Influences of β-endorphins in Ethanol Consumption Patterns and Acquisition of a Conditioned Taste Aversion Mediated by the Drug

Abstract

Rewarding effects of ethanol may be mediated in part by endogenous opioids. Ethanol alters β-endorphin synthesis and release. β-endorphin heterozygous (HT) and knockout (KO) mice consume higher levels of a low-concentrated alcohol solution and show heightened predisposition to self-administer ethanol in comparison with wild-type (WT) mice (Grisel et al., 1999). This study was conducted in order to: i) re-analyze and extend previous results in terms of ethanol consumption profiles of β-endorphin deficient mice; and ii) analyze conditioned aversive learning mediated by ethanol postabsorptive effects as a function of genetic capabilities to synthesize β-endorphin. In Experiment 1, mice were evaluated in terms of consumption of a low (7%) ethanol solution in a two-bottle free choice paradigm. Ethanol concentration was then increased to 10 % and voluntary intake consumption was tested. WT mice displayed significantly higher consumption levels and ethanol-preference scores than did KO mice, independently from ethanol concentration. HT mice drank more ethanol than did KO mice. In Experiment 2, mice (KO, HT and WT) were tested in a conditioned taste aversion paradigm in which a sodium chloride (NaCl) solution was paired with a 2-g/kg ethanol dose. Only HT and KO displayed a conditioned aversion when using 2-g/kg ethanol as unconditioned stimulus. The present results indicate that total or partial deficiency of β-endorphin synthesis reduces ethanol preference and consumption. Furthermore, this study indicates that the lack of β-endorphin synthesis exacerbates ethanol’s aversive postabsorptive effects which can in turn modulate self-administration patterns of the drug