Resting and action membrane potential. General physiology of excitable tissues
To conduct a signal from the preceding cell to the next, the neuron generates electrical signals within itself. Your eye movements while reading this paragraph, the feeling of an easy chair under your booty, the perception of music from your headphones and much more are based on the fact that hundreds of billions of electrical signals pass inside you. Such a signal can originate in the spinal cord and travel to the tip of the toe along a long axon. Or it can overcome a negligibly small distance in the depths of the brain, limiting itself to the limits of an interneuron with short processes. Any neuron that receives a signal sends it through its body and outgrowths, and this signal is electrical in nature.
As early as 1859, scientists were able to measure the speed at which these electrical signals are transmitted. It turned out that the electricity transmitted along a living axon is fundamentally different from the electric current in metals. An electrical signal is transmitted through a metal wire at a speed close to the speed of light (300,000 kilometers per second), because there are a lot of free electrons in the metal. However, despite this speed, the signal is significantly weakened, overcoming long distances. If signals were transmitted along the axons in the same way that they are transmitted in metals, then the nerve impulse coming from the nerve ending in the skin of your big toe would completely attenuate before reaching your brain - the electrical resistance of organic matter is too high, and the signal is too weak .
Research has shown that electricity travels much more slowly through axons than through wires, and that this transmission is based on a previously unknown mechanism that causes the signal to travel at about 30 meters per second. Electrical signals traveling through nerves, unlike signals traveling through wires, do not weaken as they travel. The reason for this is that the nerve endings do not passively pass the signal through, simply allowing the charged particles in them to pass it on to each other. They are at each of their points an active emitter of this signal, relaying it, and a detailed description of this mechanism will require a separate chapter. Thus, sacrificing the high speed of nerve impulse conduction, due to the active transmission of the signal, the neuron receives a guarantee that the signal that has arisen in the big toe reaches the spinal cord without weakening at all.
To observe the passage of an electrical excitation wave, or action potential (action potential [‘ækʃən pə’tenʃəl]), in a living cell, a simple device is sufficient: one end of a thin metal wire is placed on the outer surface of the axon of the sensory neuron of the skin, and the other is brought to the recorder, which draws a line up when the signal is amplified, and down when it is weakened. Each touch on the skin triggers one or more action potentials. At each potential occurrence, the recorder draws a narrow long peak.
The action potential of a sensory neuron lasts only about 0.001 second and includes two phases: a rapid increase, reaching a peak, and then an almost equally rapid decrease in excitation, leading to the initial position. And then the recorder reports an unexpected fact: all action potentials arising in the same nerve cell are approximately the same. This can be seen in the picture on the left: all the peaks drawn by the recorder have approximately the same shape and amplitude, regardless of how strong or prolonged the touch to the skin that caused them was. A slight stroke or a perceptible pinch will be transmitted by action potentials of the same magnitude. An action potential is a constant signal that obeys the all-or-nothing principle: after the stimulus exceeds a certain threshold value, approximately the same signal always appears, no more and no less than usual. And if the stimulus is less than the threshold value, then the signal will not be transmitted at all: for example, you can touch the skin so lightly with the tip of the pen that this touch will not be felt.
The principle of "all or nothing" in the emergence of the action potential raises new questions. How does a sensory neuron report the strength of a stimulus - strong or weak pressure, bright or dim light? How does he report the duration of the stimulus? Finally, how do neurons distinguish one type of sensory information from another—for example, how do they distinguish between touch and pain, light, smell, or sound? And how do they distinguish sensory information for perception from motor information for action?
Evolution has solved the problem of how to communicate the strength of a stimulus by using the same kind of signals of the same magnitude: this strength is determined by frequency(frequency [‘friːkwənsɪ] ), with which action potentials are emitted. A weak stimulus, such as a light touch on the arm, results in the emission of only two or three action potentials per second, while strong pressure, as when pinching or hitting the elbow, can cause a burst of hundreds of action potentials per second. In this case, the duration of sensation is determined by the duration of the occurrence of action potentials.
Do neurons use different electrical codes to tell the brain that they carry information about different stimuli, such as pain, light, or sound? It turned out not! Surprisingly, there is very little difference between the action potentials generated by neurons from different sensory systems (such as visual or tactile)! Thus, the nature and nature of the sensation is independent of differences in action potentials (which opens up a rather exciting perspective for thinking about the "matrix" from the movie of the same name). The neuron that transmits auditory information is built in exactly the same way as the neuron from the optic nerve circuit, and they conduct the same action potentials in the same way. Without knowing which neural circuit a particular neuron belongs to, it is impossible to determine what information it carries only by analyzing its functioning.
The nature of the transmitted information depends primarily on the type of excitable nerve fibers and the specific brain systems with which these fibers are associated. Sensations of each type are transmitted along their own conducting paths, and the type of information transmitted by a neuron depends precisely on the path that this neuron is part of. In any sensory pathway, information is transmitted from the first sensory neuron (a receptor that responds to an external stimulus such as touch, smell, or light) to specialized neurons in the spinal cord or brain. Thus, visual information differs from auditory information only in that it is transmitted along other pathways that begin in the retina of the eye and end in the area of the brain that is responsible for visual perception.
The signals sent from the motor neurons of the brain to the muscles are also almost identical to those sent by the sensory neurons from the skin to the brain. They follow the same “all or nothing” principle, they also transmit the intensity of the signal using the frequency of action potentials, and the result of the signal also depends only on which neural circuit this neuron is included in. Thus, a rapid succession of action potentials along a certain pathway causes the movement of your fingers, and not, say, the perception of colored lights, only because this path is associated with the muscles of the hands, and not with the retina of the eyes.
The universality of action potentials is not limited by the similarity of their manifestation in different neurons within the same organism. They are so similar in different animals that even an experienced researcher is not able to accurately distinguish the recording of the action potential of the nerve fiber of a whale, mouse, monkey, or his supervisor. Nevertheless, action potentials in different cells are not identical: there is still a slight difference in their amplitude and duration, and the statement "all action potentials are the same" is just as inaccurate as the statement "all bougainvilleas are the same."
So, each neuron transmits a signal through its body and processes in the same way. All the variety of information we receive from sensory neurons, all the movements that our body can make, are the result of the transmission of a single type of signal within neurons. There remains a "trifle": to understand what kind of signal it is and how it is transmitted.
We habitually separate everything that we consider living nature, including ourselves, from “non-living” things, including metals and the electric current transmitted through them. It is all the more surprising to realize that metals are not just present in our bodies - they are necessary, without them the body cannot exist. An electric current is not a one-time phenomenon, but continuously occurring in hundreds of billions of neurons that have pierced our entire body with their processes. Right now you can feel all sorts of signs of his presence: your awareness of this text is the result of countless transmissions of electric current. The feeling of hunger and pleasure from the smell of food being prepared, the very perception of this smell, the touch of the wind flying through the window to your skin ... The list is endless. And the desire to understand how all this happens is also made up of electrical impulses that arise in neurons.
Since the purpose of this chapter is to communicate only the most general information about the passage of a nerve impulse, it is also necessary here to consider the environment in which it occurs, those conditions in the cell that make its occurrence and transmission possible. Therefore, it is worth starting with studying the springboard on which events will develop, namely from a neuron to resting state (dormant state [‘dɔːmənt steɪt]).
Back in the middle of the last century, scientists found a way to determine in which part of the neuron there is an electric charge. For this use voltmeter (voltmeter [‘vəultˌmiːtə]) (a device for measuring the voltage of an electric field) with two electrodes. One electrode is placed inside the neuron, placing it close to the cell membrane, and the second electrode is placed in the environment surrounding the neuron, on the other side of the same membrane. The voltmeter shows that on different sides of the cell membrane there are electric charges, negative inside the cell and positive outside. The existence of such electric charges of different poles on both sides of the membrane creates an electric field, an important characteristic of which is potential. Potential, in simple terms, is the ability to do work, such as the work of dragging a charged particle from place to place. The more negative charges accumulated on one side, and the more positive charges accumulated on the other side of the membrane, the stronger the electric field they create, and the more force they are able to drag charged particles back and forth. The difference between external and internal electric charges is called membrane potential (membrane potential [‘membreɪn pə’tenʃəl]) rest. For a neuron, it is approximately 70 mV (millivolts), that is, 70 thousandths of a volt, or seven hundredths of a volt. For comparison, the potential difference in an AA battery is 1.5 volts - 20 times more. That is, the resting membrane potential of a neuron is only 20 times weaker than between the terminals of an AA battery - quite large, it turns out. The electric potential exists only on the membrane, and in its other parts the neuron is electrically neutral.
More precisely, the resting membrane potential of a neuron is -70 mV (minus seventy millivolts). The minus sign only means that the negative charge is inside the cell, and not outside, and thus the electric field created is able to drag positively charged ions through the membrane into the cell.
Actors in the creation of the resting membrane potential:
1 . IN cell membrane neurons have channels through which ions carrying an electric charge can travel through it. At the same time, the membrane is not just a passive "partition" between the internal environment of the neuron and the intercellular fluid surrounding it: special proteins embedded in the flesh of the membrane open and close these channels, and thus the membrane controls the passage of ions - atoms that have an electric charge. Accumulating negatively charged ions inside the cell, the neuron increases the amount of negative charges inside, thereby leading to an increase in positive charges outside, and thus the electrical potential increases. Since the proton has a positive charge, and the electron is negative, then with an excess of protons, a positively charged ion is obtained, and with an excess of electrons, a negatively charged one. If you want more detailed information about atoms and ions, you can return to. It is important to understand that the membrane potential exists exactly at the border of the cell membrane, and the fluids in general inside and outside the neuron remain electrically neutral. Ions, for which the membrane is permeable, remain close to it, since positive and negative charges are mutually attracted to each other. As a result, a layer of positive ions “sitting” on it is formed outside the membrane, and negative ions inside. Thus, the membrane plays the role of an electrical capacitance that separates charges, inside which there is an electric field. The membrane is therefore a natural capacitor.
2 . negatively charged proteins located inside the neuron near the inner surface of the membrane. The charge on proteins always remains the same and is only a fraction of the total charge on the inner surface of the membrane. Unlike ions, proteins cannot enter and leave the cell - they are too large for this. The total charge varies depending on the number of positively charged ions located near the membrane, the concentration of which can change due to their movement from the cell to the outside, and from the outside to the inside.
3 . positively charged potassium ions (K+) can move freely between the internal and external environment when the neuron is at rest. They move through permanently open flow potassium channels (flow potassium passage), through which only K + ions can pass, and nothing else. Flow channels are channels that do not have gates, which means that they are open in any state of the neuron. There are much more potassium ions inside the cell than outside. This is due to the constant operation of the sodium-potassium pump (it will be discussed below), therefore, in the resting state of the neuron, K + ions begin to move into the external environment, since the concentration of the same substance tends to equalize in the general system. If we pour some substance into a pool of water in one corner, then its concentration in this corner will be very large, and in other parts of the pool it will be zero or very small. However, after some time, we will find that the concentration of this substance has leveled off throughout the basin due to Brownian motion. In this case, one speaks of the "partial pressure" of a particular substance, be it a liquid or a gas. If alcohol is poured into one corner of the pool, there will be a large difference in the concentration of alcohol between this corner and the rest of the pool. There will be a partial pressure of alcohol molecules, and they will gradually be distributed evenly over the pool so that the partial pressure will disappear, since the concentration of alcohol molecules will even out everywhere. Thus, K + ions carry a positive charge from the neuron with them, leaving due to the partial pressure, which is stronger than the attractive force of negatively charged proteins, if the difference in the concentration of ions inside and outside the cell is large enough. Since negatively charged proteins remain inside, a negative charge is thus formed on the inside of the membrane. For a clear understanding of the work of cellular mechanisms, it is important to remember that despite the constant outflow of potassium ions from the cell, there are always more of them inside the neuron than outside.
4 . positively charged sodium ions (Na +) are on the outside of the membrane and create a positive charge there. During the resting phase of the neuron, the sodium channels of the cell closed, and Na + cannot pass inside, and their concentration outside increases due to the work of the sodium-potassium pump, which removes them from the neuron.
5 . the role of negatively charged chloride ions (Cl -) and positively charged calcium ions (Ca 2+) to create a membrane potential is small, so their behavior will remain behind the scenes for the time being.
Formation of the resting membrane potential takes place in two stages:
Stage I. a small (-10 mV) potential difference is created using sodium potassium pump.
Unlike other membrane channels, the sodium-potassium channel is capable of passing both sodium and potassium ions through itself. Moreover, Na + can pass through it only from the cell to the outside, and K + from the outside to the inside. One cycle of this channel includes 4 steps:
1 . The "gates" of the sodium-potassium channel are open only on the inner side of the membrane, and 3 Na + enter there
2 . the presence of Na + inside the channel affects it so that it can partially destroy one molecule ATP(ATP) ( adenosine triphosphate), (adenosine triphosphate) which is the "accumulator" of the cell, storing energy and giving it away when necessary. With such partial destruction, which consists in the splitting off of one phosphate group PO 4 3− from the end of the molecule, energy is released, which is exactly what is spent on the transfer of Na + to the external space.
3 . when the channel opens for Na + to come out, it remains open, and two K + ions enter it - they are attracted by the negative charges of proteins from the inside. The fact that only two potassium ions are placed in a channel containing three sodium ions is quite logical: the potassium atom has a larger diameter.
4 . the presence of potassium ions now, in turn, acts on the channel so that the outer “gates” close and the inner ones open, and K + enters the internal environment of the neuron.
This is how the sodium-potassium pump works, "exchanging" three sodium ions for two potassium ions. Since the electric charge of Na + and K + is the same, it turns out that three positive charges are removed from the cell, and only two get inside. Due to this, the internal positive charge of the cell membrane decreases, and the external one increases. In addition, a difference is created in the concentration of Na + and K + on opposite sides of the membrane:
=) there are a lot of sodium ions outside the cell, and few inside. At the same time, sodium channels are closed, and Na + cannot get back into the cell, and it does not go far from the membrane, since it is attracted by the negative charge existing on the inside of the membrane.
=) there are a lot of potassium ions inside the cell, but there are few of them outside, and this leads to the leakage of K + from the cell through the potassium channels open during the resting phase of the neuron.
Stage II The formation of the resting membrane potential is just based on this outflow of potassium ions from the neuron. The figure on the left shows the ionic composition of the membrane at the beginning of the second stage of the formation of the resting potential: a lot of K + and negatively charged proteins (designated A 4-) inside, and Na + stuck around the membrane outside. Moving into the external environment, potassium ions carry away their positive charges from the cell, while the total charge of the inner membrane decreases. Just like positive sodium ions, potassium ions flowing out of the cell remain outside the membrane, attracted by the internal negative charge, and the external positive charge of the membrane is the sum of the Na + and K + charges. Despite the outflow through the flow channels, there are always more potassium ions inside the cell than outside.
The question arises: why don't potassium ions continue to flow out until the moment when their number inside the cell and outside it becomes the same, that is, until the partial pressure created by these ions disappears? The reason for this is that when K+ leaves the cell, there is an increase in positive charge on the outside and an excess of negative charge on the inside. This reduces the desire of potassium ions to leave the cell, because the external positive charge repels them, and the internal negative one attracts them. Therefore, after some time, K + cease to flow out despite the fact that their concentration in the external environment is lower than in the internal one: the influence of charges on different sides of the membrane exceeds the force of partial pressure, that is, it exceeds the desire of K + to be distributed evenly in the liquid inside and outside neuron. At the moment this equilibrium is reached, the membrane potential of the neuron stops at about -70 mV.
As soon as the neuron reaches the resting membrane potential, it is ready for the emergence and conduction of the action potential, which will be discussed in the next cytological chapter.
So let's summarize: the uneven distribution of potassium and sodium ions on both sides of the membrane is caused by the action of two competing forces: a) the force of electrical attraction and repulsion, and b) the force of partial pressure arising from the difference in concentrations. The work of these two competing forces proceeds under the conditions of the existence of differently arranged sodium, potassium and sodium-potassium channels, which act as regulators of the action of these forces. The potassium channel is flow-through, meaning it is always open when the neuron is at rest, so that K+ ions can easily move back and forth under the influence of electrical repulsion/attraction forces and under the influence of forces caused by partial pressure, that is, the difference in concentration of these ions. The sodium channel is always closed when the neuron is at rest, so Na + ions cannot pass through them. And finally, the sodium-potassium channel, designed so that it works like a pump, which, with each cycle, pushes three sodium ions out, and pushes two potassium ions in.
All this construction ensures the emergence of the resting membrane potential of the neuron: i.e. a state in which two things are achieved:
a) there is a negative charge inside and a positive charge outside.
b) there are a lot of K + ions inside, clinging to the negatively charged parts of proteins, and thus potassium partial pressure arises - the tendency of potassium ions to go outside to equalize the concentration.
c) there are many Na + ions outside, partly forming pairs with Cl - ions. And thus, sodium partial pressure arises - the desire of sodium ions to enter the inside of the cell to equalize the concentration.
As a result of the operation of the potassium-sodium pump, we get three forces that exist on the membrane: the force of the electric field and the force of two partial pressures. These forces begin to work when the neuron leaves the state of rest.
All living cells have the ability, under the influence of stimuli, to move from a state of physiological rest to a state of activity or excitation.
Excitation- this is a complex of active electrical, chemical and functional changes in excitable tissues (nervous, muscular or glandular), with which the tissue responds to external influences. An important role in excitation is played by electrical processes that ensure the conduction of excitation along nerve fibers and bring tissues into an active (working) state.
Membrane potential
Living cells have an important property: the inner surface of the cell is always negatively charged with respect to its outer side. Between the outer surface of the cell, charged electropositively in relation to the protoplasm, and the inner side of the cell membrane, there is a potential difference that ranges from 60-70 mV. According to P. G. Kostyuk (2001), in a nerve cell, this difference ranges from 30 to 70 mV. The potential difference between the outer and inner sides of the cell membrane is called membrane potential. or resting potential(Fig. 2.1).
The resting membrane potential is present on the membrane as long as the cell is alive and disappears with cell death. L. Galvani, back in 1794, showed that if a nerve or muscle is damaged by making a cross section and applying electrodes connected to a galvanometer to the damaged part and to the site of damage, the galvanometer will show the current that always flows from the undamaged part of the tissue to the incision site . He called this current the quiescent current. In their physiological essence, the resting current and the resting membrane potential are one and the same. The potential difference measured in this experiment is 30-50 mV, since in case of tissue damage, part of the current is shunted in the intercellular space and the fluid surrounding the structure under study. The potential difference can be calculated using the Nernst formula:
where R - gas constant, T - absolute temperature, F - Faraday number, [K] ext. and [K] adv. - the concentration of potassium inside and outside the cell.
Rice. 2.1.
The reason for the occurrence of the resting potential is common to all cells. Between the protoplasm of the cell and the extracellular environment there is an uneven distribution of ions (ionic asymmetry). The composition of human blood in terms of salt balance resembles the composition of ocean water. The extracellular environment in the central nervous system also contains a lot of sodium chloride. The ionic composition of the cytoplasm of cells is poorer. Inside the cells, there are 8-10 times less Na + ions and 50 times less C ions! ". The main cytoplasmic cation is K +. Its concentration inside the cell is 30 times higher than in the extracellular environment, and approximately equals the extracellular concentration of Na. The main counterions for K + in the cytoplasm are organic anions, in particular anions of aspartic, histamine and other amino acids.Such asymmetry is a violation of thermodynamic equilibrium.In order to restore it, potassium ions must gradually leave the cell, and sodium ions should strive into it.However, this is not happening.
The first obstacle to leveling the difference in ion concentrations is the plasma membrane of the cell. It consists of a double layer of phospholipid molecules, covered from the inside by a layer of protein molecules, and from the outside by a layer of carbohydrates (mucopolysaccharides). Some of the cellular proteins are built directly into the lipid bilayer. These are internal proteins.
Membrane proteins of all cells are divided into five classes: pumps, channels, receptors, enzymes And structural proteins. Pumps serve to move ions and molecules against concentration gradients, using metabolic energy for this. protein channels, or pores, provide selective permeability (diffusion) through the membrane of ions and molecules corresponding to them in size. receptor proteins, having high specificity, they recognize and bind, attaching to the membrane, many types of molecules necessary for the life of the cell at any given time. Enzymes accelerate the course of chemical reactions at the membrane surface. Structural proteins ensure the connection of cells into organs and the maintenance of the subcellular structure.
All of these proteins are specific, but not strictly. Under certain conditions, a particular protein can be both a pump, an enzyme, and a receptor at the same time. Through the channels of the membrane, water molecules, as well as ions corresponding to the size of the pores, enter and leave the cell. The permeability of the membrane for different cations is not the same and changes with different functional states of the tissue. At rest, the membrane is 25 times more permeable to potassium ions than to sodium ions, and when excited, sodium permeability is about 20 times higher than potassium. At rest, equal concentrations of potassium in the cytoplasm and sodium in the extracellular environment should provide an equal amount of positive charges on both sides of the membrane. But since the permeability for potassium ions is 25 times higher, potassium, leaving the cell, makes its surface more and more positively charged with respect to the inner side of the membrane, near which negatively charged molecules of aspartic, histamine and other molecules that are too large for membrane pores accumulate more and more. amino acids that “released” potassium outside the cell, but “not allowing” it to go far due to its negative charge. Negative charges accumulate on the inside of the membrane, and positive charges accumulate on the outside. There is a potential difference. The diffuse current of sodium ions into the protoplasm from the extracellular fluid keeps this difference at the level of 60-70 mV, preventing it from increasing. The diffuse current of sodium ions at rest is 25 times weaker than the countercurrent of potassium ions. Sodium ions, penetrating into the cell, reduce the value of the resting potential, allowing it to be held at a certain level. Thus, the value of the resting potential of muscle and nerve cells, as well as nerve fibers, is determined by the ratio of the number of positively charged potassium ions diffusing out of the cell per unit time and positively charged sodium ions diffusing through the membrane in the opposite direction. The higher this ratio, the greater the value of the resting potential, and vice versa.
The second obstacle that keeps the potential difference at a certain level is the sodium-potassium pump (Fig. 2.2). It was called sodium-potassium or ionic, since it actively removes (pumps out) sodium ions penetrating into it from the protoplasm and introduces (injects) potassium ions into it. The energy source for the operation of the ion pump is the breakdown of ATP (adenosine triphosphate), which occurs under the influence of the enzyme adenosine triphosphatase, localized in the cell membrane and activated by the same ions, i.e. potassium and sodium (sodium-potassium-dependent ATP-ase).
Rice. 2.2.
It is a large protein that is larger than the thickness of the cell membrane. The molecule of this protein, penetrating the membrane through, binds predominantly sodium and ATP on the inside, and potassium and various inhibitors such as glycosides on the outside. This creates a membrane current. Due to this current, the appropriate direction of ion transport is ensured. The transfer of ions occurs in three stages. First, an ion combines with a carrier molecule to form an ion-carrier complex. This complex then passes through the membrane or transfers a charge across it. Finally, the ion is released from the carrier on the opposite side of the membrane. At the same time, a similar process takes place, transporting ions in the opposite direction. If the pump transfers one sodium ion to one potassium ion, then it simply maintains the concentration gradient on both sides of the membrane, but does not contribute to the creation of the membrane potential. To make this contribution, the ion pump must transfer sodium and potassium in a ratio of 3:2, i.e., for 2 potassium ions entering the cell, it must remove 3 sodium ions from the cell. When operating at maximum load, each pump is capable of pumping about 130 potassium ions and 200 sodium ions through the membrane per second. This is the top speed. In real conditions, each pump is regulated according to the needs of the cell. Most neurons have 100 to 200 ion pumps per square micron of membrane surface. Therefore, the membrane of any nerve cell contains 1 million ion pumps capable of moving up to 200 million sodium ions per second.
Thus, the membrane potential (resting potential) is created as a result of both passive and active mechanisms. The degree of participation of certain mechanisms in different cells is not the same, which means that the membrane potential may be different in different structures. The activity of the pumps may depend on the diameter of the nerve fibers: the thinner the fiber, the higher the ratio of the surface size to the volume of the cytoplasm, respectively, and the activity of the pumps required to maintain the difference in ion concentrations on the surface and inside the fiber should be greater. In other words, the membrane potential may depend on the structure of the nervous tissue, and hence on its functional purpose. The electrical polarization of the membrane is the main condition that ensures cell excitability. This is her constant readiness for action. This is the cell's store of potential energy, which it can use in case the nervous system needs its immediate response.
Why do we need to know what the resting potential is?
What is "animal electricity"? Where do biocurrents come from in the body? How can a living cell in an aquatic environment turn into an "electric battery"?
We can answer these questions if we learn how the cell, through redistributionelectric charges creates for himself electric potential on the membrane.
How does the nervous system work? Where does it all begin? Where does the electricity for nerve impulses come from?
We can also answer these questions if we learn how a nerve cell creates an electrical potential for itself on the membrane.
So, understanding how the nervous system works begins with understanding how a single nerve cell, a neuron, works.
And at the heart of the work of a neuron with nerve impulses lies redistributionelectric charges on its membrane and a change in the magnitude of electrical potentials. But in order for the potential to change, you must first have it. Therefore, we can say that a neuron, preparing for its nervous work, creates an electrical potential as an opportunity for such work.
Thus, our very first step to studying the functioning of the nervous system is to understand how electrical charges move on nerve cells and how, due to this, an electrical potential appears on the membrane. This is what we will do, and we will call this process of the appearance of an electrical potential in neurons - resting potential formation.
Definition
Normally, when a cell is ready to work, it already has an electrical charge on the surface of the membrane. It is called resting membrane potential .
The resting potential is the difference in electrical potential between the inner and outer sides of the membrane when the cell is in a state of physiological rest. Its average value is -70 mV (millivolts).
"Potential" is an opportunity, it is akin to the concept of "potency". The electrical potential of a membrane is its ability to move electrical charges, positive or negative. In the role of charges are charged chemical particles - sodium and potassium ions, as well as calcium and chlorine. Of these, only chloride ions are negatively charged (-), while the rest are positively charged (+).
Thus, having an electrical potential, the membrane can move the above charged ions into or out of the cell.
It is important to understand that in the nervous system, electric charges are created not by electrons, as in metal wires, but by ions - chemical particles that have an electric charge. Electric current in the body and its cells is a flow of ions, not electrons, as in wires. Note also that the membrane charge is measured from within cells, not outside.
Speaking quite primitively simply, it turns out that "pluses" will prevail outside around the cell, i.e. positively charged ions, and inside - "minus signs", i.e. negatively charged ions. We can say that inside the cage electronegative . And now we just need to explain how it happened. Although, of course, it is unpleasant to realize that all our cells are negative "characters". ((
Essence
The essence of the resting potential is the predominance of negative electric charges in the form of anions on the inside of the membrane and the lack of positive electric charges in the form of cations, which are concentrated on its outside, and not on the inside.
Inside the cell - "negativity", and outside - "positivity".
This state of affairs is achieved through three phenomena: (1) the behavior of the membrane, (2) the behavior of positive potassium and sodium ions, and (3) the relationship between chemical and electrical force.
1. Membrane behavior
Three processes are important in the behavior of the membrane for the resting potential:
1) Exchange internal sodium ions to external potassium ions. The exchange is carried out by special membrane transport structures: ion exchanger pumps. In this way, the membrane oversaturates the cell with potassium, but depletes with sodium.
2) open potash ion channels. Through them, potassium can both enter the cell and leave it. He goes out basically.
3) Closed sodium ion channels. Because of this, sodium removed from the cell by exchange pumps cannot return to it. Sodium channels open only under special conditions - and then the resting potential is disturbed and shifted towards zero (this is called depolarization membranes, i.e. decrease in polarity).
2. Behavior of potassium and sodium ions
Potassium and sodium ions move across the membrane in different ways:
1) Through ion exchange pumps, sodium is forcibly removed from the cell, and potassium is dragged into the cell.
2) Through constantly open potassium channels, potassium leaves the cell, but can also return to it back through them.
3) Sodium "wants" to enter the cell, but "can't", because channels are closed to him.
3. The ratio of chemical and electrical forces
In relation to potassium ions, a balance is established between the chemical and electrical forces at a level of - 70 mV.
1) Chemical force pushes potassium out of the cell, but tends to draw sodium into it.
2) Electrical the force tends to draw positively charged ions (both sodium and potassium) into the cell.
Resting potential formation
I will try to tell you briefly where the resting membrane potential comes from in nerve cells - neurons. After all, as everyone now knows, our cells are only positive on the outside, but inside they are very negative, and in them there is an excess of negative particles - anions and a lack of positive particles - cations.
And here one of the logical traps awaits the researcher and student: the internal electronegativity of the cell does not arise due to the appearance of extra negative particles (anions), but, on the contrary, due to the loss of a certain amount of positive particles (cations).
And therefore, the essence of our story will not be that we will explain where the negative particles come from in the cell, but that we will explain how the deficit of positively charged ions - cations - is obtained in neurons.
Where do positively charged particles go from the cell? Let me remind you that these are sodium ions - Na + and potassium - K +.
Sodium-potassium pump
And the whole point is that in the membrane of the nerve cell constantly work exchanger pumps formed by special proteins embedded in the membrane. What are they doing? They change the "own" sodium of the cell to the external "foreign" potassium. Because of this, the cell ends up with a lack of sodium, which has gone to the exchange. And at the same time, the cell is overflowing with potassium ions, which these molecular pumps have dragged into it.
To make it easier to remember, figuratively, you can say this: The cell loves potassium!"(Although true love is out of the question here!) Therefore, she drags potassium into herself, despite the fact that it is already full of it. Therefore, she unprofitably exchanges it for sodium, giving 3 sodium ions for 2 potassium ions. Therefore it spends ATP energy on this exchange, and how it spends!
By the way, it is interesting that a cell is not born with a resting potential in its finished form. For example, during differentiation and fusion of myoblasts, the potential of their membrane changes from -10 to -70 mV, i.e. their membrane becomes more electronegative, it polarizes during differentiation. And in experiments on multipotent mesenchymal stromal cells (MMSC) of human bone marrow artificial depolarization inhibited differentiation cells (Fischer-Lougheed J., Liu JH, Espinos E. et al. Human myoblast fusion requires expression of functional inward rectifier Kir2.1 channels. Journal of Cell Biology 2001; 153: 677-85; Liu JH, Bijlenga P., Fischer-Lougheed J. et al. Role of an inward rectifier K+ current and of hyperpolarization in human myoblast fusion. Journal of Physiology 1998; 510: 467-76; Sundelacruz S., Levin M., Kaplan DL Membrane potential controls adipogenic and osteogenic differentiation of mesenchymal stem cells Plos One 2008; 3).
Figuratively speaking, it can be expressed as follows:
By creating a resting potential, the cell is "charged with love."
It's love for two things:
1) cell love for potassium,
2) the love of potassium for freedom.
Oddly enough, but the result of these two types of love is emptiness!
It is this emptiness that creates a negative electric charge in the cell - the rest potential. More precisely, a negative potential is createdempty spaces left from the potassium that escaped from the cell.
So, the result of the activity of membrane ion exchanger pumps is as follows:
The sodium-potassium ion exchange pump creates three potentials (opportunities):
1. Electric potential - the ability to draw positively charged particles (ions) into the cell.
2. Ionic sodium potential - the ability to draw sodium ions into the cell (and sodium ions, and not any others).
3. Ionic potassium potential - the ability to push potassium ions out of the cell (and it is potassium, and not any others).
1. Sodium deficiency (Na +) in the cell.
2. Excess potassium (K +) in the cell.
We can say this: membrane ion pumps create concentration difference ions, or gradient (difference) concentration between the intracellular and extracellular environment.
It is because of the resulting sodium deficiency that this very sodium will now "crawl" into the cell from the outside. This is how substances always behave: they tend to equalize their concentration in the entire volume of the solution.
And at the same time, an excess of potassium ions was obtained in the cell compared to the external environment. Because the membrane pumps pumped it into the cell. And he seeks to equalize his concentration inside and outside, and therefore seeks to get out of the cage.
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 in a cell, it is necessary to separately compare the concentrations of sodium and potassium ions. Those. it is necessary to separately compare the concentration of sodium inside and outside the cell and separately the concentration of potassium inside and outside the cell, but it makes no sense to compare sodium with potassium, as is often done in textbooks.
According to the law of concentration equalization, which operates in solutions, sodium "wants" to enter the cell from the outside. But it cannot, since the membrane in its normal state does not pass it well. It enters a little and the cell again immediately exchanges it for external potassium. Therefore, sodium in neurons is always in short supply.
But potassium just can easily go out of the cell! The cage is full of him, and she can't keep him. So it comes out through special protein holes in the membrane (ion channels).
Analysis
From chemical to electrical
And now - the most important thing, follow the stated thought! We must move from the movement of chemical particles to the movement of electric charges.
Potassium is charged with a positive charge, and therefore, when it leaves the cell, it takes out of it not only itself, but also "pluses" (positive charges). In their place, "minuses" (negative charges) remain in the cell. This is the resting membrane potential!
The resting membrane potential is a deficit of positive charges inside the cell, formed due to the leakage of positive potassium ions from the cell.
Conclusion
Rice. Resting potential (RP) formation scheme. The author thanks Ekaterina Yurievna Popova for her help in creating the drawing.
Components of the resting potential
The resting potential is negative from the side of the cell and consists, as it were, of two parts.
1. The first part is approximately -10 millivolts, which are obtained from the non-equilateral operation of the membrane exchanger pump (after all, it pumps out more “pluses” with sodium than it pumps back with potassium).
2. The second part is potassium leaking out of the cell all the time, dragging positive charges out of the cell. It gives most of the membrane potential, bringing it down to -70 millivolts.
Potassium will stop leaving the cell (more precisely, its input and output will be equal) only when the electronegativity level of the cell is -90 millivolts. But this is hindered by sodium constantly leaking into the cell, which drags its positive charges with it. And the cell maintains an equilibrium state at the level of -70 millivolts.
Note that it takes energy to create the resting potential. These costs are produced by ion pumps that exchange "own" internal sodium (Na + ions) for "foreign" external potassium (K +). Recall that ion pumps are ATPase enzymes and break down ATP, receiving energy from it for the indicated exchange of different types of ions with each other. It is very important to understand that 2 potentials “work” with the membrane at once: chemical (concentration gradient of ions) and electric ( electric potential difference on opposite sides of the membrane). Ions move in one direction or another under the action of both of these forces, on which energy is spent. In this case, one of the two potentials (chemical or electrical) decreases, while the other increases. Of course, if we consider the electric potential (potential difference) separately, then the "chemical" forces that move the ions will not be taken into account. And then there may be an incorrect impression that the energy for the movement of the ion is taken, as it were, from nowhere. But it's not. Both forces must be considered: chemical and electrical. In this case, large molecules with negative charges located inside the cell play the role of "extras", because they are not moved across the membrane by either chemical or electrical forces. Therefore, these negative particles are usually not considered, although they exist and it is they that provide the negative side of the potential difference between the inner and outer sides of the membrane. But nimble potassium ions are just capable of moving, and it is their leakage from the cell under the influence of chemical forces that creates the lion's share of the electrical potential (potential difference). After all, it is potassium ions that move positive electric charges to the outer side of the membrane, being positively charged particles.
So it's all about the sodium-potassium membrane exchanger pump and the subsequent outflow of "excess" potassium from the cell. Due to the loss of positive charges during this leakage, electronegativity increases inside the cell. It is this "membrane resting potential". It is measured inside the cell and is usually -70 mV.
conclusions
Figuratively speaking, "the membrane turns the cell into an "electric battery" by controlling ionic flows."
The resting membrane potential is formed due to two processes:
1. Operation of the sodium-potassium membrane pump.
The work of the potassium-sodium pump, in turn, has 2 consequences:
1.1. Direct electrogenic (generating electrical phenomena) action of the ion pump-exchanger. This is the creation of a small electronegativity inside the cell (-10 mV).
The unequal exchange of sodium for potassium is to blame for this. More sodium is expelled from the cell than potassium is metabolized. And along with sodium, more “pluses” (positive charges) are removed than are returned with potassium. There is a small deficit of positive charges. The membrane is negatively charged from the inside (approximately -10 mV).
1.2. Creation of prerequisites for the emergence of large electronegativity.
These prerequisites are an unequal concentration of potassium ions inside and outside the cell. Excess potassium is ready to leave the cell and carry positive charges out of it. We will talk about this below.
2. Leakage of potassium ions from the cell.
From the zone of increased concentration inside the cell, potassium ions go to the zone of low concentration outside, at the same time carrying positive electrical charges. There is a strong deficit of positive charges inside the cell. As a result, the membrane is additionally charged negatively from the inside (up to -70 mV).
The final
The potassium-sodium pump creates the prerequisites for the emergence of the resting potential. This is the difference in ion concentration between the inside and outside of the cell. Separately, the difference in concentration for sodium and the difference in concentration for potassium manifest themselves. The cell's attempt to equalize the concentration of ions with potassium leads to a loss of potassium, a loss of positive charges, and generates electronegativity within the cell. This electronegativity makes up most of the resting potential. A smaller part of it is the direct electrogenicity of the ion pump, i.e. the predominant loss of sodium during its exchange for potassium.
Video: Resting membrane potential
It has been established that the most important ions that determine the membrane potentials of cells are inorganic ions K + , Na + , SG, and in some cases Ca 2 + . It is well known that the concentrations of these ions in the cytoplasm and in the intercellular fluid differ tenfold.
From Table. 11.1 it can be seen that the concentration of K + ions inside the cell is 40-60 times higher than in the intercellular fluid, while for Na + and SG the distribution of concentrations is opposite. The uneven distribution of the concentrations of these ions on both sides of the membrane is provided both by their different permeability and by the strong electric field of the membrane, which is determined by its resting potential.
Indeed, at rest the total flux of ions through the membrane is zero, and then it follows from the Nernst-Planck equation that
Thus, at rest concentration gradients - and
electric potential - directed at the membrane
opposite to each other and therefore, in a resting cell, a high and constant difference in the concentrations of the main ions ensures that an electrical voltage is maintained on the cell membrane, which is called equilibrium membrane potential.
In turn, the resting potential arising on the membrane prevents the release of ions from the K + cell and the excessive entry of SG into it, thereby maintaining their concentration gradients on the membrane.
A complete expression for the membrane potential, taking into account the diffusion fluxes of these three types of ions, was obtained by Goldman, Hodgkin and Katz:
where R k, P Na , P C1 - membrane permeability for the corresponding ions.
Equation (11.3) determines the resting membrane potentials of various cells with high accuracy. It follows from this that for the resting membrane potential, it is not the absolute values of the membrane permeability for various ions that are important, but their ratios, since by dividing both parts of the fraction under the sign of the logarithm, for example, by P k, we will move on to the relative permeability of ions.
In cases where the permeability of one of these ions is much greater than the others, equation (11.3) goes into the Nernst equation (11.1) for this ion.
From Table. 11.1 it can be seen that the resting membrane potential of cells is close to the Nernst potential for K + and CB ions, but differs significantly from it in Na +. This testifies
The fact that at rest the membrane is well permeable to K + and SG ions, while its permeability to Na + ions is very low.
Despite the fact that the equilibrium Nernst potential for SG is closest to the resting potential of the cell, the latter has a predominantly potassium nature. This is due to the fact that a high intracellular concentration of K + cannot decrease significantly, since K + ions must balance the volume negative charge of anions inside the cell. Intracellular anions are mainly large organic molecules (proteins, organic acid residues, etc.) that cannot pass through the channels in the cell membrane. The concentration of these anions in the cell is practically constant and their total negative charge prevents a significant release of potassium from the cell, maintaining its high intracellular concentration together with the Na-K pump. However, the main role in the initial establishment of a high concentration of potassium ions and a low concentration of sodium ions inside the cell belongs to the Na-K pump.
The distribution of C1 ions is established in accordance with the membrane potential, since there are no special mechanisms in the cell to maintain the concentration of SG. Therefore, due to the negative charge of chlorine, its distribution is reversed with respect to the distribution of potassium on the membrane (see Table 11.1). Thus, the concentration diffusion of K + from the cell and C1 into the cell are practically balanced by the resting membrane potential of the cell.
As for Na + , at rest its diffusion is directed into the cell under the action of both the concentration gradient and the electric field of the membrane, and the entry of Na + into the cell is limited at rest only by the low permeability of the membrane for sodium (sodium channels are closed). Indeed, Hodgkin and Katz experimentally established that at rest the permeability of the squid axon membrane for K + , Na + and SG is related as 1: 0.04: 0.45. Thus, at rest, the cell membrane is poorly permeable only for Na + , and for SG it is permeable almost as well as for K + . In nerve cells, the permeability for SG is usually lower than for K + , but in muscle fibers, the permeability for SG even somewhat predominates.
Despite the low permeability of the cell membrane for Na + at rest, there is, albeit a very small, passive transfer of Na + into the cell. This current of Na + should have led to a decrease in the potential difference across the membrane and to the release of K + from the cell, which would eventually lead to equalization of the concentrations of Na + and K + on both sides of the membrane. This does not happen due to the operation of the Na + - K + pump, which compensates for the leakage currents of Na + and K + and thus maintains the normal values of the intracellular concentrations of these ions and, consequently, the normal value of the resting potential of the cell.
For most cells, the resting membrane potential is (-60) - (-100) mV. At first glance it may seem that this is a small value, but it must be taken into account that the membrane thickness is also small (8-10 nm), so the electric field strength in the cell membrane is huge and amounts to about 10 million volts per 1 m (or 100 kV per 1 cm):
Air, for example, cannot withstand such an electric field strength (electrical breakdown in air occurs at 30 kV/cm), but the membrane does. This is a normal condition for its activity, since it is precisely such an electric field that is necessary to maintain the difference in the concentrations of sodium, potassium and chlorine ions on the membrane.
The value of the resting potential, which is different in cells, can change when the conditions of their life activity change. Thus, the violation of bioenergetic processes in the cell, accompanied by a drop in the intracellular level of macroergic compounds (in particular, ATP), primarily excludes the component of the resting potential associated with the work of Ma + -K + -ATPase.
Damage to the cell usually leads to an increase in the permeability of cell membranes, as a result of which the differences in the permeability of the membrane for potassium and sodium ions decrease; the resting potential in this case decreases, which can cause a violation of a number of cell functions, such as excitability.
- Since the intracellular concentration of potassium is maintained almost constant, even relatively small changes in the extracellular concentration of K * can have a noticeable effect on the resting potential and on the activity of the cell. Similar changes in the concentration of K "in the blood plasma occur in some pathologies (for example, renal failure).
The membrane of all living cells is polarized. The inner side of the membrane carries a negative charge compared to the intercellular space (Fig. 1). The amount of charge carried by the membrane is called membrane potential (MP). In non-excitable tissues, the MP is low, and is about -40 mV. In excitable tissues, it is high, about -60 - -100 mV and is called resting potential (RP).
The resting potential, like any membrane potential, is formed due to the selective permeability of the cell membrane. As is known, the plasmolemma consists of a lipid bilayer through which the movement of charged molecules is hindered. Proteins embedded in the membrane can selectively change the permeability of the membrane to various ions, depending on incoming stimuli. At the same time, potassium ions play a leading role in the formation of the resting potential, in addition to them, sodium and chlorine ions are important.
Rice. one. Concentrations and distribution of ions from the inside and outside of the membrane.
Most of the ions are distributed unevenly on the inside and outside of the cell (Fig. 1). Inside the cell, the concentration of potassium ions is higher, and sodium and chlorine are lower than outside. At rest, the membrane is permeable to potassium ions and practically impermeable to sodium and chloride ions. Despite the fact that potassium can freely leave the cell, its concentrations remain unchanged due to the negative charge on the inside of the membrane. Thus, two forces that are in equilibrium act on potassium: osmotic (K + concentration gradient) and electrical (membrane charge), due to which the number of potassium ions entering the cell is equal to those leaving. The movement of potassium is carried out through potassium channels leak open at rest. The value of the membrane charge at which potassium ions are in equilibrium can be calculated using the Nernst equation:
E m \u003d E k \u003d RT / nF ln [ K + ] n / [ K + ] ext
where E k is the equilibrium potential for K + ; R is the gas constant; T is the absolute temperature; F is the Faraday number; n - valence K + (+1), [K + n] - [K + ext] - external and internal concentrations of K +.
If we substitute the values from the table in Fig. 43, then we get the value of the equilibrium potential, equal to approximately -95 mV. This value fits into the range of the membrane potential of excitable cells. Differences in the PP of different cells (even excitable ones) can arise for three reasons:
- differences in intracellular and extracellular concentrations of potassium ions in different tissues (the table shows data on the average statistical neuron);
- sodium-potassium ATPase can contribute to the charge value, since it removes 3 Na + from the cell in exchange for 2 K + ;
- despite the minimal permeability of the membrane for sodium and chlorine, these ions can still enter the cells, although from 10 to 100 times worse than potassium.
To take into account the penetration of other ions into the cell, there is the Nernst-Goldman equation:
E m \u003d RT / nF ln P k [ K + ] ext + P Na [ Na + ] ext + P Cl [ Cl - ] n / P k [ K + ] n + P Na [ Na + ] n + P Cl [ Cl - ] ext,
Where Em is the membrane potential; R is the gas constant; T— absolute temperature; F is the Faraday number; P K , P Na And P Cl - membrane permeability constants for K + Na + and Cl, respectively; [TO+ n ], , , , [Cl - n] and [Cl - ext] - concentrations of K + , Na + and Cl outside (n) and inside (ext) of the cell.
This equation allows you to set a more accurate value of the PP. Typically, the membrane is a few mV less polarized than the equilibrium potential for K + .
Action potential (AP) may occur in excitable cells. If a nerve or muscle is irritated above the excitation threshold, then the RI of the nerve or muscle will quickly decrease and for a short period of time (millisecond) there will be a short-term recharging of the membrane: its inner side will become positively charged relative to the outer, after which the RI will be restored. This short-term change in the PP, which occurs when the cell is excited, is called the action potential.
The occurrence of PD is possible due to the fact that, unlike potassium ions, sodium ions are far from equilibrium. If we substitute sodium instead of potassium into the Nernst equation, we get an equilibrium potential of about +60 mV. During PD, there is a transient increase in Na+ permeability. At the same time, sodium will begin to penetrate into the cell under the action of two forces: along the concentration gradient and along the membrane charge, trying to adjust the membrane charge to its equilibrium potential. The movement of sodium is carried out along potential dependent sodium channels, which open in response to a shift in the membrane potential, after which they themselves are inactivated.
Rice. 2. The action potential of the nerve fiber (A) and the change in the conductivity of the membrane for sodium and potassium ions (B).
On the record, the PD looks like a short-term peak (Fig. 44), which has several phases.
- Depolarization (rising phase) (Fig. 44) - an increase in sodium permeability due to the opening of sodium channels. Sodium tends to its equilibrium potential, but does not reach it, since the channel has time to become inactivated.
- Repolarization - the return of the charge to the magnitude of the resting potential. In addition to the potassium channels of the leak, voltage-dependent potassium channels are connected here (activated by depolarization). At this time, potassium leaves the cell, returning to its equilibrium potential.
- Hyperpolarization (not always) - occurs in cases where the equilibrium potential for potassium exceeds the modulus of PP. The return to the PP occurs after the return to the equilibrium potential for K + .
During PD, the polarity of the membrane charge changes. The PD phase in which the membrane charge is positive is called overshot(Fig. 2).
The system of activation and inactivation is very important for AP generation. voltage-gated sodium channels(Fig. 3). These channels have two doors: activation (M-gate) and inactivation (H-gate). At rest, the M-gate is open and the H-gate is closed. During membrane depolarization, the M gate opens rapidly and the H gate begins to close. The flow of sodium into the cell is possible while the M-gate is already open, and the H-gate has not yet closed. The entry of sodium leads to further depolarization of the cell, leading to the opening of more channels and starting a positive feedback loop. Membrane depolarization will continue until all voltage-gated sodium channels are inactivated, which occurs at the peak of AP. The minimum amount of stimulus leading to the occurrence of AP is called threshold. Thus, the emerging AP will obey the all-or-nothing law and its value will not depend on the magnitude of the stimulus that caused the AP.
Due to the H-gate, channel inactivation occurs before the potential on the membrane reaches the equilibrium value for sodium. After the cessation of sodium entry into the cell, repolarization occurs due to potassium ions leaving the cell. At the same time, potential-activated potassium channels are also connected to the leakage channels in this case. During repolarization, the M-gate closes rapidly in the fast sodium channel. The H-gate opens much more slowly and remains closed for some time after the charge returns to the resting potential. This period is called refractory period.
Rice. 3. Operation of a voltage-gated sodium channel.
The concentration of ions inside the cell is restored by sodium-potassium ATPase, which, using energy in the form of ATP, pumps 3 sodium ions out of the cell and pumps 2 potassium ions.
On unmyelinated fiber or along the muscle membrane, the action potential propagates continuously. The resulting action potential due to the electric field is able to depolarize the membrane of the neighboring area to a threshold value, resulting in depolarization in the neighboring area. The main role in the emergence of a potential in a new section of the membrane is the previous section. At the same time, at each site, immediately after the AP, a period of refractory occurs, due to which the AP propagates unidirectionally. Ceteris paribus, the propagation of the action potential along the unmyelinated axon occurs the faster, the larger the fiber diameter. In mammals, the speed is 1-4 m / s. Since invertebrates lack myelin, the AP speed in giant squid axons can reach 100 m/s.
By myelinated fiber The action potential propagates spasmodically (saltatory conduction). Myelinated fibers are characterized by a concentration of voltage-gated ion channels only in the areas of Ranvier intercepts; here their density is 100 times greater than in the membranes of unmyelinated fibers. There are almost no voltage-gated channels in the area of myelin couplings. The action potential that arose in one interception of Ranvier, due to the electric field, depolarizes the membrane of neighboring interceptions to a threshold value, which leads to the emergence of new action potentials in them, that is, excitation passes abruptly, from one interception to another. In the event of damage to one node of Ranvier, the action potential excites the 2nd, 3rd, 4th, and even 5th, since the electrical insulation created by the myelin sleeves reduces the dissipation of the electric field. Saltatory conduction increases the speed of AP conduction 15-20 times up to 120 m/s.
The work of neurons
The nervous system is made up of neurons and glial cells. However, the main role in the conduction and transmission of nerve impulses is played by neurons. They receive information from many cells along the dendrites, analyze it and transmit it or not to the next neuron.
The transmission of a nerve impulse from one cell to another is carried out with the help of synapses. There are two main types of synapses: electrical and chemical (Fig. 4). The task of any synapse is to transmit information from presynaptic membrane(axon membrane) on postsynaptic(membrane of a dendrite, another axon, muscle, or other target organ). Most synapses of the nervous system are formed between the end of axons and dendrites, which form dendritic spines in the area of the synapse.
Advantage electrical synapse is that the signal from one cell to another passes without delay. In addition, such synapses do not get tired. To do this, pre- and postsynaptic membranes are connected by transverse bridges through which ions from one cell can move to another. However, a significant disadvantage of such a system is the lack of unidirectional transmission of PD. That is, it can be transmitted both from the presynaptic membrane to the postsynaptic one, and vice versa. Therefore, such a construction is quite rare and mainly in the nervous system of invertebrates.
Rice. 4. Diagram of the structure of chemical and electrical synapses.
chemical synapse very common in nature. O is more complicated, since a system is needed for converting an electrical impulse into a chemical signal, then again into an electrical impulse. All this gives rise to synaptic delay, which can be 0.2-0.4 ms. In addition, chemical depletion can occur, resulting in synapse fatigue. However, such a synapse provides unidirectional transmission of AP, which is its main advantage.
Rice. five. Scheme of work (a) and electron micrograph (b) of a chemical synapse.
At rest, the end of the axon, or presynaptic terminal, contains membrane vesicles (vesicles) with a neurotransmitter. The surface of the vesicles is negatively charged to prevent binding to the membrane and is coated with special proteins involved in the release of the vesicles. Each vial contains the same amount of a chemical called quantum neurotransmitter. Neurotransmitters are very diverse in chemical structure, however, most of them are produced right at the end. Therefore, it may contain systems for the synthesis of a chemical mediator, as well as the Golgi apparatus and mitochondria.
postsynaptic membrane contains receptors to the neurotransmitter. Receptors can be in the form of ion channels that open upon contact with their ligand ( ionotropic), and membrane proteins that trigger an intracellular cascade of reactions ( metabotropic). One neurotransmitter can have several ionotropic and metabotropic receptors. At the same time, some of them can be excitatory, and some - inhibitory. Thus, a cell's response to a neurotransmitter will determine the type of receptor on its membrane, and different cells can respond quite differently to the same chemical.
Between the pre- and postsynaptic membrane is located synaptic cleft, 10-15 nm wide.
When AP arrives at the presynaptic ending, voltage-activated calcium channels open on it and calcium ions enter the cell. Calcium binds to proteins on the surface of the vesicles, which leads to their transport to the presynaptic membrane, followed by membrane fusion. After such an interaction, the neurotransmitter finds itself in the synaptic cleft (Fig. 5) and can bind to its receptor.
Ionotropic receptors are ligand-activated ion channels. This means that the channel only opens in the presence of a certain chemical. For different neurotransmitters, these can be sodium, calcium, or chloride channels. The current of sodium and calcium causes membrane depolarization, therefore, such receptors are called excitatory. Chlorine current leads to hyperpolarization, which makes it difficult to generate AP. Therefore, such receptors are called inhibitory.
Metabotropic neurotransmitter receptors belong to the class of G protein-associated receptors (GPCRs). These proteins trigger a variety of intracellular cascades of reactions that ultimately lead to either further transmission of excitation or inhibition.
After signal transmission, it is necessary to quickly remove the neurotransmitter from the synaptic cleft. For this, either enzymes that decompose a neurotransmitter are present in the gap, or transporters pumping the mediator into the cells can be located on the presynaptic ending or neighboring glial cells. In the latter case, it can be reused.
Each neuron receives impulses from 100 to 100,000 synapses. A single depolarization on one dendrite will not result in further signal transmission. A neuron can receive both excitatory and inhibitory stimuli simultaneously. All of them summed up on the soma of the neuron. This summation is called spatial. Further, PD may or may not occur (depending on the incoming signals) in the area axon colliculus. The axon hillock is the region of the axon that is adjacent to the soma and has a minimum AP threshold. Further, the impulse propagates along the axon, the end of which can strongly branch and form synapses with many cells. In addition to the spatial, there is time summation. It occurs in the case of the receipt of frequently repeated impulses from one dendrite.
In addition to classical synapses between axons and dendrites or their spines, there are also synapses that modulate transmission in other synapses (Fig. 6). These include axo-axonal synapses. Such synapses are able to enhance or inhibit synaptic transmission. That is, if an AP arrives at the end of the axon that forms the axo-spinous synapse, and at that time an inhibitory signal arrives at it via the axo-axonal synapse, the release of the neurotransmitter in the axo-spinous synapse will not occur. Axodendritic synapses can change the conduction of AP by the membrane on the way from the spine to the cell soma. There are also axo-somatic synapses that can affect signal summation in the region of the soma of the neuron.
Thus, there is a huge variety of different synapses, differing in the composition of neurotransmitters, receptors and their location. All this provides a variety of reactions and plasticity of the nervous system.
Rice. 6. Variety of synapses in the nervous system.
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