Formation of the resting membrane potential. Resting and action membrane potential

• managed. By control mechanism: electrically, chemically and mechanically controlled;
• uncontrollable. They do not have a gate mechanism and are always open, ions flow constantly, but slowly.

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

The mechanism of formation of resting potentials. The immediate cause of the resting potential is the unequal concentration of anions and cations inside and outside the cell. Firstly, this arrangement of ions is justified by the difference in permeability. Secondly, significantly more potassium ions leave the cell than sodium.

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

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

As a result, ions quickly diffuse into or out of the cell along an electrochemical gradient. This is excitement. Based on 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 towards the cell according to a concentration and electrical gradient. Motion condition: sodium channel gate open;
• 2nd phase - inversion. Reversing the charge sign. Inversion involves two parts: ascending and descending.

The ascending part. Sodium continues to move into the cell according to the concentration gradient, but against the electrical gradient (it interferes).

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

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

Excitability criteria

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

During the period of development of the spike (peak potential), there is an avalanche-like flow of sodium ions into the cell, as a result of which the membrane is recharged, and it loses the ability to respond with excitation to stimuli of above-threshold strength. This phase of excitability is called absolute refractoriness, i.e. absolute inexcitability, which lasts until the end of membrane recharging. Absolute membrane refractoriness occurs due to the fact that sodium channels completely open and then inactivate.

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

The next period corresponds increased level excitability: 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 reduced, i.e. cell excitability is increased. During this phase, new excitation can arise from the action of stimuli of subthreshold strength. Sodium channels are not completely inactivated during this phase. Membrane potential increases - a state of membrane hyperpolarization occurs. Moving away from critical level depolarization, the threshold of stimulation slightly increases, and new excitation can arise only under the action of stimuli of a supra-threshold value.

The mechanism of occurrence of the resting membrane potential

Each cell at rest is characterized by the presence of a transmembrane potential difference (resting potential). Typically, the charge difference between the inner and outer surfaces of the membranes is -80 to -100 mV and can be measured using external 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 the resting potential is ensured by two main processes - the uneven distribution of inorganic ions between the intra- and extracellular spaces and the unequal permeability of the cell membrane to them. Analysis chemical composition extra- and intracellular fluid indicates an extremely uneven distribution of ions (Table 1).

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

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

Rice. 1. Measuring the resting potential of a muscle fiber (A) using an intracellular microelectrode: M - microelectrode; I - 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 equal to zero. At the moment of puncture (shown by an arrow), a potential difference was detected, indicating that the inner side of the membrane is negatively charged relative to its outer surface (according to B.I. Khodorov)

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

	Intracellular concentration	Extracellular concentration
A- (anions of organic compounds)

Due to the concentration gradient, K+ reaches the outer surface of the cell, carrying out its positive charge. High molecular weight anions cannot follow K+ because the membrane is impermeable to them. The Na+ ion also cannot replace the lost potassium ions, because the permeability of the membrane for it is much less. CI- along the concentration gradient can only move inside the cell, thereby increasing the negative charge inner surface membranes. As a result of this movement of ions, polarization of the membrane occurs when its outer surface is charged positively and the inner surface is charged negatively.

The electric field that is created on the membrane actively interferes with the distribution of ions between the internal and external contents of the cell. As the positive charge on the outer surface of the cell increases, it becomes increasingly difficult for the K+ ion, which is positively charged, to move from inside to outside. It seems to be moving uphill. The greater the positive charge on the outer surface, the less K+ ions can reach the cell surface. At a certain potential on the membrane, the number of K+ ions crossing the membrane in both directions turns out to be equal, i.e. The potassium concentration gradient is balanced by the potential present across the membrane. The potential at which the diffusion flux of ions becomes equal to the flux of like ions going into reverse 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, despite the fact that the concentration of CI- ions outside the fiber is greater 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 should enter into the cell (its equilibrium potential is +60 mV), and the presence of a negative charge inside the cell should not interfere with 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 in the cell membrane there is a system of carriers, each of which is bound by the stirrup Na+ ions located inside the cell and carries them out. WITH outside the transporter binds to two K+ ions located outside the cell, which are transferred into the cytoplasm. The energy supply for the operation of transporter systems is provided by ATP. The operation of a pump using such a system leads to the following results:

• a high concentration of K+ ions is maintained inside the cell, which ensures a constant value 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 the resting potential. In this case, they talk about an electrogenic pump, since it itself creates a small, but D.C. positive charges from the cell, and therefore makes a direct contribution to the formation of a negative potential inside it. However, the magnitude of the contribution of the electrogenic pump to general meaning the resting potential is usually small and amounts to several millivolts;
• a low concentration of Na + ions is maintained inside the cell, which, on the one hand, ensures the operation of the action potential generation mechanism, and on the other hand, ensures the preservation of normal osmolarity and cell volume;
• maintaining a stable concentration gradient of Na +, the sodium-potassium pump promotes the coupled K +, Na + -transport of amino acids and sugars across the cell membrane.

Thus, the occurrence 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.

Nerve fiber action potential, 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.

The action potential is the main specific sign of excitation. Its registration indicates that the cell or its structures responded to the impact with excitation. 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. AP is used as a carrier of information, transmitting it in the form of electrical signals (electrical signaling) along afferent and efferent nerve fibers, the conduction system of the heart, and also to initiate contraction muscle cells.

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

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

With an increase in the pressure force on the Pacinian body, causing an increase in the receptor potential to 10 mV, a rapid oscillation of the membrane potential is usually recorded at the nearest node of Ranvier, accompanied by recharging of the membrane - the action potential (AP), or 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 for converting the receptor potential into an action potential (nerve impulse) and propagating the impulse along the nerve fiber

The essence of the mechanism of AP generation 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 node of Ranvier. These currents, carried by Na+, K+, CI- and other mineral ions, “flow” not only along, but also across the membrane of the nerve fiber in the area of ​​the node of Ranvier. In the membrane of the nodes of Ranvier, in contrast to the receptor membrane of the nerve ending itself, there is high density voltage-gated ion sodium and potassium channels.

When the depolarization value of about 10 mV is reached at the Ranvier interception membrane, fast voltage-dependent sodium channels open and through them a flow of Na+ ions rushes into the axoplasm along the electrochemical gradient. It causes rapid depolarization and recharging of the membrane at the node of Ranvier. However, simultaneously with the opening of fast voltage-gated sodium channels in the membrane of the node of Ranvier, slow voltage-gated potassium channels open and K+ ions begin to leave the axoillasma. Their output lags behind the entry of Na+ ions. Thus, Na+ ions entering the axoplasm at high speed quickly depolarize and recharge to a short time(0.3-0.5 ms) membrane, and the outgoing K+ ions restore the original distribution of charges on the membrane (repolarize the membrane). As a result, during a mechanical impact on the Pacinian corpuscle with a force equal to or exceeding the threshold, a short-term potential oscillation is observed on the membrane of the nearest node of Ranvier in the form of rapid depolarization and repolarization of the membrane, i.e. PD (nerve impulse) is generated.

Since the direct cause of AP generation is the receptor potential, in this case it is also called the generator potential. The number of generated per unit time, identical in amplitude and duration nerve impulses proportional to the amplitude of the receptor potential, and therefore to the force of pressure on the receptor. The process of converting information about the force of influence contained in the amplitude of the receptor potential into a number of discrete nerve impulses is called discrete information coding.

In more detail, ionic mechanisms and time dynamics processes of AP generation were studied under experimental conditions under artificial influence of electric current on the nerve fiber different strengths and duration.

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

The nerve fiber membrane at the point of localization of the stimulating electrode responds to the influence of a very weak current that has not yet reached the threshold value. This response is called local, and the oscillation of the potential difference on the membrane is called local potential.

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

If the membrane is exposed to an electric current of increasing strength, then at this value, called the threshold, the depolarization of the membrane can reach a critical level - Ec, at which the opening of fast voltage-dependent sodium channels occurs. As a result, an avalanche-like increase in the flow of Na+ ions into the cell occurs through them. The induced depolarization process becomes self-accelerating, and the local potential develops into an action potential.

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

Table. Comparative characteristics local potential and action potential

Characteristic	Local potential	Action potential
Conductivity	Spreads locally, 1-2 mm with attenuation (decrement)	Spreads without attenuation over long distances along the entire length of the nerve fiber
Law of "force"	Submits	Doesn't obey
All or nothing law	Doesn't obey	Submits
Summation phenomenon	Summarizes, increases with repeated frequent subthreshold stimulation	Does not add up
Amplitude value
Excitability	Increases	Decreases to the point of complete inexcitability (refractoriness)
Stimulus magnitude	Subliminal	Threshold and superthreshold

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 call the entire ascending part of the PD, in which areas corresponding to the local potential are identified (from the level E 0 before E k), rapid depolarization (from the level E k to level 0 mV), inversions charge sign (from 0 mV to the peak value or the beginning of repolarization). Repolarization called the descending part of the AP, which reflects the process of restoration of the original polarization of the membrane. At first, repolarization occurs quickly, but as it approaches 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 AP is also called peak, or spike. It includes phases of depolarization and rapid repolarization.

In the mechanism of development of PD vital role belongs to voltage-gated ion channels and a non-simultaneous increase in the permeability of the cell membrane for Na+ and K+ ions. Thus, when an electric current acts on a cell, it causes depolarization of the membrane and, when the membrane charge decreases to a critical level (Ec), voltage-gated sodium channels open. As already mentioned, these channels are formed by protein molecules embedded in the membrane, inside which there is a pore and two gate mechanisms. One of the gate mechanisms, activation, ensures (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) ensures its inactivation, which develops when the membrane is recharged (Fig. 4). Because both of these mechanisms rapidly change the position of the channel gate, voltage-gated sodium channels are fast ion channels. This circumstance is of decisive importance for the generation of PD in excitable tissues and for its conduction along the membranes of nerve and muscle fibers.

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

Rice. 4. Gate position and 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 allow Na+ ions into the cell, only the activation gate must be opened, since the inactivation gate is open under resting conditions. This is what happens when membrane depolarization reaches a level E k(Fig. 3, 4).

The opening of the activation gate of sodium channels leads to an avalanche-like entry of sodium into the cell, driven by the forces of its electrochemical gradient. Since Na+ ions carry a positive charge, they neutralize excess 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 for only about 0.5 ms and after this period of time from the moment of onset

AP 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 k activation of potassium channels and opening of their gates for K+ ions are also observed. K+ ions, under the influence of concentration gradient forces, leave the cell, removing positive charges from it. However, the gate mechanism of potassium channels is slow-functioning and the rate of exit of positive charges with K+ ions from the cell to the outside lags behind the entry of Na+ ions. The flow of K+ ions, removing excess positive charges from the cell, causes the restoration of the original distribution of charges on the membrane or its repolarization, and on the inner side, a moment after recharging, the negative charge is restored.

The occurrence of AP on excitable membranes and the subsequent restoration of the original resting potential on the membrane is possible because the dynamics of the entry into and exit of the positive charges of Na+ and K+ ions into the cell and exit from the cell are different. The entrance of the Na+ ion is ahead of the exit of the K+ ion. 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 APs by excitable muscle and nerve cells was due to the formation of two types of different-speed ion channels in their membrane - fast sodium and slow potassium.

To generate a single AP, a relatively small amount of energy is required to enter the cell. large number Na+ ions, which does not disrupt its distribution outside and inside the cell. If a large number of APs are generated, the distribution of ions on both sides of the cell membrane could be disrupted. However, in normal conditions this is prevented by the operation of the Na+, K+ pump.

Under natural conditions, in neurons of the central nervous system, the action potential primarily arises in the region of the axon hillock, in afferent neurons - in the node of Ranvier of the nerve ending closest to the sensory receptor, i.e. in those parts 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 channels, but also calcium channels play a role in the occurrence of AP.

The mechanisms of perception and transformation of signals into action potentials in secondary sensory receptors differ from the mechanisms discussed for primary sensory receptors. In these receptors, the perception of signals is carried out by specialized neurosensory (photoreceptor, olfactory) or sensoroepithelial (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 an oscillation of the potential difference of the plasma membrane, i.e. into receptor potential.

Thus, the key point in the mechanisms by which sensory cells convert perceived signals into receptor potential is a change in the permeability of ion channels in response to the stimulus. 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 that arises 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 described in detail in the chapter on sensory systems.

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

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

The resting membrane potential is the electrical potential (reserve) formed between the outer surface of the cell membrane and inside The inner side of the membrane relative to the outer surface always has a negative charge. For cells of each type, the resting potential is almost constant. So, in warm-blooded animals in the fibers of skeletal muscles it is 90 mV, for myocardial cells - 80, for nerve cells - 60-70. Membrane potential is present in all living cells.

In accordance with modern theory the electrical reserve under consideration is formed as a result of active and passive movement of ions.

Passive movement occurs without requiring any energy expenditure. at rest it is more permeable to potassium ions. In the cytoplasm of nerve and muscle cells there are thirty to fifty times more of them (potassium ions) than in the intercellular fluid. In the cytoplasm, ions are in free form and diffuse, in accordance with the concentration gradient, into the extracellular fluid through the membrane. In the intercellular fluid they are retained by intracellular anions on the outer surface of the membrane.

The intracellular space contains mainly anions of pyruvic, acetic, aspartic and other organic acids. Inorganic acids are contained in relatively small quantities. Anions cannot penetrate through the membrane. They remain in the cage. Anions are located on the inner side of the membrane.

Due to the fact that anions have a negative charge, and cations have a positive charge, the outer surface of the membrane has a positive charge, and the inner one has a negative charge.

There are eight to ten times more sodium ions in the extracellular fluid than in the cell. Their permeability is negligible. However, due to the penetration of sodium ions, the membrane potential decreases to some extent. At the same time, diffusion of chlorine ions into the cell also takes place. The content of these ions is fifteen to thirty times higher in extracellular fluids. Due to their penetration, the membrane potential increases slightly. In addition, there is a special molecular mechanism in the membrane. It ensures the active promotion of potassium and sodium ions towards higher concentrations. In this way, ionic asymmetry is maintained.

Under the influence of the enzyme adenosine triphosphatase, ATP is broken down. Poisoning with cyanide, monoiodoacetate, dinitrophenol and other substances, including those that stop the processes of ATP synthesis and glycolysis, provokes its (ATP) decrease in the cytoplasm and the cessation of the “pump” functioning.

The membrane is also permeable to chloride ions (especially in muscle fibers). In cells with high permeability, potassium and chlorine ions in equally form membrane dormancy. At the same time, in other cells the contribution of the latter to this process is insignificant.

Electric charge, like mass, is a fundamental property of substances. There are two types of charges, conventionally designated as positive and negative.

Each substance has electric charge, the value of which can be positive, negative or equal to zero. For example, electrons are negatively charged and protons are positively charged. Since each atom contains one or more electrons and an equal number of protons, total number charges in a macroscopic object is extremely large, but in general such an object is not charged or has a small charge.

The charge of an electron is absolute value the smallest.

Electric field. Coulomb's law

Every charged object creates an electric field in the space surrounding it. Electric field is a type of matter through which charged objects interact with each other. A test charge introduced into the electric field of another charge “feels” the presence of this field. It will be attracted to or repelled by the charge creating the electric field.

Coulomb's law defines the electric force F acting between two point charges q 1 And q 2:

k- constant determined by the selected conditions; r- distance between charges.

According to Coulomb's law, a force acts in the direction of a line connecting two charges. The magnitude of the force acting on the charges is proportional to the size of each of the charges and inversely proportional to the square of the distance between them.

The electric field can be represented as power lines showing direction electrical forces. These forces are directed away from the charge when it is positive and towards the charge when it is negative. If a positive charge is placed in an electric field, it experiences a force in the direction of the field. A negative charge is subject to a force opposite to the direction of the field.

Electric field characteristics

1) Tension electric field. Every electric charge produces an electric field around itself. If another charge q enter into this field, then a force will act on it F, proportional q and electric field strength E:

The electric field strength E (or simply intensity) at any point is defined as the electric force F that acts on a positive charge q, placed at this point:

E is a vector quantity, that is, it has both magnitude and direction. The unit of measurement for voltage is volt per meter [V/m].

The principle of superposition (superposition) indicates that if an electric field is created by many charges, the total intensity will be determined by the addition of the intensities created by each charge, according to the rules of vector addition.

2) Electric potential. To move a charge against the electrical force acting on it, work must be done. This work does not depend on the path of movement of the charge in the electric field, but depends on the initial and final position of the charge.

If a charge is moved from one point to another against an electric force, its electrostatic potential energy increases. Electric potential at any point is equal to electrostatic potential energy Wp, which has a positive charge q at this point: φ = W p /q (4).

We can also say that the electric potential at a point equal to work which must be done against electric forces in order to move a positive charge from a given point to a large distance where the electric field potential is zero. Electric potential is scalar quantity and is measured in volts ( IN).

The electric field strength is the negative gradient of the electric potential - an indicator of the change in potential with distance x: E → = - dφ/dx. Using instruments, you can measure the potential difference, but not the field strength. The latter can be calculated using the dependence between E → and Δφ: where Δφ = E l- the distance between two electric field currents.

Resting membrane potential

Each cell converts some of its metabolic energy into electrostatic energy. The source of the cell's electric field is the plasma membrane. There is a potential difference between the inner and outer surfaces of the plasma membrane. This potential difference is called membrane potential .

Potential difference between internal and external environment cells can be measured directly and quite accurately. For this purpose, a microelectrode is used, which is a glass micropipette with a tip diameter of up to 1 µm filled with concentrated KCl solution. The microelectrode is connected to the voltage amplifier of the recording device. The membrane potential of muscle cells, nerve cells, or other tissue cells can be measured. Another electrode (reference) is installed on the surface of the tissue.

When the microelectrode tip is outside the cell, its potential relative to the reference electrode is zero. If the end of the electrode is immersed in the cell, piercing plasma membrane, the potential difference sharply becomes negative. The potential difference between the internal and external environments of the cell is recorded on the scale of the measuring device. This potential difference is called transmembrane, or membrane potential.


If a cell is at rest, its membrane potential is negative meaning and a stable value. It is usually called resting membrane potential . The resting membrane potential of cells of various tissues ranges from - 55 millivolts (mV) before - 100mV.

Under certain physiological conditions, changes in membrane potential can occur. Changes in a positive direction are called depolarization plasma membrane. A shift in membrane potential in a negative direction is called hyperpolarization .

Biophysical basis of resting membrane potential

Electrical phenomena in the plasma membrane are determined by the distribution of ions between the inner and external sides membranes. From chemical analysis It is known that the concentration of ions in the intracellular fluid is very different from the concentration of ions in the extracellular fluid. The term "extracellular fluid" refers to all fluids outside of cells (intercellular substance, blood, lymph, etc.). The table shows the concentrations of major ions in mammalian muscle cells and extracellular fluid (millimoles per liter).

Exist significant differences between the concentration of major ions inside and outside the cell. Extracellular fluid has a high concentration of sodium and chlorine ions. The intracellular fluid has a high concentration of potassium and various organic anions (A -) (charged protein groups).

The difference between the concentrations of sodium and potassium in extracellular and intracellular fluids is due to the activity sodium-potassium pump, which pumps 3 sodium ions out of the cell in one cycle and pumps 2 potassium ions into the cell against the electrochemical gradient of these ions. The main function of the sodium-potassium pump is to maintain differences in the concentrations of sodium and potassium ions on both sides of the plasma membrane.

At rest, the permeability of the plasma membrane for potassium ions significantly exceeds the permeability of the membrane for sodium ions. In nerve cells, the permeability ratio of the corresponding ions is 1:0.04.

This fact makes it possible to explain the existence of the resting membrane potential.

Potassium ions tend to leave the cell due to their high internal concentration. In this case, intracellular anions do not move through the membrane due to their large size. The insignificant entry of sodium ions into the cell also does not compensate for the release of potassium ions outside, since the permeability of the membrane at rest for sodium ions is small.

Consequently, the outside of the cell acquires an additional positive charge and an excess of negative charge remains inside.

Potassium diffusion through the membrane is a limited process. Potassium ions passing through the membrane create an electric field that retards the diffusion of other potassium ions. As potassium leaves the cell, the electric field increases and, ultimately, the voltage reaches such a value that the flow of potassium through the membrane stops. The state in which the flow of ions along their concentration gradient is balanced by the membrane potential is called state of electrochemical equilibrium ions. The magnitude of this membrane equilibrium potential is determined Nernst equation ( it is believed that the membrane is permeable to only one type of ion ) :

R- universal gas constant, T- thermodynamic temperature, z- electric charge of the ion, F- Faraday constant, i and o - intracellular and extracellular concentrations of potassium ions, respectively.

Calculations based on the Nernst equation indicate that the internal and external concentration of chlorine ion also corresponds to a state of electrochemical equilibrium, but the sodium concentration is far from equilibrium with the membrane potential.

The Nernst equation shows that the concentration gradient of potassium ions determines the value of the resting membrane potential only in a first approximation. The calculated values ​​of the membrane potential coincide with those obtained experimentally only when high concentration potassium outside the cell.

A more accurate value for the resting membrane potential can be calculated from the Goldman-Hodgkin equation, which takes into account the concentrations and membrane permeability of the three main ions in intra- and extracellular fluids:

Also, the sodium-potassium pump directly participates in maintaining the resting membrane potential, pumping three sodium ions out of the cell and pumping only two potassium ions. As a result, the resting membrane potential becomes more negative than it would be if it were generated solely by the passive movement of ions across the membrane.

Action potential

If a short-term electricity, then the membrane potential undergoes consistent changes that are specific and unique to excitable cells. Excitable tissues can also be stimulated mechanically or chemicals, but experimental work typically uses electrical stimuli.

Rice. 1. Action potential nerve cell.

Action potential - a rapid fluctuation in the membrane potential caused by the action of an electrical or other stimulus on an excitable cell.

In Fig. Figure 1 shows the action potential of a nerve cell recorded using a microelectrode. If a brief electrical stimulus is applied to a cell, the membrane potential decreases rapidly to zero. This deviation is characterized as depolarization phase And. For a short time internal environment cells becomes electropositive with respect to the outside ( membrane potential reversal phase, or overshoot ). The membrane potential then returns to the level of the resting membrane potential ( repolarization stage ) (Fig. 2.).

Rice. 2. Action potential phases

Action potential duration ranges from 0.5 to 1 millisecond in large nerve cells and several milliseconds in skeletal muscle cells. Total amplitude - almost 100 - 120 mV, deviation from the zero line is about 30-50 mV.

The action potential plays a leading role in information processing in the nervous system. It has a constant amplitude, which is not a probabilistic quantity. It is of great importance in information processing nervous system. The intensity of stimulation is encoded by the number of action potentials and the frequency with which action potentials follow each other.

Biophysical basis of action potential

Action potentials arise from specific changes in ion permeability in the plasma membrane. The English physiologist Hodgkin showed that the main mechanism of the action potential is a short-term and very specific change in the permeability of the membrane to sodium ions. In this case, sodium ions enter the cell until the membrane potential reaches the electrochemical equilibrium potential of sodium ions.

Rice. 3. Changes in membrane permeability to sodium and potassium ions during an action potential

The permeability of the membrane to sodium when an electrical stimulus is applied to the cell increases approximately 500 times and becomes significantly greater than the permeability of the membrane to potassium ions. The concentration of sodium ions in the cell increases sharply. As a result, the membrane potential takes positive value, and the flow of sodium ions into the cell slows down.

During the occurrence of an action potential, depolarization of the plasma membrane occurs. Rapid depolarization of the membrane under the influence of an electrical stimulus causes an increase in its permeability to sodium ions. The increased intake of sodium ions into the cell increases the depolarization of the membrane, which, in turn, causes a further increase in the permeability of the membrane to sodium, etc.

But the value of the membrane potential during depolarization does not reach the level of the electrochemical equilibrium potential of sodium ions. The reason for this is a decrease in the permeability of the membrane to sodium ions due to inactivation of sodium transmembrane transport. This process sharply reduces the permeability of the membrane to sodium ions and stops the influx of sodium into the cell.

At this moment, the membrane permeability to potassium ions increases, which leads to rapid decline the magnitude of the membrane potential to the level of the resting potential. The permeability of the membrane to potassium ions also decreases to its normal value. Thus, inactivation of the incoming sodium current and increasing the permeability of the membrane to potassium ions (outgoing current) limit the duration of the action potential and lead to repolarization membranes.

Thus, during an action potential, some sodium ions enter the cell. But this amount is quite small. The change in ion concentration in large nerve cells is only about 1/300,000 of the initial value.

The main mechanism of changes in membrane permeability is due to events in the sodium and potassium channels of the membrane. The state of their gates is controlled by the magnitude of the membrane potential. Sodium channels have two types of gates. One of them, called the activation gate, is closed at rest and opens when the membrane is depolarized. The entry of sodium ions into the cell causes the opening of everything more activation gate. The second type of gate of sodium channels - inactivated by increasing depolarization, the membranes gradually close, which stops the flow of sodium into the cell. Depolarization of the membrane also causes the opening of an additional number of potassium channels, as a result of which the permeability of the membrane for potassium ions increases and membrane repolarization occurs.

Rice. 4. Changes in the state of sodium and potassium channels of the membrane depending on the value of the membrane potential

Propagation of action potential

The action potential propagates along the membrane of nerve and muscle cells without decreasing in amplitude with distance. This process is due cable properties plasma membrane, i.e. ability to conduct electric current over short distances. Local electrical current flows into the cell in the active region (where the action potential occurs) and out of the cell in the adjacent inactive region. These ionic currents cause some changes in the membrane potential in the area adjacent to the site of the action potential.

A cyclic local current reduces the membrane charge in the inactive zone and depolarizes it. If depolarization reaches a threshold level, the permeability of the membrane to sodium ions increases and an action potential occurs. Thus, the action potential propagates along nerve and muscle fibers at a constant speed.

Rice. 5. Action potential propagation along the nerve fiber membrane

The speed of action potential propagation in nerve fibers depends on their diameter. It is maximum in the thickest fibers, reaching about 100 meters per second.

PP- this is the difference in electrical potential between the outer and inner sides.

The PP plays an important role in the life of the neuron itself and the organism as a whole. It forms the basis for information processing in the nerve cell, provides regulation of activity internal organs and the musculoskeletal system by triggering the processes of excitation and contraction in the muscle.

Reasons for the formation of PP is the unequal concentration of anions and cations inside and outside the cell.

Formation mechanism:

As soon as at least a little Na + appears in the cell, the potassium-sodium pump begins to operate. The pump begins to exchange its own internal Na + for external K +. Because of this, the cell becomes deficient in Na +, and the cell itself becomes overfilled with potassium ions. K+ begins to leave the cell, because there is an excess of it. In this case, there are more anions in the cell than cations and the cell becomes negatively charged.

13. Characteristics of the action potential and the mechanism of its occurrence.

PD is an electrical process expressed in the fluctuation of membrane potential as a result of the movement of ions into and out of the cell.

Provides signal transmission between nerve cells, between nerve centers and working organs.

The PD consists of three phases:

1. Depolarization (i.e. the disappearance of the cell charge - a decrease in the membrane potential to zero)

2. Inversion (change of cell charge to the opposite, when the inner side of the cell membrane is charged positively, and the outer side is negatively charged)

3. Repolarization (restoration of the original charge of the cell, when the inner surface of the cell membrane is again charged negatively, and the outer surface – positively)

Mechanism of occurrence of PD: if the action of a stimulus on the cell membrane leads to the occurrence of PD, then the process of PD development itself causes phase changes in the permeability of the cell membrane, which ensures the rapid movement of the Na+ ion into the cell, and the K+ ion out of the cell.

14. Synaptic transmission to the central nervous system. Properties of synapses.

Synapse– the point of contact between a nerve cell and another neuron.

1.According to the transmission mechanism:

A. Electrical. In them, excitation is transmitted through an electric field. Therefore, it can be transmitted in both directions. There are few of them in the central nervous system.

b. Chemical. Excitation is transmitted through them using PAF, a neurotransmitter. They are the majority in the central nervous system.

V. Mixed.

2.By localization:

A. Axonodendritic

b. Axosomtic (axon + cell)

V. Axoaxonic

d. Dendrosomatic (dendrite + cell)

d. Dendrodendritic

3. By effect:

A. Exciting (triggering the generation of PD)

b. Inhibiting (preventing the occurrence of PD)

The synapse consists of:

Presynaptic terminal (axon terminal);

Synaptic cleft;

Postsynaptic part (end of dendrite);

Through the synapse, trophic influences are carried out, leading to changes in the metabolism of the innervated cell, its structure and function.

Properties of synapses:

Lack of strong connection between axon and dendrite;

Low lability;

Increased dysfunction;

Transformation of the rhythm of excitation;

Excitation transmission mechanism;

One-sided conduction of excitation;

High sensitivity to drugs and poisons;

The difference in electrical potential (in volts or mV) between the liquid on one side of the membrane and the liquid on the other side is called membrane potential(MP) and is designated Vm. The magnitude of the MF of living cells is usually from -30 to -100 mV and all this potential difference is created in the areas immediately adjacent to the cell membrane on both sides. A decrease in the magnitude of the MP is called depolarization, increase - hyperpolarization, restoration of the original value after depolarization - repolarization. Membrane potential exists in all cells, but in excitable tissues (nervous, muscle, glandular), membrane potential, or as it is also called in these tissues, resting membrane potential, plays a key role in their implementation physiological functions. The membrane potential is determined by two main properties all eukaryotic cells: 1) asymmetric distribution of ions between extra- and intracellular fluid, maintained metabolic processes; 2) Selective permeability of ion channels of cell membranes. To understand how MF occurs, let us imagine that a certain vessel is divided into two compartments by a membrane permeable only to potassium ions. Let the first compartment contain 0.1 M, and the second 0.01 M KCl solution. Since the concentration of potassium ions (K +) in the first compartment is 10 times higher than in the second, then in starting moment for every 10 K+ ions diffusing from compartment 1 to the second, there will be one ion diffusing in the opposite direction. Since chlorine anions (Cl-) cannot pass through the membrane together with potassium cations, an excess of positively charged ions will form in the second compartment and, on the contrary, an excess of Cl- ions will appear in compartment 1. As a result, there arises transmembrane potential difference, preventing further diffusion of K + into the second compartment, since for this they need to overcome the attraction of negative Cl- ions at the moment of entering the membrane from compartment 1 and the repulsion of like ions at the exit from the membrane into compartment 2. Thus, for each K ion + passing through the membrane at this moment, two forces act - a chemical concentration gradient (or a chemical potential difference), facilitating the transition of potassium ions from the first compartment to the second, and an electrical potential difference, causing the K + ions to move in the opposite direction. After these two forces are balanced, the number of K+ ions moving from compartment 1 to compartment 2 and back will be equal and established electrochemical equilibrium. The transmembrane potential difference corresponding to this state is called equilibrium potential, in this particular case, the equilibrium potential for potassium ions ( Ek). At the end of the 19th century, Walter Nernst established that the equilibrium potential depends on the absolute temperature, the valence of the diffusing ion and the ratio of the concentrations of this ion according to different sides membranes:

Where Ex- equilibrium potential for ion X, R- universal gas constant = 1.987 cal/(mol deg), T- absolute temperature in degrees Kelvin, F- Faraday number = 23060 cal/v, Z- charge of the transferred ion, [X] 1 And [X] 2- ion concentration in compartments 1 and 2.

If you go from natural logarithm to decimal, then for a temperature of 18˚C and a monovalent ion we can write the Nernst equation as follows:

Ex = 0.058 lg

Using the Nernst equation, we calculate the potassium equilibrium potential for an imaginary cell, assuming that the extracellular potassium concentration is [K + ]n = 0.01 M, and the intracellular potassium concentration is [K + ]v = 0.1 M:

Ek = 0.058 log = 0.058 log = 0.058 (-1) = -0.058 = -58 mv

IN in this case, Ek negative because potassium ions would leave the hypothetical cell, negatively charging the layer of cytoplasm adjacent to the inside of the membrane. Since there is only one diffusing ion in this hypothetical system, the potassium equilibrium potential will be equal to the membrane potential ( Ek= Vm).

The above mechanism is also responsible for the formation of the membrane potential in real cells, but in contrast to the simplified system considered, in which only one ion could diffuse through the “ideal” membrane, real cell membranes All inorganic ions pass through in one way or another. However, the less permeable the membrane is to any ion, the less effect it has on the MP. Considering this circumstance, Goldman in 1943. an equation was proposed for calculating the value of the MP of real cells, taking into account the concentrations and relative permeability through the plasma membrane of all diffusing ions:

Vm = 0.058 lg

Using the labeled isotope method, Richard Keynes in 1954 determined the permeability of frog muscle cells to major ions. It turned out that the permeability for sodium is approximately 100 times less than for potassium, and the Cl- ion does not make any contribution to the creation of MP. Therefore, for muscle cell membranes, the Goldman equation can be written in the following simplified form:

Vm = 0.058 lg

Vm = 0.058 lg

Studies using microelectrodes inserted into cells have shown that the resting potential of frog skeletal muscle cells ranges from -90 to -100 mV. Such good agreement between the experimental data and the theoretical data confirms that the resting potential is determined by the diffusion fluxes of inorganic ions. Moreover, in real cells the membrane potential is close to the equilibrium potential of the ion, which is characterized by maximum transmembrane permeability, namely the equilibrium potential of the potassium ion.