Charge of the cell membrane at rest. The action potential of an excitable cell and its phases. Electrical and physiological manifestations of arousal

»: Resting potential is an important phenomenon in the life of all body cells, and it is important to know how it is formed. However, this is a complex dynamic process, difficult to understand as a whole, especially for undergraduate students (biological, medical and psychological specialties) and unprepared readers. However, when considering the points, it is quite possible to understand its main details and stages. The paper introduces the concept of the rest potential and identifies the main stages of its formation using figurative metaphors that help to understand and remember the molecular mechanisms of the formation of the rest potential.

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

Let's understand in more detail.

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

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

These questions can only be answered if we find out how the cell creates for itself a difference in electrical potentials (resting potential) across the membrane.

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

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

Definition of the concept of "resting potential"

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

Thus, the membrane is polarized. This means that it has a different electrical potential of the outer and inner surfaces. It is quite possible to register the difference between these potentials.

This can be verified by inserting a microelectrode connected to a recording device into the cell. As soon as the electrode enters the cell, it instantly acquires a certain constant electronegative potential with respect to the electrode located in the fluid surrounding the cell. The magnitude of the intracellular electrical potential in nerve cells and fibers, for example, giant nerve fibers squid, at rest is about -70 mV. This value is called the resting membrane potential (RMP). At all points of the axoplasm, this potential is practically the same.

Nozdrachev A.D. etc. Beginnings of Physiology.

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

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

It is important to take into account that in nervous system electric charges are not represented by electrons, as in ordinary metal wires, but by ions - chemical particles that have an electric charge. And in general in aqueous solutions It is not electrons that move in the form of an electric current, but ions. That's why everything electric currents in cells and their environment is ion currents.

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

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

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

The essence of resting potential formation

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

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

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

The main secret of the appearance of negativity inside the cell

Let's open this secret right away and say that the cell loses some of its positive particles and becomes negatively charged due to two processes:

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

These two processes we need to explain.

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

In the membrane nerve cell proteins are constantly working exchanger pumps(adenosine triphosphatase, or Na + /K + -ATPase), embedded in the membrane. They change the "own" sodium of the cell to the external "foreign" potassium.

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

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

To make it easier to remember the operation of exchanger pumps, it can be figuratively expressed as follows: "The cell loves potassium!" Therefore, the cell drags potassium towards itself, despite the fact that it is already full of it. And therefore, she unprofitably exchanges it for sodium, giving 3 sodium ions for 2 potassium ions. And so it spends on this exchange the energy of ATP. And how to spend! Up to 70% of all neuron energy consumption can be spent on the work of sodium-potassium pumps. (That's what love does, even if it's not real!)

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

Figuratively speaking, it can be expressed as follows: By creating the potential for rest, the cell is "charged with love." It's love for two things:

1. the love of the cell for potassium (therefore, the cell forcibly drags him to itself);
2. the love of potassium for freedom (therefore, potassium leaves the cell that has captured it).

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

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

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

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

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

Due to the resulting sodium deficiency inside the cell, this ion strives at every opportunity rush inward: solutes always tend to equalize their concentration in the entire volume of the solution. But this does not work well for sodium, since sodium ion channels are usually closed and open only when certain conditions: under the influence of special substances (transmitters) or with a decrease in negativity in the cell (membrane depolarization).

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

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

Here it is also important to understand that sodium and potassium ions, as it were, "do not notice" each other, they react only "to themselves." Those. sodium reacts to the concentration of sodium, 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, it is necessary to consider separately the concentrations of sodium and potassium ions. Those. it is necessary to separately compare the sodium concentration inside and outside the cell and separately the potassium concentration inside and outside the cell, but it makes no sense to compare sodium with potassium, as it happens in textbooks.

According to the law of equalization of chemical concentrations, which operates in solutions, sodium "wants" to enter the cell from the outside; the electric force also draws him there (as we remember, the cytoplasm is negatively charged). He wants to want something, but he cannot, since the membrane in its normal state does not pass it well. The sodium ion channels present in the membrane are normally closed. If, nevertheless, it enters a little, then the cell immediately exchanges it for external potassium with the help of its sodium-potassium exchange pumps. It turns out that sodium ions pass through the cell as if in transit and do not linger in it. Therefore, sodium in neurons is always in short supply.

But potassium just can easily go out of the cell! The cage is full of him, and she can't keep him. It exits through special channels in the membrane - "potassium leak channels", which are normally open and release potassium.

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

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

From chemical to electrical

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

Potassium (K +) is positively charged, and therefore, when it leaves the cell, it takes out of it not only itself, but also a positive charge. Behind him from the inside of the cell to the membrane stretch "minuses" - negative charges. But they cannot seep through the membrane - unlike potassium ions - because. there are no suitable ion channels for them, and the membrane does not let them through. Remember the -60 mV negativity that we didn't explain? This is the very part of the resting membrane potential, which is created by the leakage of potassium ions from the cell! And this - most of resting potential.

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

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

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

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

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

Conclusion

So, the rest potential consists of two parts:

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

Interestingly, potassium will stop leaving the cell (more precisely, its input and output are equalized) only at a cell negativity level of −90 mV. In this case, the chemical and electrical forces will equalize, pushing potassium through the membrane, but directing it to opposite sides. But this is hindered by sodium constantly leaking into the cell, which carries with it positive charges and reduces the negativity for which potassium “fights”. And as a result, the equilibrium state at the level of −70 mV is maintained in the cell.

Now the resting membrane potential is finally formed.

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

Literature

1. Jacqueline Fischer-Lougheed, Jian-Hui Liu, Estelle Espinos, David Mordasini, Charles R. Bader, et. al. (2001). Human Myoblast Fusion Requires Expression of Functional Inward Rectifier Kir2.1 Channels . J Cell Biol. 153 , 677-686;
2. Liu J.H., Bijlenga P., Fischer-Lougheed J. et al. (1998). Role of an inward rectifier K + current and of hyperpolarization in human myoblast fusion . J Physiol. 510 , 467–476;
3. Sarah Sundelacruz, Michael Levin, David L. Kaplan. (2008). Membrane Potential Controls Adipogenic and Osteogenic Differentiation of Mesenchymal Stem Cells. PLOS ONE. 3 , e3737;
4. Pavlovskaya M.V. and Mamykin A.I. Electrostatics. Dielectrics and conductors in an electric field. DC / Electronic manual on general exchange rate physics. St. Petersburg: St. Petersburg State Electrotechnical University;
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6. Makarov A.M. and Luneva L.A. Fundamentals of electromagnetism / Physics at the Technical University. T. 3;
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The resting membrane potential (MPS) is the potential difference between the outer and inner sides of the membrane under conditions when the cell is not excited. The cytoplasm of the cell is charged negatively to the extracellular fluid by the uneven distribution of anions and cations on both sides of the membrane. Potential difference (voltage) for various cells has a value from -50 to -200 mV (minus means that inside the cell is more negatively charged than outside). The resting membrane potential occurs on the membranes of all cells - excitatory (nerves, muscles, secretory cells) and non-waking ones.

MPS is required to maintain the excitability of cells such as muscle and nerve cells. It also affects the transport of all charged particles in any cell type: it promotes the passive transport of anions out of the cell and cations into the cell.

Formation and maintenance of membrane potential provide different types ion pumps (in particular sodium-potassium pump or sodium-potassium ATPase) and ion channels (potassium, sodium, chloride ion channels).

Registration of the resting potential

To register the resting potential, a special microelectrode technique is used. A microelectrode is a thin glass tube with an elongated end, less than 1 µm in diameter, filled with an electrolyte solution (usually potassium chloride). The reference electrode is a silver chlorinated plate located in the extracellular space, both electrodes are connected to an oscilloscope. First, both electrodes are located in the extracellular space and there is no potential difference between them, if you enter the recording microelectrode through the membrane into the cell, then the oscilloscope will show a jump potential shift up to about -80 mV. This potential shift is called the resting membrane potential.

Resting potential formation

Two factors lead to the emergence of the resting membrane potential: firstly, the concentrations of various ions differ externally and inside the cell, and secondly, the membrane is semipermeable: some ions can penetrate through it, others cannot. Both of these phenomena depend on the presence of special proteins in the membrane: concentration gradients create ion pumps, and ion channels provide membrane permeability for ions. critical role ions of potassium, sodium and chlorine play in the formation of the membrane potential. The concentrations of these ions are visible on both sides of the membrane. For a mammalian neuron, the K + concentration is 140 mmol inside the cell and only 5 mM outside, the Na + concentration gradient is almost the opposite - 150 mmol outside and 15 mM inside. This distribution of ions is maintained by the sodium-potassium pump in the plasma membrane, a protein that uses the energy of ATP to pump K + into the cell and download Na + from it. There is also a concentration gradient for other ions, for example, the chloride anion Cl -.

The concentration gradients of potassium and sodium cations are chemical form potential energy. Ion channels are involved in the conversion of energy into electrical energy - pores are formed by accumulations of special transmembrane proteins. When ions diffuse through a channel, they carry a unit of electrical charge. Any net movement of positive or negative ions across the membrane will create a voltage, or potential difference, on either side of the membrane.

The ion channels involved in the establishment of MPS have selective permeability, that is, they allow only a certain type of ions to penetrate. In the membrane of a neuron at rest, potassium channels are open (those that mainly allow only potassium to pass through), most sodium channels are closed. Diffusion of K+ ions through potassium channels is critical for the creation of a membrane potential. Since the concentration of K + is much higher inside the cell, the chemical gradient promotes the outflow of these cations from the cell, so anions that cannot pass through potassium channels begin to predominate in the cytoplasm.

The outflow of potassium ions from the cell is limited by the membrane potential itself, since, at a certain level, the accumulation of negative charges in the cytoplasm will limit the movement of cations outside the cell. Thus, the main factor in the occurrence of MPS is the distribution of potassium ions under the action of electric and chemical potentials.

Equilibrium potential

In order to determine the influence of the movement of a certain ion through a semipermeable membrane on the formation of the membrane potential, model systems are built. Such a model system consists of a vessel divided into two cells by an artificial semi-permeable membrane, into which ion channels are embedded. An electrode can be immersed in each cell and the potential difference can be measured.

Let us consider the case when the artificial membrane is permeable only for potassium. On both sides of the membrane of the model system, a concentration gradient is created similar to that of a neuron: a 140 mM solution of potassium chloride (KCl) is placed in the cell corresponding to the cytoplasm (inner cell), in the cell corresponding to interstitial fluid(outer cell) - 5 mmol solution KCl. Potassium ions will diffuse through the membrane into the outer cell along the concentration gradient. But since the anions Cl - penetrate through the membrane, an excess of negative charge cannot arise in the inner cell, which will prevent the outflow of cations. When such model neurons reach a state of equilibrium, the action of the chemical and electrical potential will be balanced, and no total K + diffusion will be observed. The value of the membrane potential, viinkae under such conditions, is called the equilibrium potential for a particular ion (E ion). The equilibrium potential for potassium is approximately -90 mV.

A similar experiment can be carried out for sodium by installing a membrane between the cells that penetrates only for this cation, and placing a solution of sodium chloride with a concentration of 150 mM in the outer cell, and 15 mM in the inner cell. The sodium will move into the inner cell, and its significant potential will be approximately 62 mV.

The number of ions that must diffuse to generate an electric potential is very small (approximately 10 -12 mol K + per 1 cm 2 membrane), this fact has two important consequences. First of all, this means that the concentrations of ions that can pass through the membrane remain stable outside and inside the cell, even after their movement has provided the electrical potential. Secondly, the meager flows of ions through the membrane do not violate the electrical neutrality of the cytoplasm and the extracellular fluid as a whole, only in the area immediately adjacent to the plasma membrane, only to establish the potential.

Nernst equation

The equilibrium potential for a particular ion, such as potassium, can be calculated using the Nernst equation, which looks like this:

where R is the universal gas constant, T is the absolute temperature (on the Kelvin scale), z is the charge of the ion, F is the Faraday number, o, i are the concentration of potassium outside and inside the cell, respectively. Since the described processes occur at body temperature - 310 ° K, and decimal logarithms in calculus it is easier to use than natural ones, this equation is converted as follows:

Substituting the concentration of K + in the Nernst equation, we obtain the equilibrium potential for potassium, which is -90 mV. Since the zero potential is taken outer side membrane, then the minus sign means that under conditions of equilibrium potassium potential, the inner Storn membrane is comparatively more electronegative. Similar calculations can be made for the equilibrium Natium potential, which is 62 mV.

Goldman's equations

Although the equilibrium potential for potassium ions is -90 mV, the MPS of the neuron is somewhat less negative. This difference reflects a small but constant flow of Na + ions across the membrane at rest. Since the concentration gradient for sodium is opposite to that for potassium, Na + moves into the cell and shifts the net charge on the inside of the membrane to positive side. In fact, the MPS of a neuron is from -60 to -80 mV. This value is much closer to E K than to E Na, because at rest a lot of potassium channels and very little sodium. The movement of chloride ions also influences the establishment of MPS. In 1943, David Goldaman proposed to improve the Nernst equation so that it reflects the effect of various ions on the membrane potential, this equation takes into account relative permeability membranes for each type of ions:

where R is the universal gas constant, T is the absolute temperature (on the Kelvin scale), z is the charge of the ion, F is the Faraday number, [ion] o, [ion] i are the concentrations of ions inside and inside the cells, P is the relative permeability of the membrane for the corresponding ion. The value of the charge in this equation is not preserved, but it is taken into account - for chlorine, the external and internal concentrations are reversed, since its charge is 1.

The value of the resting membrane potential for various tissues

• Separated muscles -95 mV;
• Unsmoothed muscles -50 mV;
• Astroglia from -80 to -90 mV;
• Neurons -70 mV.

The role of the sodium-potassium pump in the formation of MPS

The resting membrane potential can exist only under the condition of an uneven distribution of ions, which is ensured by the functioning of the sodium-potassium pump. In addition, this protein also does electrogenic power - it transfers 3 sodium cations in exchange for 2 potassium ions moving inside the cell. Thus, Na + -K + -ATPase reduces MPS by 5-10 mV. Suppression of the activity of this protein leads to an insignificant (by 5-10 mV) instantaneous increase in the membrane potential, after which it will exist for some time at a fairly stable level, while Na + and K + concentration gradients remain. Subsequently, these gradients will begin to decrease, due to the penetration of the membrane to ions, and after a few tens of minutes, the electric potential on the membrane will disappear.

Between the outer surface of the cell and its cytoplasm at rest there is a potential difference of about 0.06-0.09 V, and the cell surface is charged electropositively with respect to the cytoplasm. This potential difference is called resting potential or membrane potential. Accurate measurement resting potential is possible only with the help of microelectrodes designed for intracellular current diversion, 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 micron. This capillary is filled saline solution, immerse a metal electrode in it and connect it to an amplifier and an oscilloscope (Fig. 68). As soon as the microelectrode pierces the membrane covering the cell, the oscilloscope beam deviates downward from its original position and sets to a new level. This indicates the presence of a potential difference between the outer and inner surface of the cell membrane.

The most complete explanation of the origin of the resting potential is the so-called membrane-ion theory. According to this theory, all cells are covered with a membrane that has unequal permeability to different ions. In this regard, inside the cell in the cytoplasm there are 30-50 times more potassium ions, 8-10 times less sodium ions and 50 times less chloride ions than on the surface. At rest, the cell membrane is more permeable to potassium ions than to sodium ions. Diffusion of positively charged potassium ions from the cytoplasm to the cell surface imparts outer surface membranes are positively charged.

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

action potential

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

An action potential can be registered either by means of electrodes applied to outer surface fiber (extracellular lead), or a microelectrode introduced into the cytoplasm (intracellular lead).

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

The cause of the action potential is a change in the ion permeability of the membrane. When irritated, the permeability of the cell membrane for sodium ions increases. Sodium ions tend to enter the cell, because, firstly, they are positively charged and are attracted by electrostatic forces, and secondly, their concentration inside the cell is low. At rest, the cell membrane was impermeable 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 to the cytoplasm significantly exceeds the flow of potassium ions from the cell to the outside. As a result inner surface the membrane becomes positively charged, and the outer one, due to the loss of positively charged sodium ions, negatively. At this point, the peak of the action potential is recorded.

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

The accumulation of sodium ions inside the cell with 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 data on the active transport of potassium ions with the help of 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 causes 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-ion theory are still debatable and need further development.

Discovery history

In 1902, Julius Bernstein put forward a hypothesis according to which the cell membrane allows K + ions to enter the cell, and they accumulate in the cytoplasm. The calculation of the resting potential according to the Nernst equation for a potassium electrode satisfactorily coincided with the measured potential between the muscle sarcoplasm and the environment, which was about - 70 mV.

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

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

General provisions

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

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

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

Resting potential formation

The PP is formed in two stages.

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

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

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

2. An excess of potassium ions (K +) in the cell.

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

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

So, the resting membrane potential is a deficit of positive electric charges inside the cell, which occurs due to the leakage of positive potassium ions from it and the electrogenic action of the sodium-potassium pump.

see also

Notes

Links

Dudel J., Ruegg J., Schmidt R. et al. Human Physiology: in 3 volumes. Per. from English / edited by R. Schmidt and G. Thevs. - 3. - M .: Mir, 2007. - T. 1. - 323 with illustrations. With. - 1500 copies. - ISBN 5-03-000575-3

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resting potential

The membranes, including plasma membranes, are in principle impenetrable to charged particles. True, the membrane contains Na + /K + -ATPase (Na + /K + -ATPase), which actively transfers Na + ions from the cell in exchange for K + ions. This transport is energy dependent and is associated with the hydrolysis of ATP (ATP). Due to the operation of the “Na +, K + -pump”, a non-equilibrium distribution of Na + and K + ions between the cell and the environment is maintained. Since the splitting of one ATP molecule ensures the transfer of three Na + ions (out of the cell) and two K + ions (into the cell), this transport is electrogenic, that is, the cell cytoplasm is negatively charged with respect to the extracellular space.

Electrochemical potential. The contents of the cell are negatively charged with respect to the extracellular space. The main reason for the appearance of an electric potential on the membrane (membrane potential Δψ, is the existence of specific ion channels. The transport of ions through the channels occurs along a concentration gradient or under the action of a membrane potential. In an unexcited cell, part of the K + channels is in an open state and K + ions constantly diffuse from to environment(along the concentration gradient). Leaving the cell, K + ions carry away a positive charge, which creates resting potential equal to approximately -60 mV. It can be seen from the permeability coefficients of various ions that the channels permeable to Na + and Cl - are mostly closed. Phosphate ions and organic anions, such as proteins, practically cannot pass through membranes. Using the Nernst equation, it can be shown that the membrane potential is primarily determined by the K + ions, which make the main contribution to the membrane conductivity.

ion channels. The membranes have channels permeable to Na + , K + , Ca 2+ and Cl - ions. These channels are most often in a closed state and open only for a short time. The channels are subdivided into voltage-gated (or electrically excitable), for example, fast Na + channels, and ligand-gated (or chemo-excitable), for example, nicotinic cholinergic channels. Channels are integral membrane proteins composed of many subunits. Depending on the change in the membrane potential or interaction with the corresponding ligands, neurotransmitters and neuromodulators, receptor proteins can be in one of two conformational states, which determines the permeability of the channel ("open" - "closed" - etc.).

A nerve cell under the action of a chemical signal (less often an electrical impulse) leads to the appearance action potential. This means that the resting potential of -60 mV jumps to +30 mV and after 1 ms returns to its original value. The process begins with the opening of the Na+ channel. Na + ions rush into the cell (along the concentration gradient), which causes a local reversal of the sign of the membrane potential. In this case, the Na + channels are immediately closed, i.e., the flow of Na + ions into the cell lasts a very short time. In connection with a change in the membrane potential, voltage-controlled K + channels open (for a few ms), and K + ions rush in the opposite direction, out of the cell. As a result, the membrane potential takes on its original value, and even exceeds for a short time resting potential. After that, it becomes excitable again.

In one pulse, a small part of the Na + and K + ions pass through the membrane, and the concentration gradients of both ions are preserved (the level of K + is higher in the cell, and the level of Na + is higher outside the cell). Therefore, as the cell receives new impulses, the process of local reversal of the sign of the membrane potential can be repeated many times. The propagation of an action potential over the surface of a nerve cell is based on the fact that the local reversal of the membrane potential stimulates the opening of neighboring voltage-gated ion channels, as a result of which the excitation propagates in the form of a depolarization wave to the entire cell.