[Kinetics of sodium current decay during normal axon membrane repolarization and in the presence of scorpion toxin].
Decay of sodium currents in repolarization ("tail current") was studied in from axonal membrane. The decay in the membrane repolarization to -40 divided by -60 mV has two exponential components: fast and slow. The fraction of the slow component in the total "tail current" (theta M) decreases as the repolarization potential (Vp) becomes more negative; at Vp more negative than -80 mV "tail" follows practically one-exponential time course. When lengthening the test pulse (at the given Vp) the fraction of the fast component in the "tail" decreases quicker than that of the slow component, following approximately the kinetics of inactivation during the tests pulse. Scorpion toxin treatment results in slowing down "tail" kinetics mainly at the expense of increasing the fraction of the slow component. A kinetic diagram assuming two open state for the channel is suggested. A hypothesis is advanced that scorpion toxin, DDT and trinitrophenol have a common "site" to interact with the gating mechanism of the sodium channel.
D000818:Animals; D007473:Ion Channels / Q000187:drug effects*; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D011895:Rana ridibunda; D011901:Ranvier's Nodes / Q000187:drug effects*; D012604:Scorpion Venoms / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism*
D007473:Ion Channels; D012604:Scorpion Venoms; D012964:Sodium
Kinetika spada natrievogo toka pri repoliarizatsii aksonnoĭ membrany v norme i v prisuststvii toksina skorpiona.