Kinetics of sodium currents decay in repolarization of axonal membrane under normal conditions and in the presence of scorpion toxin

Decay of sodium currents in repolarization ('tail current') was studied in the frog axonal membrane. The decay in membrane repolarization of the -40 and -60 mV has two exponential components: fast and slow. The fraction of the slow component in the total 'tail current' decreases as the repolarization potential (Vp) becomes more negative; at Vp more negative than -80, the mV 'tail' follows practically a 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 test 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 states 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.