Violation of excitation
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.
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