid membrane repolarization *

2) membrane depolarization

3) reversal of membrane potential

4) trace depolarization

5) local depolarization

2-8. With complete blockade of fast sodium channels of the cell membrane, the following is observed:

1) reduced excitability

2) decrease in the amplitude of the action potential

3) absolute refractoriness *

4) exaltation

5) trace depolarization

2-9. A negative charge on the inner side of the cell membrane is formed as a result of diffusion:

1) K + from the cell and the electrogenic function of the K-Na-pump *

2) Na + per cage

3) C1 - from the cage

4) Ca2 + into the cell

5) there is no right answer

2-10. The value of the rest potential is close to the value of the equilibrium potential for an ion:

3) calcium

2-11. The ascending phase of the action potential is associated with an increase in ion permeability:

2) there is no right answer

3) sodium *

2-12. Indicate the functional role of the resting membrane potential:

1) its electric field affects the state of protein channels and membrane enzymes *

2) characterizes an increase in cell excitability

3) is the basic unit of information coding in the nervous system

4) ensures the operation of diaphragm pumps

5) characterizes a decrease in cell excitability

2-13. The ability of cells to respond to stimuli with a specific reaction characterized by rapid, reversible membrane depolarization and metabolic changes is called:

1) irritability

2) excitability *

3) lability

4) conductivity

5) automation

2-14. Biological membranes, participating in changes in the intracellular content and intracellular reactions due to the reception of extracellular biologically active substances, performs the function of:

1) barrier

2) receptor-regulatory *

3) transport

4) cell differentiation

2-15. The minimum strength of the stimulus, necessary and sufficient for the occurrence of a response, is called:

1) threshold *

2) overthreshold

3) submaximal

4) subthreshold

5) maximum

2-16. With an increase in the threshold of irritation, the excitability of the cell:

1) increased

2) decreased *

3) has not changed

4) everything is correct

5) there is no right answer

2-17. Biological membranes, participating in the transformation of external stimuli of a non-electrical and electrical nature into bioelectric signals, perform mainly the function:

1) barrier

2) regulatory

3) cell differentiation

4) transport

5) generating action potential *

2-18. Action potential is:

1) a stable potential that is established on the membrane when two forces are in balance: diffusion and electrostatic

2) the potential between the outer and inner surfaces of the cell in a state of functional rest

3) fast, actively propagating, phase oscillation of the membrane potential, accompanied, as a rule, by recharging of the membrane *

4) a slight change in membrane potential under the action of a subthreshold stimulus

5) long-term, stagnant membrane depolarization

2-19. Membrane permeability for Na + in the phase of action potential depolarization:

1) sharply increases and a powerful sodium current entering the cell appears *

2) sharply decreases and a powerful sodium current emerging from the cell appears

3) does not change significantly

4) everything is correct

5) there is no right answer

2–20. Biological membranes, participating in the release of neurotransmitters in synaptic endings, perform mainly the function:

1) barrier

2) regulatory

3) intercellular interaction *

4) receptor

5) generating action potential

2-21. The molecular mechanism that ensures the removal of sodium ions from the cytoplasm and the introduction of potassium ions into the cytoplasm is called:

1) voltage-gated sodium channel

2) nonspecific sodium-potassium channel

3) chemically dependent sodium channel

4) sodium-potassium pump *

5) leakage channel

2-22. The system of movement of ions through the membrane along the concentration gradient, not requiring direct energy consumption is called:

1) pinocytosis

2) passive transport *

3) active transport

4) persorption

5) exocytosis

2-23. The membrane potential level at which an action potential arises is called:

1) membrane potential at rest

2) a critical level of depolarization *

3) trace hyperpolarization

4) zero level

5) trace depolarization

2-24. With an increase in the concentration of K + in the extracellular environment with a resting membrane potential in an excitable cell, the following will occur:

1) depolarization *

2) hyperpolarization

3) the transmembrane potential difference will not change

4) stabilization of the transmembrane potential difference

5) there is no right answer

2-25. The most significant change when exposed to a fast sodium channel blocker will be:

1) depolarization (decrease in resting potential)

2) hyperpolarization (increased resting potential)

3) a decrease in the steepness of the depolarization phase of the action potential *

4) slowing down the phase of repolarization of the action potential

5) there is no right answer

3. BASIC REGULATIONS OF IRRITATION

EXCITABLE TISSUE

3-1. The law, according to which, with an increase in the strength of the stimulus, the response gradually increases until the maximum is reached, is called:

1) "all or nothing"

2) strength-duration

3) accommodation

4) strength (power relations) *

5) polar

3-2. The law according to which an excitable structure responds to threshold and suprathreshold stimuli with the maximum possible response is called:

2) "all or nothing" *

3) strength-duration

4) accommodation

5) polar

3–3. The minimum time during which a current equal to twice the rheobase (twice the threshold force) causes excitation is called:

1) good time

2) accommodation

3) adaptation

4) chronaxia *

5) lability

3-4. The structure obeys the law of force:

1) heart muscle

2) a single nerve fiber

3) single muscle fiber

4) whole skeletal muscle *

5) single nerve cell

The structure is subject to the “All or Nothing” law:

1) whole skeletal muscle

2) nerve trunk

3) heart muscle *

4) smooth muscle

5) nerve center

3-6. The adaptation of tissue to a stimulus that slowly grows in strength is called:

1) lability

2) functional mobility

3) hyperpolarization

4) accommodation *

5) braking

3-7. The paradoxical phase of parabiosis is characterized by:

1) a decrease in the response with an increase in the strength of the stimulus *

2) a decrease in the response with a decrease in the strength of the stimulus

3) an increase in response with an increase in the strength of the stimulus

4) the same response with an increase in the strength of the stimulus

5) lack of reaction to stimuli of any strength

3-8. The irritation threshold is an indicator of:

1) excitability *

2) contractility

3) lability

4) conductivity

5) automation

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ROLE OF ACTIVE ION TRANSPORT IN THE FORMATION OF MEMBRANE POTENTIAL

One of the advantages of an “ideal” membrane that allows one ion to pass through is to maintain the membrane potential for an arbitrarily long time without spending energy, provided that the penetrating ion is initially distributed unevenly on both sides of the membrane. At the same time, the membrane of living cells is permeable to one degree or another for all inorganic ions in the solution surrounding the cell. Therefore, the cells must

we somehow maintain the intracellular concentration of ions at a certain level. Sodium ions are quite indicative in this respect, by the example of the permeability of which in the previous section the deviation of the membrane potential of the muscle from the equilibrium potassium potential was analyzed. According to the measured concentrations of sodium ions outside and inside the muscle cell, the equilibrium potential calculated by the Nernst equation for these ions will be about 60 mV, with a plus sign inside the cell. The membrane potential, calculated by the Goldman equation and measured with micro-electrodes, is 90 mV with a minus sign inside the cell. Thus, its deviation from the equilibrium potential for sodium ions will be 150 mV. Under the influence of such a high potential, even at low permeability, sodium ions will enter through the membrane and accumulate inside the cell, which, accordingly, will be accompanied by the release of potassium ions from it. As a result of this process, the intra- and extracellular concentrations of ions will equalize after a while.

In fact, this does not happen in a living cell, since sodium ions are constantly removed from the cell using the so-called ion pump. The assumption of the existence of an ion pump was put forward by R. Dean in the 40s of the XX century. and was an extremely important addition to the membrane theory of the formation of resting potential in living cells. It has been shown experimentally that the active “pumping out” of Na + from the cell is accompanied by the obligatory “pumping” of potassium ions into the cell (Fig. 2.8). Since the permeability of the membrane for sodium ions is small, their entry from the external environment into the cell will be slow, therefore

Low K + concentration High Na ++ concentration

the pump will effectively maintain a low sodium ion concentration in the cell. The permeability of the membrane for potassium ions at rest is quite high, and they easily diffuse through the membrane.

There is no need to spend energy to maintain a high concentration of potassium ions, it is preserved due to the emerging transmembrane potential difference, the mechanisms of the occurrence of which are described in detail in the previous sections. The transfer of ions by a pump requires the expenditure of metabolic energy of the cell. The source of energy for this process is the energy stored in the high-energy bonds of ATP molecules. Energy is released through the hydrolysis of ATP by the enzyme adenosine triphosphatase. It is believed that the same enzyme directly carries out the transfer of ions. In accordance with the structure of the cell membrane, ATPase is one of the integral proteins embedded in the lipid bilayer. A feature of the carrier enzyme is its high affinity on the outer surface for potassium ions, and on the inner surface for sodium ions. The action of inhibitors of oxidative processes (cyanides or azides) on the cell, cell cooling, blocks the hydrolysis of ATP, as well as the active transfer of sodium and potassium ions. Sodium ions gradually enter the cell, and potassium ions leave it, and as the [K +] o / [K +] ratio decreases, the resting potential will slowly decrease to zero. We discussed the situation when an ion pump removes one positively charged sodium ion from the intracellular environment and, accordingly, transfers one positively charged potassium ion from the extracellular space (1: 1 ratio). In this case, the ion pump is said to be electro-neutral.

At the same time, it was experimentally found that in some nerve cells the ion pump removes more sodium ions for the same period of time than pumps in potassium ions (the ratio can be 3: 2). In such cases, the ion pump is electrogenic, T.

Fiziologia_Otvety

That is, he himself creates a small but constant total current of positive charges from the cell and additionally contributes to the creation of a negative potential inside it. Note that the additional potential created with the help of an electrogenic pump in a resting cell does not exceed several millivolts.

Let us summarize the information about the mechanisms of formation of the membrane potential - the resting potential in the cell. The main process, due to which most of the potential with a negative sign on the inner surface of the cell membrane is created, is the emergence of an electric potential that delays the passive exit of potassium ions from the cell along its concentration gradient through potassium channels -

tegral proteins. Other ions (for example, sodium ions) participate in the creation of potential only to a small extent, since the membrane permeability for them is much lower than for potassium ions, i.e., the number of open channels for these ions at rest is small ... An extremely important condition for maintaining the resting potential is the presence in the cell (in the cell membrane) of an ion pump (integral protein), which ensures the concentration of sodium ions inside the cell at a low level and thereby creates the prerequisites for the main potential-forming intracellular ions became potassium ions. A small contribution to the resting potential can be made directly by the ion pump itself, but provided that its work in the cell is electrogenic.

Concentration of ions 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 much higher than in the extracellular environment. 2 ... The membrane at rest is selectively permeable for K +, and for Na +, the membrane permeability at rest is insignificant. If the potassium permeability is taken to be 1, then the sodium permeability at rest is only 0.04. Hence, there is a constant flux of K + ions from the cytoplasm along the concentration gradient... Potassium current from the cytoplasm creates a relative deficit of positive charges on the inner surface, the cell membrane is impermeable for anions, as a result of which the cytoplasm of the cell turns out to be negatively charged with respect 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 current 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 depends on the charge of the membrane. The intracellular negative charge, which is created due to the current 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 RT / nF * ln /, (n is the valence 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, just like 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 membrane resting potential is extremely important, because it is it that determines the cell's ability to excite - a specific response to a stimulus.

Excitation of the cell

V agitation cells (transition from dormancy 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 can be a change in the membrane potential - electrically excitable channels are activated, and the interaction of membrane receptors with a biologically 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 an irritant. 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 ionic current arises and the membrane potential decreases - depolarization membranes.

Table 4

Change in membrane potential upon excitation of a cell.

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 one is negative. Potassium channels are activated at the same time, but sodium (fast) channels are activated and inactivated within 1 - 1.5 milliseconds, and potassium channels longer.

It is customary to depict changes in membrane potential graphically. The upper figure shows the initial depolarization of the membrane - a change in potential in response to a stimulus. For each excitable cell, there is a special level of membrane potential, upon reaching which the properties of sodium channels change dramatically. This potential is named critical level of depolarization (KUD). When the membrane potential changes to KUD, fast, potential-dependent sodium channels open, the flow of sodium ions rushes into the cell. When positively charged ions pass into the cell, in the cytoplasm, the positive charge increases. As a result, the transmembrane potential difference decreases, the MF value decreases to 0, and then, as sodium further enters the cell, the membrane is recharged and the charge reverses (overshoot) - now the surface becomes electronegative with respect to the cytoplasm - the membrane is DEPOLARIZED completely - the middle pattern. 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 is so strong that it depolarizes the membrane to KUD, this stimulus is called a threshold stimulus, it causes excitation of the cell. The reversal point of the potential 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) - a rapid change in the membrane potential in response to the action of the threshold strength stimulus. 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 active transport process 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 pass potassium ions until an 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 - a short-term increase in MF after its recovery, which is due to an increase in the membrane permeability for potassium and chlorine ions. Hyperpolarization occurs only after PD and is not typical for all cells. Let us try again to represent graphically the phases of the action potential and ionic processes underlying the changes in the membrane potential (Fig.

Resting potential of a neuron

nine). On the abscissa we plot the values ​​of the membrane potential in millivolts, on the ordinate - time in milliseconds.

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

2. Rapid entry of sodium into the cell - fast, voltage-dependent sodium channels open, and depolarization reaches the reversal point of the potential - 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 passes from the cell to the extracellular environment - repolarization, restoration of the MPP begins

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

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

Figure 9 Phases of action potential

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

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

2. KUD - the critical level of depolarization (or the threshold of generation of the membrane action potential) - this is the value of the membrane potential, upon reaching which they open fast, potential-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 KUD, the less excitable such a cell is.

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

Under the action of an irritant subthreshold strength incomplete depolarization occurs - LOCAL RESPONSE (LO).

Incomplete, or partial, depolarization is a change in the membrane charge that does not reach the critical level of depolarization (CCD).

Figure 10. Change in membrane potential in response to the action of a stimulus of subthreshold force - local response

The local response has basically the same mechanism as PD, its ascending phase is determined by the input of sodium ions, and the descending phase is determined by the output of potassium ions.

However, the LO amplitude is proportional to the strength of subthreshold stimulation, and not standard, as in AP.

Table 5

It is easy to see that there are conditions in cells under which a potential difference should arise between the cell and the intercellular environment:

1) cell membranes are well permeable to cations (primarily potassium), while the membrane permeability to anions is much less;

2) the concentrations of most substances in cells and in the extracellular fluid are very different (compare with what was said on p.

). Therefore, a double electrical layer will appear on the cell membranes ("minus" on the inner side of the membrane, "plus" on the outside), and a constant potential difference should exist on the membrane, which is called the resting potential. The membrane is said to be polarized at rest.

For the first time the hypothesis of a similar nature of PP cells and diffusion potential was expressed by Nernst in 1896.

Knowledge base

student of the Military Medical Academy Yu.V. Chagovets. Now this point of view has been confirmed by numerous experimental data. True, there are some discrepancies between the measured PP values ​​and those calculated by formula (1), but they are explained by two obvious reasons. First, there is not one cation in the cells, but many (K, Na, Ca, Mg, etc.). This can be taken into account by replacing the Nernst formula (1) with a more complex formula, worn out by Goldman:

Where pK is the membrane permeability for potassium, pNa is the same for sodium, pCl is the same for chlorine; [K +] e - concentration of potassium ions outside the cell, [K +] i - the same inside the cell (similar for sodium and chlorine); ellipses denote the corresponding terms for other ions. Chlorine ions (and other anions) go in the opposite direction to potassium and sodium ions, so the "e" and "i" signs for them are set in reverse order.

The calculation using the Goldman formula gives a much better agreement with the experiment, but some discrepancies still remain. This is due to the fact that when deriving formula (2), the work of active transport was not considered. Taking into account the latter makes it possible to achieve almost complete agreement with experience.

19. Sodium and potassium channels in the membrane and their role in bioelectrogenesis. Gate mechanism. Features of voltage-gated channels. The mechanism of the action potential emergence. The state of the channels and the nature of ion fluxes in different phases of AP. The role of active transport in bioelectrogenesis. Critical membrane potential. The all-or-nothing law for excitable membranes. Refractoriness.

It turned out that the selective filter has a "rigid" structure, that is, it does not change its lumen under different conditions. Channel transitions from open to closed state and back are associated with the operation of a non-selective filter, a gate mechanism. Gate processes occurring in one or another part of the ion channel, which is called a gate, are understood as any changes in the conformation of protein molecules that form the channel, as a result of which its pair can open or close. Therefore, it is customary to call a gate the functional groups of protein molecules that provide gate processes. It is important that the gate is set in motion by physiological stimuli, that is, those that are present in natural conditions. Among physiological stimuli, shifts in membrane potential play a special role.

There are channels that are controlled by the potential difference on the membrane, being open at some values ​​of the membrane potential and closed at others. Such channels are called voltage-gated. It is with them that the generation of AP is associated. Due to their special importance, all ion channels of biomembranes are subdivided into 2 types: voltage-dependent and voltage-independent. The natural stimuli that control the movement of the gate in the channels of the second type are not shifts of the membrane potential, but other factors. For example, in chemosensitive channels, chemicals play the role of a controlling stimulus.

An essential component of a voltage-gated ion channel is a voltage sensor. This is the name of a group of protein molecules capable of responding to changes in the electric field. So far there is no specific information about what they are and how they are located, but it is clear that an electric field can interact in a physical environment only with charges (either free or bound). It was assumed that Ca2 + (free charges) serves as a voltage sensor, since changes in its content in the intercellular fluid lead to the same consequences as shifts in the membrane potential. For example, a tenfold decrease in the concentration of calcium ions in the interstitium is equivalent to depolarization of the plasma membrane by about 15 mV. However, later it turned out that Ca2 + is necessary for the voltage sensor to work, but it is not itself. AP is generated even when the concentration of free calcium in the intercellular medium falls below 10 ~ 8 mol. In addition, the content of Ca2 + in the cytoplasm generally has little effect on the ionic conductivity of the plasmolemma. Obviously, the voltage sensor is bound charges - groups of protein molecules with a large dipole moment. They are immersed in a lipid bilayer, which is characterized by a rather low viscosity (30 - 100 cP) and a low dielectric constant. This conclusion was reached by studying the kinetic characteristics of the motion of the stress sensor upon shifts of the membrane potential. This movement represents a typical displacement current.

The modern functional model of the sodium voltage-gated channel provides for the existence of two types of gates in it, operating in antiphase. They differ in inertial properties. More mobile (light) are called m-gates, more inertial (heavy) - h - gates. At rest, the h-gate is open, m - the gate is closed, the movement of Na + along the channel is impossible. When the plasmolemma is depolarized, the gates of both types begin to move, but due to the unequal inertia, the m-gates have time

open before the h-gate closes. At this moment, the sodium channel is open and Na + rushes through it into the cell. The delay in the movement of the h-gate relative to the m-gate corresponds to the duration of the AP depolarization phase. When the h-gate closes, the flow of Na + through the membrane will stop and repolarization will begin. Then h - and m - gates return to their initial state. Voltage-gated sodium channels are activated (turned on) during rapid (abrupt) depolarization of the plasma membrane. ,

PD is created due to faster diffusion of sodium ions through the plasma membrane in comparison with anions that form salts with it in the intercellular medium. Consequently, depolarization is associated with the entry of sodium cations into the cytoplasm. With the development of PD, sodium does not accumulate in the cell. When excited, sodium flows in and out are observed. The appearance of PD is not caused by a violation of ionic concentrations in the cytoplasm, but by a drop in the electrical resistance of the plasma membrane due to an increase in its permeability to sodium.

As already mentioned, under the action of the threshold and suprathreshold stimuli, the excitable membrane generates AP. This process is characterized by law "all or nothing. He is the antithesis of gradualism. The meaning of the law is that the parameters of AP do not depend on the intensity of the stimulus. As soon as the CMF is reached, changes in the potential difference across the excitable membrane are determined only by the properties of its voltage-dependent ion channels, which provide the incoming current. Among them, an external stimulus opens only the most sensitive. Others open at the expense of the previous ones, already regardless of the stimulus. It is said that the process of involving new potential-dependent ion channels in the transmembrane transfer of ions is spanty. Therefore the amplitude. The duration and steepness of the leading and trailing fronts of AP depends only on ionic gradients on the cell membrane and the kinetic characteristics of its channels. The “all or nothing” law is a characteristic property of single cells and fibers with an excitable membrane. It is not characteristic of most multicellular formations. The exception is structures organized by the syncytium type.

Date of publication: 2015-01-25; Read: 421 | Page copyright infringement

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• managed. By the control mechanism: electro-, chemo- and mechanically controlled;
• uncontrollable. They do not have a gate mechanism and are always open, ions go constantly, but slowly.

Resting potential Is the difference in electrical potentials between the external and internal environment of the cell.

Resting potential formation mechanism. The immediate cause of the resting potential is the unequal concentration of anions and cations inside and outside the cell. First, this arrangement of ions is based on the difference in permeability. Secondly, much more potassium ions leave the cell than sodium.

Action potential- this is the excitation of the cell, a rapid fluctuation of the membrane potential due to the diffusion of ions into and out of the cell.

When the stimulus acts on the cells of the excitable tissue, at first, sodium channels are very quickly activated and inactivated, then, with some delay, potassium channels are activated and inactivated.

As a consequence, ions rapidly diffuse into or out of the cell according to an electrochemical gradient. This is excitement. According to the change in the magnitude and sign of the cell charge, three phases are distinguished:

• 1st phase - depolarization. Reducing the cell charge to zero. Sodium moves to the cell according to the concentration and electrical gradient. Condition of movement: the gate of the sodium channel is open;
• 2nd phase - inversion. Reversal of charge sign. Inversion involves two parts: upward and downward.

Ascending part. Sodium continues to move into the cell according to the concentration gradient, but contrary to the electrical gradient (it interferes).

Descending part. Potassium begins to leave the cell according to the concentration and electrical gradient. The gates of the potassium channel are open;

• 3rd phase - repolarization. Potassium continues to leave the cell according to the concentration, but in spite of the electrical gradient.

Criteria for excitability

With the development of the action potential, a change in the excitability of the tissue occurs. This change occurs in phases. The state of the initial membrane polarization characteristically reflects the resting membrane potential, which corresponds to the initial state of excitability and, consequently, the initial state of the excitable cell. This is a normal level of excitability. The pre-soldering period is the period of the very beginning of the action potential. The excitability of the tissue is slightly increased. This phase of excitability is primary exaltation (primary supernormal excitability). During the development of the prejunction, the membrane potential approaches the critical level of depolarization, and to reach this level, the strength of the stimulus may be less than the threshold.

During the period of development of the spike (peak potential), an avalanche-like flow of sodium ions into the cell occurs, as a result of which the membrane recharges, and it loses its ability to respond with excitation to stimuli of suprathreshold force. This phase of excitability is called absolute refractoriness, i.e. absolute non-excitability, which lasts until the end of the membrane recharge. The absolute refractoriness of the membrane occurs due to the fact that sodium channels are completely opened and then inactivated.

After the end of the recharge phase, its excitability is gradually restored to its original level - this is the phase of relative refractoriness, i.e. relative non-excitability. It continues until the membrane charge is restored to a value corresponding to the critical level of depolarization. Since during this period the membrane potential of rest has not yet been restored, the excitability of the tissue is reduced, and new excitation can arise only under the action of a suprathreshold stimulus. A decrease in excitability in the phase of relative refractoriness is associated with partial inactivation of sodium channels and activation of potassium channels.

The next period corresponds to an increased level of excitability: the phase of secondary exaltation or secondary supernormal excitability. Since the membrane potential in this phase is closer to the critical level of depolarization, compared to the resting state of the initial polarization, the stimulation threshold is lowered, i.e. the excitability of the cell is increased. In this phase, new excitement can arise under the action of stimuli of the subthreshold force. Sodium channels in this phase are not completely inactivated. The membrane potential increases - a state of membrane hyperpolarization arises. Moving away from the critical level of depolarization, the threshold of stimulation rises slightly, and new excitation can arise only under the action of stimuli of a suprathreshold magnitude.

The Mechanism of the Occurrence of the Resting Membrane Potential

Each cell at rest is characterized by the presence of a transmembrane potential difference (resting potential). Typically, the difference in charge between the inner and outer surfaces of membranes is from -80 to -100 mV and can be measured using the outer and intracellular microelectrodes (Fig. 1).

The potential difference between the outer and inner sides of the cell membrane in its resting state is called membrane potential (resting potential).

The creation of resting potential is provided by two main processes - the uneven distribution of inorganic ions between the intra- and extracellular spaces and the unequal permeability of the cell membrane for them. Analysis of the chemical composition of the extra- and intracellular fluid indicates an extremely uneven distribution of ions (Table 1).

At rest, inside the cell there are many anions of organic acids and K + ions, the concentration of which is 30 times higher than outside; Na + ions, on the contrary, are 10 times more outside the cell than inside; CI- is also larger on the outside.

At rest, the membrane of nerve cells is most permeable for K +, less for CI- and very little permeable for Na + / The permeability of the nerve fiber membrane for Na + B at rest is 100 times less than for K +. For many anions of organic acids, the membrane at rest is completely impermeable.

Rice. 1. Measurement of the resting potential of muscle fiber (A) using an intracellular microelectrode: M - microelectrode; And - an indifferent electrode. The beam on the oscilloscope screen (B) shows that before the membrane was pierced by the microelectrode, the potential difference between M and I was zero. At the moment of puncture (shown by an arrow), a potential difference was detected, indicating that the inner side of the membrane is charged negatively with respect to its outer surface (according to B.I.Khodorov)

Table. Intra- and extracellular concentrations of muscle cell ions in a warm-blooded animal, mmol / l (according to J. Dudel)

Due to the concentration gradient, K + comes out to the outer surface of the cell, carrying out its positive charge. High molecular weight anions cannot follow K + because of their impermeability to the membrane. The Na + ion also cannot replace the left potassium ions, because the membrane permeability for it is much lower. СI- along the concentration gradient can mix only inside the cell, thereby increasing the negative charge of the inner surface of the membrane. Due to this movement of ions, polarization of the membrane occurs when its outer surface is charged positively, and its inner surface is negatively charged.

The electric field that is created on the membrane actively interferes with the distribution of ions between the inner and outer contents of the cell. As the positive charge on the outer surface of the cell increases, the K + ion, as a positively charged one, becomes more and more difficult to move from the inside to the outside. It moves uphill, as it were. The greater the value of the positive charge on the outer surface, the smaller the amount of K + ions can go to the cell surface. At a certain value of the potential on the membrane, the number of K + ions crossing the membrane in either direction turns out to be equal, i.e. the potassium concentration gradient is balanced by the potential on the membrane. The potential at which the diffusion flux of ions becomes equal to the flux of like ions going in the opposite direction is called the equilibrium potential for a given ion. For K + ions, the equilibrium potential is -90 mV. In myelinated nerve fibers, the value of the equilibrium potential for CI- ions is close to the value of the resting membrane potential (-70 mV). Therefore, in spite of the fact that the concentration of СI- ions outside the fiber is higher than inside it, their one-way current is not observed in accordance with the concentration gradient. In this case, the concentration difference is balanced by the potential present on the membrane.

The Na + ion along the concentration gradient would have to enter the cell (its equilibrium potential is +60 mV), and the presence of a negative charge inside the cell should not impede this flow. In this case, the incoming Na + would neutralize the negative charges inside the cell. However, this does not actually happen, since the membrane at rest is poorly permeable to Na +.

The most important mechanism that maintains a low intracellular concentration of Na + ions and a high concentration of K + ions is the sodium-potassium pump (active transport). It is known that there is a system of carriers in the cell membrane, each of which binds to the stirrup by the Na + ions inside the cell and removes them outside. From the outside, the carrier binds to two K + ions outside the cell, which are carried into the cytoplasm. The power supply for the operation of the carrier systems is provided by ATP. The operation of the pump on such a system leads to the following results:

• a high concentration of K + ions is maintained inside the cell, which ensures the constancy of the resting potential. Due to the fact that during one cycle of ion exchange, one more positive ion is removed from the cell than is introduced, active transport plays a role in creating resting potential. In this case, they speak of an electrogenic pump, since it itself creates a small but constant current of positive charges from the cell, and therefore makes a direct contribution to the formation of a negative potential inside it. However, the contribution of the electrogenic pump to the total value of the resting potential is usually small and amounts to several millivolts;
• maintains a low concentration of Na + ions inside the cell, which, on the one hand, ensures the operation of the mechanism for generating the action potential, on the other hand, ensures the maintenance of normal osmolarity and cell volume;
• maintaining a stable concentration gradient of Na +, the sodium-potassium pump promotes the conjugated K +, Na + transport of amino acids and sugars across the cell membrane.

Thus, the emergence of a transmembrane potential difference (resting potential) is due to the high conductivity of the cell membrane at rest for K +, CI- ions, ionic asymmetry of the concentrations of K + ions and CI- ions, the work of active transport systems (Na + / K + -ATPase), which create and maintain ionic asymmetry.

Action potential of nerve fiber, nerve impulse

Action potential - this is a short-term fluctuation in the potential difference of the membrane of an excitable cell, accompanied by a change in its charge sign.

Action potential is the main specific sign of arousal. Its registration indicates that the cell or its structures responded to the stimulation. However, as already noted, PD in some cells can occur spontaneously (spontaneously). Such cells are found in the pacemakers of the heart, the walls of blood vessels, and the nervous system. PD is used as a carrier of information, transmitting it in the form of electrical signals (electrical signaling) along afferent and efferent nerve fibers, the conducting system of the heart, as well as to initiate contraction of muscle cells.

Let us consider the causes and mechanism of AP generation in afferent nerve fibers that form primary sensory receptors. The immediate cause of the onset (generation) of AP in them is the receptor potential.

If we measure the potential difference on the membrane of the Ranvier interception closest to the nerve ending, then in the intervals between the impacts on the capsule of the Pacini corpuscle it remains unchanged (70 mV), and during the impact it depolarizes almost simultaneously with the depolarization of the receptor membrane of the nerve ending.

With an increase in the force of pressure on the Pacini body, causing an increase in the receptor potential up to 10 mV, in the nearest interception of Ranvier, a rapid oscillation of the membrane potential is usually recorded, accompanied by a recharge of the membrane - the action potential (AP), or a nerve impulse (Fig. 2). If the force of pressure on the body increases even more, the amplitude of the receptor potential increases and a number of action potentials with a certain frequency are generated in the nerve ending.

Rice. 2. Schematic representation of the mechanism of transformation of the receptor potential into an action potential (nerve impulse) and propagation of the impulse along the nerve fiber

The essence of the AP generation mechanism is that the receptor potential causes the appearance of local circular currents between the depolarized receptor membrane of the unmyelinated part of the nerve ending and the membrane of the first interception of Ranvier. These currents, which are carried by the ions Na +, K +, CI- and other mineral ions, "flow" not only along, but also across the membrane of the nerve fiber in the area of ​​interception of Ranvier. In the membrane of Ranvier's interceptions, in contrast to the receptor membrane of the nerve ending itself, there is a high density of ionic voltage-dependent sodium and potassium channels.

When the depolarization value of about 10 mV reaches the Ranvier interception membrane on the membrane, fast voltage-dependent sodium channels are opened and through them the flow of Na + ions rushes into the axoplasm along the electrochemical gradient. It causes rapid depolarization and recharge of the Ranvier interception membrane. However, simultaneously with the opening of fast voltage-gated sodium channels, slow voltage-gated potassium channels open in the Ranvier interception membrane and K + ions begin to leave the axoilasm. Thus, the Na + ions entering the axoplasm at a high rate quickly depolarize and recharge the membrane for a short time (0.3-0.5 ms), while the outgoing K + ions restore the initial distribution of charges on the membrane (repolarize the membrane). As a result, during mechanical action on the Pacini body with a force equal to or exceeding the threshold, a short-term fluctuation of potential is observed on the membrane of the nearest interception of Ranvier in the form of rapid depolarization and repolarization of the membrane, i.e. PD (nerve impulse) is generated.

Since the immediate cause of AP generation is the receptor potential, in this case it is also called the generator potential. The number of nerve impulses of the same amplitude and duration generated per unit time is proportional to the amplitude of the receptor potential, and, consequently, to the force of pressure on the receptor. The process of converting information about the strength of the impact, embedded in the amplitude of the receptor potential, into the number of discrete nerve impulses is called discrete coding of information.

The ionic mechanisms and the temporal dynamics of the processes of AP generation have been studied in more detail under experimental conditions when the nerve fiber is artificially exposed to electric currents of various strengths and durations.

The nature of the action potential of the nerve fiber (nerve impulse)

The membrane of the nerve fiber at the point of localization of the irritating electrode responds to the effect of a very weak current that has not yet reached the threshold value. This answer is called local, and the fluctuation of the potential difference across the membrane is called local potential.

A local response on the membrane of an excitable cell can precede the emergence of an action potential or arise as an independent process. It is a short-term fluctuation (depolarization and repolarization) of the resting potential, which is not accompanied by membrane recharge. Depolarization of the membrane during the development of the local potential is due to the advanced entry into the axoplasm of Na + ions, and repolarization is due to the delayed exit from the axoplasm of K + ions.

If you act on the membrane with an electric current of increasing force, then at this value, called the threshold, the depolarization of the membrane can reach a critical level - E k, at which fast voltage-dependent sodium channels open. As a result, through them there is an avalanche-like increase in the flow of Na + ions into the cell. The evoked process of depolarization acquires a self-accelerating character, and the local potential develops into an action potential.

It has already been mentioned that a characteristic feature of PD is a short-term inversion (change) of the sign of the charge on the membrane. Outside, it for a short time (0.3-2 ms) becomes negatively charged, and inside - positively. The magnitude of the inversion can be up to 30 mV, and the magnitude of the entire action potential - 60-130 mV (Fig. 3).

Table. Comparative characteristics of local potential and action potential

The action potential, depending on the nature of the change in charges on the inner surface of the membrane, is divided into phases of depolarization, repolarization and hyperpolarization of the membrane. Depolarization the entire ascending part of the AP is called, on which the sections corresponding to the local potential (from the level E 0 before E to), rapid depolarization (from the level E to to the level of 0 mV), inversions the sign of the charge (from 0 mV to the peak value or the beginning of repolarization). Repolarization is called the descending part of the AP, which reflects the process of restoration of the initial membrane polarization. At first, repolarization is carried out quickly, but approaching the level E 0, the speed can slow down and this section is called trace negativity(or trace negative potential). In some cells, following repolarization, hyperpolarization develops (an increase in membrane polarization). They call her trace positive potential.

The initial high-amplitude fast-flowing part of the PD is also called peak, or spike. It includes phases of depolarization and rapid repolarization.

In the mechanism of PD development, the most important role belongs to voltage-dependent ion channels and a non-simultaneous increase in the permeability of the cell membrane for Na + and K + ions. So, when an electric current acts on a cell, it causes membrane depolarization and when the membrane charge decreases to a critical level (E to), voltage-dependent sodium channels open. As already mentioned, these channels are formed by protein molecules built into the membrane, inside which there are a pore and two gate mechanisms. One of the gate mechanisms - the activation one, provides (with the participation of segment 4) the opening (activation) of the channel during membrane depolarization, and the second (with the participation of the intracellular loop between the 3rd and 4th domains) - its inactivation, which develops during membrane recharging (Fig. 4). Since both of these mechanisms rapidly change the position of the channel gates, voltage-gated sodium channels are fast ion channels. This circumstance is of decisive importance for the generation of AP in excitable tissues and for its conduction through the membranes of nerve and muscle fibers.

Rice. 3. Action potential, its phases and ionic currents (a, o). Description in text

Rice. 4. Position of the gate and the state of activity of voltage-gated sodium and potassium channels at different levels of membrane polarization

In order for the voltage-gated sodium channel to pass Na + ions into the cell, it is only necessary to open the activation gates, since the inactivation gates are open under resting conditions. This happens when membrane depolarization reaches the level E to(Fig. 3, 4).

The opening of the activation gates of sodium channels leads to an avalanche-like entry of sodium into the cell, driven by the action of the forces of its electrochemical gradient. Since Na + ions carry a positive charge, they neutralize the excess of negative charges on the inner surface of the membrane, reduce the potential difference across the membrane and depolarize it. Soon, Na + ions impart an excess of positive charges to the inner surface of the membrane, which is accompanied by an inversion (change) of the charge sign from negative to positive.

However, sodium channels remain open only for about 0.5 ms, and after this period of time from the moment of the beginning

PD closes the inactivation gate, sodium channels become inactivated and impermeable to Na + ions, the entry of which into the cell is sharply limited.

From the moment of membrane depolarization to the level E to activation of potassium channels and opening of their gates for K + ions are also observed. K + ions under the action of the forces of the concentration gradient leave the cell, carrying out positive charges from it. However, the gate mechanism of potassium channels is slowly functioning and the rate of release of positive charges with K + ions from the cell to the outside is delayed in relation to the entrance of Na + ions. The flow of K + ions, removing the excess of positive charges from the cell, causes the restoration of the initial distribution of charges on the membrane or its repolarization, and a negative charge is restored on the inner side after a moment from the moment of recharge.

The appearance of AP on excitable membranes and the subsequent restoration of the initial resting potential on the membrane are possible because the dynamics of the entry into and exit from the cell of positive charges of Na + and K + ions are different. The entry of the Na + ion is ahead of the exit of the K + ion in time. If these processes were in equilibrium, then the potential difference across the membrane would not change. The development of the ability to excite and generate AP by excitable muscle and nerve cells was due to the formation in their membrane of two types of different-speed ion channels - fast sodium and slow potassium.

The generation of a single AP requires the entry of a relatively small number of Na + ions into the cell, which does not disturb its distribution outside and inside the cell. When a large number of APs are generated, the distribution of ions on both sides of the cell membrane could be disturbed. However, under normal conditions this is prevented by the operation of the Na +, K + -pump.

Under natural conditions, in CNS neurons, the action potential primarily arises in the area of ​​the axonal knoll, in afferent neurons - in the Ranvier interception of the nerve ending closest to the sensory receptor, i.e. in those areas of the membrane where there are fast selective voltage-gated sodium channels and slow potassium channels. In other types of cells (for example, pacemaker, smooth myocytes), not only sodium and potassium, but also calcium channels play a role in the development of AP.

The mechanisms of perception and conversion of signals into AP in the secondary sensory sensory receptors differ from the mechanisms analyzed for the primary sensory receptors. In these receptors, the perception of signals is carried out by specialized neurosensory (photoreceptor, olfactory) or sensorepithelial (taste, auditory, vestibular) cells. Each of these sensitive cells has its own, special mechanism for perceiving signals. However, in all cells, the energy of the perceived signal (stimulus) is converted into fluctuations in the potential difference of the plasma membrane, i.e. into receptor potential.

Thus, the key moment in the mechanisms of transformation of perceived signals by sensory cells into receptor potential is the change in the permeability of ion channels in response to exposure. The opening of Na +, Ca 2+, K + -ion channels during signal perception and transformation is achieved in these cells with the participation of G-proteins, second intracellular messengers, binding to ligands, and phosphorylation of ion channels. As a rule, the receptor potential arising in sensory cells causes the release of a neurotransmitter from them into the synaptic cleft, which ensures the transmission of a signal to the postsynaptic membrane of the afferent nerve ending and the generation of a nerve impulse on its membrane. These processes are detailed in the chapter on sensory systems.

The action potential can be characterized by the amplitude and duration, which for the same nerve fiber remain the same when AP propagates along the fiber. Therefore, the action potential is called discrete potential.

There is a definite connection between the nature of the effect on sensory receptors and the number of APs arising in the afferent nerve fiber in response to the effect. It consists in the fact that for large but strength or duration of exposure in the nerve fiber, a greater number of nerve impulses are formed, i.e. with an increase in the impact, impulses of a higher frequency will be sent to the nervous system from the receptor. The processes of converting information about the nature of the impact into the frequency and other parameters of nerve impulses transmitted to the central nervous system are called discrete coding of information.

To conduct a signal from a previous cell to the next, the neuron generates electrical signals within itself. Your eye movements while reading this paragraph, the feeling of a soft chair under your booty, the perception of music from headphones and much more are based on the fact that hundreds of billions of electrical signals pass through you. Such a signal can originate in the spinal cord and travel along a long axon to the tip of the toe. Or it can cover a negligible distance in the depths of the brain, confining itself to the limits of an interneuron with short processes. Any neuron that receives a signal sends it through its body and outgrowths, and this signal is electrical in nature.

Back in 1859, scientists were able to measure the speed at which these electrical signals are transmitted. It turned out that the electricity transmitted by a living axon is fundamentally different from the electric current in metals. Through a metal wire, an electrical signal is transmitted at a speed close to the speed of light (300,000 kilometers per second), because there are many free electrons in the metal. However, despite this speed, the signal is noticeably weakened, overcoming long distances. If signals were transmitted along axons in the same way that they are transmitted in metals, then the nerve impulse coming from the nerve endings in the skin of your big toe would completely decay without reaching your brain - the electrical resistance of organic matter is too high, and the signal is too weak ...

Studies have shown that electricity travels much slower along axons than wires, and that this transmission is based on a previously unknown mechanism that causes the signal to travel at a speed of about 30 meters per second. Electrical signals traveling along nerves, unlike signals traveling through wires, do not weaken as they move. The reason for this is that the nerve endings do not pass the signal through themselves passively, simply allowing the charged particles in them to transmit it to each other. At each point they are an active emitter of this signal, relaying it, and a detailed description of this mechanism will require a separate chapter. Thus, by sacrificing the high speed of nerve impulses, due to the active signal transmission, the neuron receives a guarantee that the signal that has arisen in the big toe will reach the spinal cord without weakening at all.

To observe the passage of an electrical excitation wave, or action potential (action potential [‘ækʃən pə’tenʃəl]), in a living cell, a simple device is sufficient: one end of a thin metal wire is placed on the outer surface of the axon of the sensory neuron of the skin, and the other is brought to a recorder, which draws a line upward when the signal is amplified, and downward when the signal is weakened. Each contact with the skin triggers one or more action potentials. At each potential, the recorder draws a narrow, long peak.

The action potential of a sensory neuron lasts only about 0.001 seconds and includes two phases: a rapid rise, reaching a peak, and then an almost equally rapid decline in excitation, leading to the initial position. And here the recorder reports an unexpected fact: all action potentials arising in one and the same nerve cell are approximately the same. This can be seen in the picture on the left: all the peaks drawn by the recorder have approximately the same shape and amplitude, no matter how hard or how long the touch on the skin that caused them was. A slight stroke or a tangible pinch will be transmitted by action potentials of the same magnitude. The action potential is a constant signal that obeys the principle of "all or nothing": after the stimulus exceeds a certain threshold value, approximately the same signal always appears, no more and no less than usual. And if the stimulus is less than the threshold value, then the signal will not be transmitted at all: for example, you can touch the skin so easily with the tip of the pen that this touch will not be felt.

The all-or-nothing principle in the emergence of an action potential raises new questions. How does the sensory neuron report the strength of the stimulus - strong or weak pressure, bright or dim light? How does he report the duration of the stimulus? Finally, how do neurons distinguish one type of sensory information from another - for example, how do they distinguish touch from pain, light, smell, or sound? And how do they distinguish sensory information for perception from motor information for action?

Evolution has solved the question of how to communicate the strength of a stimulus using the same type of signals of the same magnitude: this strength is determined frequency(frequency [‘friːkwənsɪ]) with which action potentials are emitted. A weak stimulus, such as a light touch on the arm, emits only two to three action potentials per second, while strong pressure, like pinching or hitting the elbow, can cause a burst of hundreds of action potentials per second. In this case, the duration of sensation is determined by the duration of the emergence of action potentials.

Do neurons use different electrical codes to tell the brain that they carry information about different stimuli, such as pain, light, or sound? It turned out that no! It is surprising, but there is very little difference between the action potentials generated by neurons from different sensory systems (for example, visual or tactile)! Thus, the character and nature of sensation does not depend on differences in action potentials (which opens up a rather exciting perspective for thinking about the "matrix" from the film of the same name). A neuron that transmits auditory information is designed in exactly the same way as a neuron from the visual nerve circuit, and they conduct the same action potentials in the same way. Without knowing which nerve circuit a particular neuron belongs to, it is impossible to determine what information it carries only by analyzing its functioning.

The nature of the transmitted information depends primarily on the type of excited nerve fibers and the specific brain systems with which these fibers are connected. Feelings of each type are transmitted along their own pathways, and the type of information transmitted by a neuron depends precisely on the path that this neuron is part of. In any sensory pathway, information travels from the first sensory neuron (a receptor that responds to an external stimulus, such as touch, smell, or light) to specialized neurons in the spinal cord or brain. Thus, visual information differs from auditory information only in that it is transmitted along other pathways starting in the retina and ending in the part of the brain that is responsible for visual perception.

The signals sent from the motor neurons in the brain to the muscles are also almost identical to those transmitted by sensory neurons from the skin to the brain. They obey the same principle "all or nothing", they also transmit the intensity of the signal using the frequency of action potentials, and also the result of the signal depends only on which nerve circuit this neuron is included in. Thus, a quick succession of action potentials, following a certain conductive path, causes precisely the movement of your fingers, and not, say, the perception of colored lights, only because this path is associated with the muscles of the hands, and not with the retina of the eyes.

The universality of action potentials is not limited to the similarity of their manifestation in different neurons located within the same organism. They are so similar in different animals that even an experienced researcher is not able to accurately distinguish the recording of the action potential of the nerve fiber of a whale, mouse, monkey, or its scientific adviser. Nevertheless, the action potentials in different cells are not identical: there is still a slight difference in their amplitude and duration, and the statement “all action potentials are the same” is just as imprecise as “all bougainvilleas are the same”.

So, each neuron transmits a signal through its body and processes in the same way. All the variety of information we receive from sensory neurons, all the movements that our body can perform are the result of the transmission of a single type of signal inside neurons. There remains a "trifle": to understand what kind of signal it is and how it is transmitted.

We habitually separate everything that we consider living nature, including ourselves, from “inanimate” things, including metals and the electric current transmitted through them. It is all the more surprising to realize that metals are not only present in our bodies - they are necessary, without them the body cannot exist. Electric current is not a one-time phenomenon, but continuously arising in hundreds of billions of neurons, which have penetrated our entire body with their processes. Right now, you can sense all sorts of signs of his presence: the fact that you are aware of this text is the result of countless transmissions of electric current. The feeling of hunger and pleasure from the smell of cooking food, the very perception of this smell, the touch of the wind blowing through the window to your skin ... The list is endless. And the desire to understand how all this happens also consists of electrical impulses arising in neurons.

Since the purpose of this chapter is to communicate only the most general information about the passage of a nerve impulse, here it is necessary to consider the environment in which it arises, those conditions in the cell that make it possible for its occurrence and transmission. Therefore, it is worth starting by studying the bridgehead on which events will develop, namely from the neuron in resting state (dormant state ['dɔːmənt steɪt]).

Back in the middle of the last century, scientists found a way to determine in which part of the neuron there is an electric charge. To do this, use voltmeter (voltmeter ['vəultˌmiːtə]) (device for measuring electric field voltage) with two electrodes. One electrode is placed inside the neuron, placing it close to the cell membrane, and the second electrode is located in the environment surrounding the neuron, on the other side of the same membrane. The voltmeter shows that on different sides of the cell membrane there are electric charges, negative inside the cell and positive outside. The existence of such opposite-polarity electric charges on both sides of the membrane creates an electric field, an important characteristic of which is potential... Potential, in simple terms, is the ability to do work, such as the work of dragging a charged particle from place to place. The more negative charges have accumulated on one side, and the more positive ones are on the other side of the membrane, the stronger the electric field they create, and the more force they are able to drag charged particles back and forth. The difference between external and internal electric charges is called membrane potential (membrane potential [‘membreɪn pə’tenʃəl]) rest. For a neuron, it is approximately 70 mV (millivolts), that is, 70 thousandths of a volt, or seven hundredths of a volt. For comparison, the potential difference in an AA battery is 1.5 volts - 20 times more. That is, the resting membrane potential of a neuron is only 20 times weaker than between the terminals of an AA battery - quite large, it turns out. The electrical potential exists only on the membrane, and in its other parts the neuron is electrically neutral.

More precisely, the resting membrane potential of a neuron is -70 mV (minus seventy millivolts). The minus sign only means that the negative charge is inside the cell, and not outside, and thus the generated electric field is able to drag positively charged ions through the membrane into the cell.

Actors in the creation of the resting membrane potential:

1 ... V cell membrane a neuron, there are channels through which ions carrying an electric charge can travel through it. At the same time, the membrane is not just a passive "partition" between the inner environment of the neuron and the intercellular fluid surrounding it: special proteins embedded in the membrane flesh open and close these channels, and thus the membrane controls the passage of ions - atoms with an electric charge. By accumulating negatively charged ions inside the cell, the neuron increases the number of negative charges inside, thereby leading to an increase in positive charges outside, and thus the electrical potential is increased. Since a proton has a positive charge, and an electron is negative, then with an excess of protons, a positively charged ion is obtained, and with an excess of electrons, a negatively charged one. If you would like more information about atoms and ions, you can return to. It is important to understand that the membrane potential exists precisely at the border of the cell membrane, and fluids in general inside and outside the neuron remain electrically neutral. Ions, for which the membrane is permeable, remain close to it, since positive and negative charges are mutually attracted to each other. As a result, a layer of positive ions "sitting" on it is formed outside the membrane, and negative ions inside. Thus, the membrane plays the role of an electrical capacitance separating charges, inside which there is an electric field. The membrane is therefore a natural condenser.

2 . negatively charged proteins located inside the neuron near the inner surface of the membrane. The charge of proteins always remains the same and is only a part of the total charge of the inner surface of the membrane. Unlike ions, proteins cannot leave the cell and enter it - they are too large for that. The total charge changes depending on the number of positively charged ions near the membrane, the concentration of which can change due to their transition from the cell to the outside, and from the outside to the inside.

3 ... positively charged potassium ions (K +) can freely move between the internal and external environment when the neuron is at rest. They move through constantly open flow potassium channels (flow potassium passage), through which only K + ions can pass, and nothing else. Flow channels are called channels that do not have gates, which means they are open in any state of the neuron. There are much more potassium ions inside the cell than outside. This is due to the constant operation of the sodium-potassium pump (it will be discussed below), therefore, in the state of rest of the neuron, the K + ions begin to move into the external environment, since the concentration of the same substance tends to equalize in the general system. If we pour some substance into a pool with water in one corner, then its concentration in this corner will be very high, and in other parts of the pool - zero or very small. However, after some time we will find that the concentration of this substance has leveled off throughout the basin due to the Brownian motion. In this case, they speak of the "partial pressure" of a particular substance, be it a liquid or a gas. If alcohol is poured into one corner of the pool, there will be a large difference in alcohol concentration between that corner and the rest of the pool. There will be a partial pressure of alcohol molecules, and they will gradually be distributed evenly over the basin so that the partial pressure will disappear, since the concentration of alcohol molecules will equalize everywhere. Thus, K + ions carry away the positive charge from the neuron, leaving outside due to the partial pressure, which is stronger than the attractive force of negatively charged proteins, if the difference in the concentration of ions inside and outside the cell is large enough. Since negatively charged proteins remain inside, a negative charge is thus formed on the inner side of the membrane. For a clear understanding of the work of cellular mechanisms, it is important to remember that despite the constant leakage of potassium ions from the cell, there are always more of them inside the neuron than outside.

4 ... positively charged sodium ions (Na +) are located on the outside of the membrane and create a positive charge there. During the resting phase of the neuron, the sodium channels of the cell closed, and Na + cannot pass inside, and their concentration outside increases due to the work of the sodium-potassium pump, which removes them from the neuron.

5 ... the role of negatively charged chlorine ions (Cl -) and positively charged calcium ions (Ca 2+) to create a membrane potential is small, so their behavior will remain behind the scenes.

Resting membrane potential formation takes place in two stages:

Stage I... a small (-10 mV) potential difference is created using sodium potassium pump.

Unlike other channels of the membrane, the sodium-potassium channel is able to pass both sodium and potassium ions through itself. Moreover, Na + can pass through it only from the cell to the outside, and K + from the outside to the inside. One cycle of operation of this channel includes 4 steps:

1 ... The "gate" of the sodium-potassium channel is open only from the inner side of the membrane, and 3 Na + enter there

2 ... the presence of Na + inside the channel affects it so that it can partially destroy one molecule ATF(ATP) ( adenosine triphosphate), (adenosine triphosphate [ə’dɛnəsiːn trai’fɔsfeɪt]) which is the "accumulator" of the cell, storing energy and giving it away when necessary. With such a partial destruction, which consists in the elimination of one phosphate group PO 4 3− from the end of the molecule, energy is released, which is exactly spent on the transfer of Na + to the outer space.

3 ... when the channel opens so that Na + comes out, it remains open, and two K + ions enter it - they are attracted by negative charges of proteins from the inside. The fact that only two potassium ions are placed in the channel containing three sodium ions is quite logical: the potassium atom has a larger diameter.

4 ... the presence of potassium ions now, in turn, affects the channel so that the external "gates" are closed, and the internal ones are opened, and K + enters the internal environment of the neuron.

This is how the sodium-potassium pump works, "exchanging" three sodium ions for two potassium ions. Since the electric charge of Na + and K + is the same, it turns out that three positive charges are removed from the cell, and only two get inside. Due to this, the internal positive charge of the cell membrane decreases, and the external one increases. In addition, a difference is created in the concentration of Na + and K + on different sides of the membrane:

=) there are many sodium ions outside the cell, and few inside. At the same time, sodium channels are closed, and Na + cannot get back into the cell, and it does not go far from the membrane, since it is attracted by the negative charge existing on the inner side of the membrane.

=) there are many potassium ions inside the cell, but there are few of them outside, and this leads to the outflow of K + from the cell through the potassium channels that are open during the resting phase of the neuron.

Stage II the formation of the resting membrane potential is just based on this outflow of potassium ions from the neuron. The figure on the left shows the ionic composition of the membrane at the beginning of the second stage of the formation of the resting potential: a lot of K + and negatively charged proteins (designated A 4-) inside, and Na + stuck to the membrane outside. Moving to the external environment, potassium ions carry away their positive charges from the cell, while the total charge of the inner membrane decreases. Just like the positive sodium ions, the potassium ions flowed out of the cell remain outside the membrane, attracted by the internal negative charge, and the external positive charge of the membrane is the sum of the charges Na + and K +. Despite the leakage through the flow channels, there are always more potassium ions inside the cell than outside.

The question arises: why do not potassium ions continue to flow out until the moment when their number inside the cell and outside it becomes the same, that is, until the partial pressure created by these ions disappears? The reason for this is that when the K + leaves the cell, the positive charge increases on the outside, and an excess of negative charge forms on the inside. This reduces the desire of potassium ions to leave the cell, because the external positive charge repels them, and the internal negative one attracts them. Therefore, after some time, K + stops flowing out despite the fact that in the external environment their concentration is lower than in the internal one: the effect of charges on different sides of the membrane exceeds the force of partial pressure, that is, it exceeds the tendency of K + to be distributed evenly in the liquid inside and outside. neuron. At the moment of reaching this equilibrium, the membrane potential of the neuron stops at about -70 mV.

As soon as the neuron reaches the resting membrane potential, it is ready for the emergence and conduct of the action potential, which will be discussed in the next cytological chapter.

Thus, to summarize: the uneven distribution of potassium and sodium ions on both sides of the membrane is caused by the action of two competing forces: a) the force of electrical attraction and repulsion, and b) the force of partial pressure arising from a difference in concentration. The work of these two rival forces takes place in the conditions of the existence of differently arranged sodium, potassium and sodium-potassium channels, which act as regulators of the action of these forces. The potassium channel is a flow channel, that is, it is always open at rest of the neuron, so that the K + ions can easily walk back and forth under the influence of the forces of electrical repulsion / attraction and under the influence of forces caused by partial pressure, that is, the difference in the concentration of these ions. The sodium channel is always closed at rest of the neuron, so that Na + ions cannot pass through them. And finally, the sodium-potassium channel, designed in such a way that it works as a pump, which drives three sodium ions outward with each cycle, and drives two potassium ions inward.

All this construction ensures the emergence of the resting membrane potential of the neuron: i.e. a state in which two things are achieved:

a) there is a negative charge inside and a positive charge outside.

b) there are many K + ions inside, stuck to the negatively charged parts of the proteins, and thus a potassium partial pressure arises - the tendency of potassium ions to come out to equalize the concentration.

c) there are many Na + ions outside, partly forming pairs with Cl - ions. And thus, sodium partial pressure arises - the desire of sodium ions to enter the cell to equalize the concentration.

As a result of the operation of the potassium-sodium pump, we obtain three forces existing on the membrane: the strength of the electric field and the strength of two partial pressures. These forces begin to work when the neuron leaves the resting state.

Why do we need to know what the potential for rest is?

What is "animal electricity"? Where do "biocurrents" come from in the body? How can a living cell in an aquatic environment turn into an "electric battery"?

We can answer these questions if we learn how a cell, due to redistributionelectric charges creates itself electrical potential on the membrane.

How does the nervous system work? How does it all begin in her? Where does the electricity for nerve impulses come from?

We can also answer these questions if we learn how a nerve cell creates an electrical potential for itself on a membrane.

So, understanding how the nervous system works begins with understanding how a single nerve cell, a neuron, works.

And at the heart of the work of a neuron with nerve impulses lies redistributionelectric charges on its membrane and a change in the magnitude of electrical potentials. But in order to change the potential, you must first have it. Therefore, we can say that a neuron, preparing for its nervous work, creates an electric potential as an opportunity for such a job.

Thus, our very first step towards studying the work of the nervous system is to understand how electrical charges move on nerve cells and how, due to this, an electrical potential appears on the membrane. This is what we will do, and we will call this process of the appearance of electrical potential in neurons - building resting potential.

Definition

Normally, when a cell is ready for work, it already has an electrical charge on the membrane surface. It is called resting membrane potential .

Resting potential is the difference in electrical potential between the inner and outer sides of the membrane when the cell is in a state of physiological rest. Its average value is -70 mV (millivolt).

"Potential" is an opportunity, it is akin to the concept of "potency". The electric potential of a membrane is its ability to move electric charges, positive or negative. Charged chemical particles - sodium and potassium ions, as well as calcium and chlorine ions - act as charges. Of these, only chlorine ions are negatively charged (-), and the rest are positively (+).

Thus, having an electric potential, the membrane can move the above charged ions into or out of the cell.

It is important to understand that in the nervous system, electric charges are created not by electrons, as in metal wires, but by ions - chemical particles that have an electric charge. The electric current in the body and its cells is a flow of ions, not electrons, as in wires. Note also that the membrane charge is measured from within cells, not outside.

To put it quite primitively simply, it turns out that the outside around the cell will be dominated by "plus signs", ie. positively charged ions, and inside - "minus", ie. negatively charged ions. We can say that inside the cage electronegative ... And now we just need to explain how it happened. Although, of course, it is unpleasant to realize that all our cells are negative "characters". ((

The essence

The essence of the resting potential is the predominance of negative electric charges in the form of anions on the inner side of the membrane and the lack of positive electric charges in the form of cations, which are concentrated on its outer side, and not on the inner side.

Inside the cell is "negativity", and outside - "positivity".

This state of affairs is achieved through three phenomena: (1) the behavior of the membrane, (2) the behavior of positive ions of potassium and sodium, and (3) the ratio of chemical and electrical force.

1. Behavior of the membrane

Three processes are important in the behavior of the membrane for the resting potential:

1) Exchange internal sodium ions to external potassium ions. The exchange is carried out by special transport structures of the membrane: ion exchanger pumps. In this way, the membrane supersaturates the cell with potassium, but depletes it in sodium.

2) Open potassium ion channels. Through them, potassium can both enter the cell and leave it. It comes out mostly.

3) Closed sodium ion channels. Because of this, sodium removed from the cell by pump-exchangers cannot return back to it. Sodium channels open only under special conditions - and then the resting potential is violated and shifts towards zero (this is called depolarization membranes, i.e. decrease in polarity).

2. Behavior of potassium and sodium ions

Potassium and sodium ions move differently across the membrane:

1) Through ion exchanger pumps, sodium is forcibly removed from the cell, and potassium is dragged into the cell.

2) Through the constantly open potassium channels, potassium leaves the cell, but it can also return to it back through them.

3) Sodium "wants" to enter the cell, but "cannot", because channels are closed for him.

3. The ratio of chemical and electrical force

In relation to potassium ions, an equilibrium is established between the chemical and electrical forces at a level of -70 mV.

1) Chemical force pushes potassium out of the cell, but tends to draw sodium into it.

2) Electric the force tends to draw positively charged ions (both sodium and potassium) into the cell.

Resting potential formation

I will try to tell you briefly where the resting membrane potential in nerve cells - neurons comes from. After all, as everyone now knows, our cells are only positive on the outside, but inside they are very negative, and there is an excess of negative particles - anions and a lack of positive particles - cations.

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

And therefore, the essence of our story will not be that we explain where the negative particles in the cell come from, but that we explain how the deficiency of positively charged ions - cations - is obtained in neurons.

Where do the positively charged particles go from the cell? Let me remind you that these are sodium ions - Na + and potassium - K +.

Sodium-potassium pump

And the whole point is that the membrane of the nerve cell is constantly working exchanger pumps formed by special proteins embedded in the membrane. What are they doing? They change the cell's "own" sodium for external "foreign" potassium. Because of this, in the end, there is a lack of sodium in the cell, which was spent on metabolism. And at the same time, the cell is overflowing with potassium ions, which were dragged into it by these molecular pumps.

To make it easier to remember, figuratively you can say this: " The cell loves potassium!"(Although there can be no talk of true love here!) Therefore, she drags potassium into herself, despite the fact that it is already full. Therefore, it is unprofitable to exchange it for sodium, giving 3 sodium ions for 2 potassium ions. Therefore she spends ATP energy on this exchange. And how she spends! Up to 70% of all energy consumption of a neuron can go to the work of sodium-potassium pumps. This is what love does, even if not real!

By the way, it is interesting that a cell is not born ready-made with resting potential. For example, during differentiation and fusion of myoblasts, the potential of their membrane changes from -10 to -70 mV, i.e. their membrane becomes more electronegative and polarizes during differentiation. And in experiments on multipotent mesenchymal stromal cells (MMSC) of human bone marrow artificial depolarization inhibited differentiation cells (Fischer-Lougheed J., Liu JH, Espinos E. et al. Human myoblast fusion requires expression of functional inward rectifier Kir2.1 channels. Journal of Cell Biology 2001; 153: 677-85; Liu JH, Bijlenga P., Fischer-Lougheed J. et al. Role of an inward rectifier K + current and of hyperpolarization in human myoblast fusion. Journal of Physiology 1998; 510: 467-76; Sundelacruz S., Levin M., Kaplan DL Membrane potential controls adipogenic and osteogenic differentiation of mesenchymal stem cells. Plos One 2008; 3).

Figuratively speaking, you can put it like this:

By creating the potential for rest, the cell is "charged with love."

It is love for two things:

1) the cell's love for potassium,

2) the love of potassium for freedom.

Oddly enough, but the result of these two types of love is emptiness!

It is she, emptiness, that creates a negative electric charge in the cell - the rest potential. More precisely, negative potential is createdempty spaces left over from potassium escaped from the cell.

So, the result of the operation of membrane ion exchanger pumps is as follows:

The sodium-potassium ion exchanger pump creates three potentials (possibilities):

1. Electric potential - the ability to draw positively charged particles (ions) into the cell.

2. Ionic sodium potential - the ability to draw sodium ions into the cell (and specifically sodium, and not any others).

3. Ionic potassium potential - it is possible to push out potassium ions (and precisely potassium, and not any others) from the cell.

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

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

We can put it this way: membrane ion pumps create concentration difference ions, or gradient (drop) concentration, between the intracellular and extracellular environment.

It is because of the resulting sodium deficiency that this sodium will now "climb" into the cell from the outside. This is how substances always behave: they strive to equalize their concentration in the entire volume of the solution.

And at the same time, an excess of potassium ions appeared in the cell in comparison with the external environment. Because the membrane pumps pumped it into the cell. And he seeks to equalize his concentration inside and outside, and therefore seeks to get out of the cell.

It is also important to understand that sodium and potassium ions do not seem to "notice" each other, they only react "to themselves." Those. sodium reacts to the concentration of sodium the same, but "does not pay attention" to how much potassium is around. Conversely, potassium reacts only to the concentration of potassium and does not "notice" sodium. It turns out that in order to understand the behavior of ions in a cell, it is necessary to separately compare 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 often done in textbooks.

According to the law of equalization of concentrations, which operates in solutions, sodium "wants" to enter the cell from the outside. But it cannot, since the membrane in its normal state does not pass it well. It comes in a little and the cell again immediately exchanges it for external potassium. Therefore, sodium in neurons is always in short supply.

But potassium just can easily leave the cell outside! The cage is full of him, and she cannot keep him. So it comes out through special protein holes in the membrane (ion channels).

Analysis

From chemical to electrical

And now - the most important thing, follow this thought! We must move from the movement of chemical particles to the movement of electric charges.

Potassium is charged with a positive charge, and therefore, when it leaves the cell, it takes out from it not only itself, but also "plus signs" (positive charges). In their place, "minuses" (negative charges) remain in the cell. This is the resting membrane potential!

Resting membrane potential is a deficiency of positive charges inside the cell, formed due to the leakage of positive potassium ions from the cell.

Conclusion

Rice. Resting potential (RP) formation scheme. The author thanks Ekaterina Yurievna Popova for her help in creating the drawing.

The constituent parts of the resting potential

The resting potential is negative from the side of the cell and consists, as it were, of two parts.

1. The first part is about -10 millivolts, which are obtained from the uneven operation of the membrane pump-exchanger (after all, it pumps out more "plus signs" with sodium than it pumps back with potassium).

2. The second part is potassium leaking out of the cell all the time, dragging away positive charges from the cell. It gives most of the membrane potential, bringing it down to -70 millivolts.

Potassium will stop leaving the cell (more precisely, its input and output will be equal) only at a cell electronegativity level of -90 millivolts. But this is hindered by sodium constantly leaking into the cell, which drags its positive charges with it. And in the cell the equilibrium state is maintained at the level of -70 millivolts.

Note that it takes energy to build up the potential for rest. These costs are generated by ion pumps, which exchange "their" internal sodium (Na + ions) for "foreign" external potassium (K +). Recall that ion pumps are enzymes of ATPases and break down ATP, receiving energy from it for the indicated exchange of different types of ions for each other. It is very important to understand that 2 potentials "work" with the membrane at once: chemical (concentration gradient of ions) and electrical ( the difference in electrical potentials on different sides of the membrane). Ions move in one direction or another under the influence of both of these forces, on which energy is spent. In this case, one of the two potentials (chemical or electrical) decreases, while the other increases. Of course, if we consider the electric potential (potential difference) separately, then the "chemical" forces that move the ions will not be taken into account. And then the wrong impression may be formed that the energy for the movement of the ion is taken from nowhere. But this is not the case. Both forces must be considered: chemical and electrical. In this case, large molecules with negative charges inside the cell play the role of "extras", because neither chemical nor electrical forces move them across the membrane. Therefore, these negative particles are usually not considered, although they exist and it is they that provide the negative side of the potential difference between the inner and outer sides of the membrane. But the nimble potassium ions are just capable of moving, and it is their leakage from the cell under the influence of chemical forces that creates the lion's share of the electrical potential (potential difference). After all, it is the potassium ions that move positive electrical charges to the outer side of the membrane, being positively charged particles.

So it's all about the sodium-potassium membrane pump-exchanger and the subsequent leakage of "excess" potassium from the cell. Due to the loss of positive charges during this outflow, electronegativity increases inside the cell. This is the "resting membrane potential". It is measured inside the cell and is usually -70 mV.

conclusions

Figuratively speaking, "the membrane turns the cell into an" electric battery "by controlling ionic flows."

The resting membrane potential is formed by two processes:

1. Operation of the potassium-sodium membrane pump.

The operation of a potassium-sodium pump, in turn, has 2 consequences:

1.1. Direct electrogenic (generating electrical phenomena) action of the ion exchanger pump. This is the creation of a small electronegativity inside the cell (-10 mV).

The unequal exchange of sodium for potassium is to blame for this. More sodium is thrown out of the cell than is exchanged for potassium. And together with sodium, more "plus signs" (positive charges) are removed than are returned together with potassium. There is a slight deficit of positive charges. The membrane is charged negatively from the inside (approximately -10 mV).

1.2. Creation of prerequisites for the emergence of a large electronegativity.

These prerequisites are the unequal concentration of potassium ions inside and outside the cell. Excess potassium is ready to leave the cell and take out positive charges from it. We will talk about this below.

2. Leakage of potassium ions from the cell.

From the zone of increased concentration inside the cell, potassium ions go out into the zone of reduced concentration, carrying out at the same time positive electric charges. There is a strong deficit of positive charges inside the cell. As a result, the membrane is additionally charged from the inside negatively (up to -70 mV).

The final

The potassium-sodium pump creates the prerequisites for the emergence of a resting potential. This is the difference in ion concentration between the inner and outer environment of the cell. The difference in sodium concentration and the difference in potassium concentration are manifested separately. The cell's attempt to equalize the concentration of ions with respect to potassium leads to a loss of potassium, a loss of positive charges and generates electronegativity inside the cell. This electronegativity accounts for most of the resting potential. A smaller part of it is the direct electrogenicity of the ion pump, i.e. the predominant loss of sodium during its exchange for potassium.

Video: Resting membrane potential

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 electropositively charged with respect to the cytoplasm. This potential difference is called resting potential or membrane potential. An accurate measurement of the resting potential is possible only with the help of microelectrodes designed for intracellular current withdrawal, very powerful amplifiers and sensitive recording devices - oscilloscopes.

The microelectrode (Fig. 67, 69) is a thin glass capillary, the tip of which has a diameter of about 1 μm. This capillary is filled with saline, a metal electrode is immersed in it and connected to an amplifier and an oscilloscope (Fig. 68). As soon as the microelectrode pierces the membrane covering the cell, the oscilloscope beam deflects downward from its original position and sets 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 has unequal permeability to various 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 sodium ions. Diffusion of positively charged potassium ions from the cytoplasm to the cell surface imparts a positive charge to the outer membrane surface.

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

Action potential

If a section of a nerve or muscle fiber is exposed to a sufficiently strong stimulus, then excitation arises in this section, which manifests itself in a rapid oscillation of the membrane potential and is called action potential.

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

With extracellular lead it can be found that the surface of the excited area for a very short period, measured in thousandths of a second, becomes electronegatively charged with respect to the resting area.

The cause of the action potential is a change in the ionic permeability of the membrane. With irritation, the permeability of the cell membrane to sodium ions increases. Sodium ions tend to the inside of the cell, since, firstly, they are positively charged and are attracted inside 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 the external environment of the cell into the cytoplasm significantly exceeds the flow of potassium ions from the cell to the outside. As a result, the inner surface of the membrane becomes positively charged, and the outer, due to the loss of positively charged sodium ions, negatively. At this moment, the peak of the action potential is recorded.

The increase in the permeability of the membrane for sodium ions lasts for a very short time. Following this, restorative processes occur in the cell, leading to the fact that the membrane permeability for sodium ions decreases again, and for potassium ions it increases. Since potassium ions are also positively charged, then, leaving the cell, they restore the original relationship outside and inside the cell.

The 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 a different ionic composition on the surface and inside the cell, and, consequently, a different charge of these surfaces. It should be noted that many provisions of the membrane-ionic theory are still controversial and require further development.