electric potentials arising in tissues and individual cells of man, animals, and plants; the most important components of the processes of excitation and inhibition. The study of bioelectric potentials is of great importance in understanding the physicochemical and physiological processes in living systems. It is also used in clinical medicine for diagnostic purposes (electrocardiography, electroencephalography, electromyography, and so on).
The initial data on the existence of bioelectric potentials (“animal electricity”) were obtained in the third quarter of the 18th century in the course of research on the nature of the “shock” produced by the electrical organs of certain fish in cases of defense or attack. The studies of the Italian physiologist and physician L. Galvani, who laid the foundation for the study of bioelectric potentials, date to the same period. A long scholarly dispute (1791–97) between Galvani and the physicist A. Volta on the nature of animal electricity culminated in two major discoveries: facts were obtained on the existence of bioelectric phenomena in living tissues, and a new principle for obtaining electric current using different kinds of metals was discovered—the voltaic cell was created. Galvani’s observations could not be properly assessed until fairly sensitive measuring instruments (galvanometers) came into use. The first such studies were carried out by the Italian physicist C. Matteucci (1837). The systematic investigation of bioelectric potentials was begun by the German physiologist E. Du Bois-Reymond (1848), who demonstrated the existence of bioelectric potentials in nerves and muscles at rest and during excitation. However, because of the inertia of the galvanometer, he was unable to record rapid oscillations of bioelectric potentials lasting a few thousandths of a second during the conduction of impulses along nerves and muscles. In 1886 the German physiologist J. Bernstein analyzed the shape of action potential. The French scientist E.-J. Marey (1875) used a capillary electrometer to record the oscillations of potentials of a beating heart. The Russian physiologist N. E. Vvedenskii (1883) used a telephone to listen to the rhythmic discharges in nerve and muscle. The Dutch physiologist W. Einthoven (1903) introduced the string galvanometer into experimental and clinical practice. This galvanometer is a high-sensitivity and quick-response instrument for recording electric currents in tissues. Russian physiologists made important contributions to the study of bioelectric potentials. V. V. Pravdich-Neminskii (1913–21) was the first to record an electroencephalogram. A. F. Samoilov (1929) investigated neuromuscular transmission of excitation, and D. S. Vorontsov (1932) discovered action potential in nerve fibers. Further progress in the study of bioelectric potentials was closely related to advances in electronics, which made it possible to use electronic amplifiers and oscillographs (developed by the American physiologistsG. Bishop, J. Erlanger, and H. S.Gasser in the 1930’s and 1940’s) in physiological experiments. The study of bioelectric potentials in single cells and fibers was made possible by the development of microelectrode technique. The use of giant nerve fibers of cephalopod mollusks, mainly the squid, is of great value in elucidating the mechanisms of generation of bioelectric potentials. The diameter of these fibers is 50–100 times greater than in vertebrates (0.5–1 mm), which permits the insertion of microelectrodes in them and makes possible the injection of various substances into the protoplasm. The study of the ionic permeability of the membrane of the giant fiber enabled the English physiologists A. Hodgkin, A. Huxley, and B. Katz (1947–52) to formulate the modern membrane theory of excitation.
The following principal types of bioelectric potentials are distinguished in nerve and muscle cells: resting potential, action potential, excitatory and inhibitory postsynaptic potentials, and generator potentials.
Resting potential (resting membrane potential). In living cells at rest there is a difference of about 60–90 millivolts (mV)—localized on the surface membrane—between the cell contents and external solution. The inner side of the membrane is charged electronegatively with respect to the outer side (see Figure 1). Resting potential is caused by the selective
permeability of the resting membrane for K+ ions (J. Bernstein, 1902, 1912; A. Hodgkin and B. Katz, 1947). The concentration of K+ in protoplasm is 50 times higher than in the extracellular fluid. Hence, in diffusing from the cell, the ions carry positive charges to the outer side of the membrane. Meanwhile, the inner side, which is virtually impermeable to large organic anions, acquires negative potential. Since the permeability of a membrane at rest is approximately 100 times lower for Na+ than for K+, the diffusion of sodium from the extracellular fluid (where it is the main cation) into the protoplasm is low and only slightly decreases the resting potential produced by the K+ ions. In skeletal muscle cells, C1- ions that diffuse within the cell play an important role in the origin of resting potential. The result of the resting potential is resting current recorded between injured and intact portions of a nerve or muscle after the placement of deriving electrodes. Membranes of nerve and muscle cells (fibers) are capable of changing their ionic permeability in response to shifts in membrane potential. When the resting potential increases (hyperpolarization of the membrane), the permeability of the surface membranes for Na+ and K+ diminishes, but when it decreases (depolarization), the permeability increases. The rate of change in permeability for Na+ greatly exceeds the rate of increase in membrane permeability for K+.
Action potential. All stimuli acting on a cell cause at first a decrease in the resting potential; when it reaches a critical level (threshold), an active spreading response—action potential—occurs (see Figure 2). During the ascending phase of the action potential, the potential on the membrane is temporarily distorted, and the inner surface, charged electronegatively at rest, acquires positive potential. After peaking, the action potential begins to diminish (descending phase) and potential on the membrane returns almost to the original level, the resting potential. Complete restoration of the resting potential occurs only after the termination of trace oscillations of potential (trace depolarization or hyperpolarization), whose duration is usually far longer than the peak of the action potential. According to the membrane theory, membrane depolarization caused by stimulation intensifies the flow of Na+ within the cell, which decreases the negative potential of the inner side of the membrane—that is, intensifies its depolarization. This in turn increases its permeability to Na+ and again intensifies depolarization, and so on.
As a result of this explosive circular process—so-called regenerative depolarization—distortion of the membrane potential characteristic of the action potential occurs. The increased permeability for Na+ is of very short duration, and it then decreases (see Figure 3), with a resulting decrease in the flow of Na+ within the cell. The permeability for K+, unlike that for Na+, continues to increase, causing the flow of K+ from the cell to intensify. The action potential begins to diminish as a result of these changes, causing the restoration of the resting potential. This is the mechanism of generation of the action potential in most excitable tissues. However, there are cells (muscle fibers in crustaceans, nerve cells in some gastropod mollusks, some plant cells) in which the ascending phase of the action potential is caused by an increase in membrane permeability not for Na+ ions but for Ca2+ ions. Another unusual mechanism of generation of action potentials is that found in heart-muscle fibers, which are characterized by a prolonged plateau in the descending phase of the action potential (see Figure 2, c). The unequal concentrations of K+ and Na+ (or Ca2+) ions inside and outside the cell (fiber) are maintained by a special mechanism (the so-called sodium pump) which ejects Na+ ions from the
cell and forces K+ ions into the protoplasm. This requires an expenditure of energy drawn by the cell in the metabolic processes.
The amplitude of the action potential of most nerve and muscle fibers is about the same: 110–120 mV. The duration of the action potential varies widely: in warm-blooded animals, the action-potential duration of nerve fibers, which conduct excitation the most quickly, is 0.3–0.4 milliseconds (msec); in fibers of the heart muscle it is 50–600 msec. The action potential lasts about 20 sec in cells of freshwater algae of the genus Chara. A feature of the action potential that distinguishes it from other forms of cell response to stimulation is the fact that it obeys the “all or nothing” rule—that is, it arises only when the stimulus attains a certain threshold value, and a further increase in the intensity of the stimulus no longer affects either the amplitude or the duration of the action potential. The action potential is one of the most important components of the process of excitation. In nerve fibers it ensures conduction of the excitation from sensory endings (receptors) to the body of the nerve cell and from the latter to the synaptic endings located on various nerve, muscle, or glandular cells. Upon reaching the effector endings the action potential induces the secretion of a certain amount of specific chemical substances, the so-called mediators, which excite or inhibit the corresponding cells. In muscle fibers, the spreading action potential triggers a series of physicochemical reactions underlying the process of muscle contraction. The action potential is conducted along nerve and muscle fibers by so-called local or action currents that arise between the excited (depolarized) and adjacent resting portions of the membrane. Action currents are recorded
by ordinary extracellular electrodes. The curve is two-phase; the first corresponds to the arrival of the action potential at the near electrode, and the second corresponds to its arrival at the far electrode (see Figure 4).
Postsynaptic potentials. Postsynaptic potentials originate in the portions of the membrane of nerve or muscle cells that directly border on the synaptic endings. They have an amplitude on the order of several mV and a duration of 10–15 msec. Postsynaptic potentials are subdivided into excitatory and inhibitory potentials. Excitatory postsynaptic potentials represent local depolarization of the postsynaptic membrane caused by the action of the corresponding mediator (for example, acetylcholine in the myoneural junction). When excitatory postsynaptic potentials achieve a certain threshold (critical) value, a spreading action potential arises in the cell (see Figure 5, a, b). An inhibitory postsynaptic potential
reflects local hyperpolarization of the membrane caused by an inhibitory mediator (see Figure 5, c). Unlike that of action potentials, the amplitude of postsynaptic potentials gradually increases with the amount of mediator secreted by the nerve ending. Excitatory and inhibitory postsynaptic potentials are summated in cases of simultaneous or successive arrival of nerve impulses at the endings located on the membrane of the same cell.
Generator potentials. Generator potentials originate in the membrane of sensory nerve endings (receptors). Outwardly they resemble excitatory postsynaptic potentials; their amplitude is on the order of several mV and varies with the force of stimulation applied to the receptor (see Figure 6). When
the generator potential reaches a threshold (critical) value, a spreading action potential arises in the neighboring portion of the membrane of the nerve fiber. The ionic mechanism of generator potentials has not yet been adequately studied.
In addition to the relatively quickly developing bioelectric potentials described above, very slow oscillations of membrane potential of an unknown nature are also recorded in nerve cells, smooth muscle fibers, and some plant cells. Volleys of impulses often arise on the crest of the wave of membrane depolarization.
All bioelectric potentials can be recorded and accurately measured only with extracellular microelectrodes, which make it possible to derive the difference in potentials between the inner and outer surfaces of the cell membrane. When oscillations of bioelectric potentials are derived from whole nerves, muscles, or the brain using surface electrodes, only the total potential of the multitude of synchronously or, more often, asynchronously functioning cells is recorded. The electromyogram is the result of the interference of the action potentials of many skeletal muscle fibers. The electrocardiogram is the result of the oscillations of electric potentials of muscle fibers in different portions of the heart. The electroencephalogram is the result of the summation of mainly excitatory and inhibitory postsynaptic potentials of a great many cells in different layers of the cerebral cortex. Although the recording of such interference electrograms cannot be used to analyze the oscillations of the bioelectric potentials of individual cells, it is valuable in evaluating the state of the particular organ as a whole. In clinical medicine electromyograms, electrocardiograms, and electroencephalograms are recorded using electrodes placed on the skin of the corresponding parts of the body. The information obtained by these methods is evaluated by comparing the changes in the corresponding curve with the results of clinical, physiological, and pathological-anatomical studies.
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