Alcohol inhibits morphine/cocaine reward memory acquisition and reconsolidation in rats

Rationale and objective Alcohol is a recreational substance that is generally socially acceptable and legal in most areas worldwide. An alcohol overdose will produce an inhibitory effect on the brain and impair cognition and memory. In this study, we examined the effect of alcohol on the acquisition, consolidation, and reconsolidation of drug reward memory induced by morphine and cocaine in rats. Methods Rats were trained to acquire morphine sulfate (10 mg/kg, s.c.) and cocaine (10 mg/kg, i.p.) conditioned place preference (CPP) via an unbiased CPP paradigm. Vehicle or alcohol (0.25, 0.75, 1.5 g/kg, i.p.) was administered at various time-points, including 30 min before each CPP conditioning session (acquisition), immediately after each CPP conditioning session (consolidation), immediately after the reactivation of CPP (reconsolidation with re-exposure), or without reactivation to the drug-paired context (reconsolidation without re-exposure). Conditioning scores were recorded before or after each conditioning session or memory reactivation. Results Alcohol at a dose of 1.5 g/kg but not 0.25 g/kg or 0.75 g/kg significantly inhibited the acquisition and reconsolidation of morphine- and cocaine-associated memory. In contrast, alcohol had no effect on the consolidation of morphine- or cocaine-induced CPP. Conclusions The results suggested that pre-exposure alcohol dose-dependently attenuated morphine- or cocaine-induced place preference and prevented drug reinstatement in rats by disrupting memory reconsolidation, which may be explained by the inhibitory effect of alcohol on dopaminergic and glutamatergic neurotransmission.