Effects of ethanol exposure on brain sodium channels.

Abstract

Ethanol, like other general anesthetics, probably acts through an interaction with excitable membranes. When ethanol is present in membranes, the lipid structure of membranes is disordered. This effect can lead to alterations in functional entities that require a particular lipid environment. Sodium channels, requiring such an environment, have been studied for their sensitivity to ethanol. In synaptosomes, ethanol in vitro reversibly inhibits sodium influx stimulated by batrachotoxin or veratridine in concentrations equivalent to those found in animals during ethanol intoxication. Only the maximum stimulation of the toxins is altered by ethanol. The potencies of aliphatic alcohols are directly related to their lipid solubilities. Acute and chronic ethanol administration reduces the effectiveness of ethanol in vitro. This tolerance dissipates after a single dose of ethanol as it is eliminated from the body. However, after 4 days of ethanol treatment, the tolerance lasts for over 20 days. These data suggest that ethanol might disrupt one of the basic processes of neural function by acting directly on the environment of the sodium channel. The channel appears to be able to adapt to the presence of ethanol through the induction of tolerance.