Action Potential

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action potential

[′ak·shən pə‚ten·chəl]
(neuroscience)
A transient change in electric potential at the surface of a nerve or muscle cell occurring at the moment of excitation.

Potential, Action

 

rapid fluctuation of membrane potential arising in response to excitation of nerve and muscle cells or fibers; an active electrical signal by means of which information is transmitted in man and animals.

Action potential is based on rapidly reversible changes in the ionic permeability of the cell membrane that are caused by activation and inactivation of ionic membrane canals. In nerve fibers, the ascending phase of action potential is caused by activation of the rapid sodium canals, and the descending phase by inactivation of these canals and activation of the potassium canals. The same mechanism is reponsible for the generation of action potential in the fibers of vertebrate skeletal muscles.

Activation of the rapid sodium canals in myocardial fibers ensures only the initial surge of action potential: the plateau of action potential characteristic of these fibers is caused by activation of the slow sodium and calcium canals. Rapid sodium canals are not found in the membranes of smooth muscle fibers in the internal organs and blood vessels of vertebrates or in the membranes of muscle fibers of such arthropods as crustaceans and insects and in the membranes of some mollusk neurons. Action potential in these cells is stimulated by activation of the slow sodium and calcium canals or of the slow calcium canals. The descending phase of action potential is maintained by the potassium canals.

Study of the physicochemical properties of ionic canals is important both for interpreting their molecular structure and for developing methods of controlling the generation of action potential in various cells. The rapid sodium canals are specifically blocked by tetrodotoxin, derived from some species of puffer fish of the suborder Tetraodontoidea and from newts of the genus Taricha, as well as by Novocain, cocaine, and other local anesthetics. The slow sodium and calcium and slow calcium canals are not affected by these agents but are blocked by Mn2+, Co2+, Ni2+, and La3- ions and by such organic compounds as isoptin, used in cardiology, and its derivative D-600. Most of the potassium canals are effectively blocked by tetraethylammonium. The effect of action potential on such intracellular processes as the contraction of myofibrils in skeletal, smooth, and cardiac muscles and neurosecretion in some specialized neurons and nerve endings is triggered by the direct action of an electrical impulse on the intracellular structures (Ca2+ is released from the sarcoplasmic network of the muscle) and by the effect on these structures of Ca2+ ions penetrating into the cell during action potential.

B. I. KHODOROV

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