Alcohol tolerance in a cholinergic nerve terminal: relation to the membrane expansion-fluidization theory of ethanol action.

Phrenic nerve terminals from rats subjected to long-term ethanol treatment were more resistant to ethanol (in vitro) than terminals from sucrose-fed rats, as measured by the effect of ethanol on the frequency of miniature end plate potentials. Long-term ethanol exposure may thus induce the synthesis of more rigid membrane lipids, reducing membrane "fluidizability". This may provide a neurocellular basis for ethanol tolerance and cross-tolerance with anesthetics and barbiturates.