Electrophysiological analysis of the actions of strychnine, bicuculline and picrotoxin on the axonal membrane

Abstract

AbstractStrychnine, bicuculline, and picrotoxin show similar effects on the membrane of the lobster giant axon. At concentrations above 5 × 10−5 M these compounds cause depolarization of the resting potential and a broadening of the action potential contour. Also occurring is an increase in excitability as defined by a decrease in stimulus threshold. Repetitive firing of action potentials is sometimes observed during the depolarizing process. Drug levels of 5 × 10−4 M and higher may secondarily induce depolarizing inactivation of the spike generating mechanism. The loss in resting potential is accounted for by a shift in relative membrane selectivity away from potassium and towards sodium. Associated with this alteration in selectivity is a marked fall in total conductance and abolition of delayed rectification. The results indicate that strychnine, bicuculline, and picrotoxin cause potassium inactivation and further that this effect is manifest in both the resting and active electrogenic state of the membrane.