Mozhaeva G N, Naumov A P, Nosyreva E D
Neirofiziologiia. 1980;12(5):541-9.
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.
对轴突膜复极化过程中钠电流的衰减（“尾电流”）进行了研究。膜复极化至 -40 除以 -60 mV 时的衰减有两个指数成分：快成分和慢成分。慢成分在总“尾电流”（θM）中的比例随着复极化电位（Vp）变得更负而降低；当 Vp 比 -80 mV 更负时，“尾电流”实际上遵循单指数时间进程。当延长测试脉冲（在给定的 Vp 下）时，“尾电流”中快成分的比例比慢成分下降得更快，大致遵循测试脉冲期间失活的动力学。蝎毒素处理主要通过增加慢成分的比例来导致“尾电流”动力学减慢。提出了一个假设，即通道有两个开放状态的动力学图。提出了一个假说，即蝎毒素、滴滴涕和三硝基苯酚有一个共同的“位点”与钠通道的门控机制相互作用。
