Violation of excitation

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The spread of excitation along the nerve fibers provide a consistent combination of the same process: the depolarization fiber membrane area, the entrance to this site Na +, depolarization of the membrane of the neighboring area, the entrance to this site Na +, etc.

With insufficient Na + entrance disturbed the generation of the action potential, and conducting stops. This effect occurs for Na + channel blockade by local anesthetics (procaine, lidocaine, etc.) And a number of other chemical agents. A specific blocker of Na + -channels is tetrodotoxin - toxin produced by the internal organs of the puffer fish.

Initial concentration difference of Na + and Ca + on both sides of the membrane (Na + 10-15 times more on the outside, K + 50-70 times within increase) required to generate an action potential is restored and maintained by active transport of ions Na + / K + - nacocom. It pumps out Na +, ringing the interior (the cytoplasm) during excitation, in return for the external K +, which came out during arousal. Activities of the pump, which carries out the role of the built-in membrane Na + / K + -ATPase, provides the energy liberated in the cleavage of ATP. Energy deficit leads to a malfunction of the pump, resulting in the inability of the membrane to generate an action potential and pursue excitement. This effect causes uncouplers of oxidative phosphorylation (for example, dinitrophenol) and other metabolic poisons, and prolonged ischemia and nerve cooling portion. Inhibit the pump, and as a consequence disturb conductivity cardiac glycosides (e.g. ouabain, strophanthin) in high doses.

Conducting field along the axon is disturbed at various kinds of diseases of the peripheral nerves and nerve fibers in the central nervous system -. In inflammatory processes, scarring of the nerve, and compression of nerve fibers, the fibers demyelination (allergic processes, multiple sclerosis), burns, etc. Carrying out the excitation stops when degeneration axon.