The effects of ethanol on squid giant axons were studied by means of the sucrose-gap technique. The membrane action potential height is moderately reduced and the duration sometimes shortened by ethanol in sea water. Voltage clamp experiments showed that ethanol in sea water reduced the maximum membrane conductances for sodium (g'(Na)) and potassium (g'(K)). In experiments with multiple application of ethyl alcohol to the same spot of membrane, a reduction of g'(Na) to 82 per cent and of g'(K) to 80 per cent of their value in sea water was brought about by 3 per cent ethanol (by volume) while 6 per cent caused a decrease of g'(Na) to 59 per cent and of g'(K) to 69 per cent. Ethanol has no significant effect on the steady-state inactivation of g(Na) (as a function of conditioning membrane potential) or on such kinetic parameters as tau(h) or the time course of turning on gi g(Na) and g(K). It is concluded that ethanol mainly reduces g(Na) and g(K) in the Hodgkin-Huxley terminology.
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