Tolerance to alcohol at the neuromuscular junction of long-sleep and short-sleep mice

Abstract

The time constant of the decay (tau) of miniature end-plate currents (MEPCs) recorded from muscles excised from long-sleep (LS) and short-sleep (SS) mice was measured as an indicator of the mean open time of the channel which is gated by the nicotinic acetylcholine receptor. Similar tau values were recorded from LS and SS mice, and these values were similarly increased by acute ethanol (50 mM). Mice were then chronically treated with ethanol to induce tolerance to its hypnotic action. The time course of the development of tolerance was similar in the LS and SS lines. While MEPCs recorded from tolerant mice yielded similar tau values to controls, acute exposure to ethanol did not cause an increase. It is suggested that an adaptation takes place in the nicotinic acetylcholine receptor channel complex during the induction of tolerance to ethanol.