Chronic EtOH treatment is known to induce many neuroadaptative changes in the CNS. Over the past 20 years, it has been widely demonstrated that GABAergic transmission is sensitive to EtOH in distinct brain regions and is clearly involved in EtOH tolerance and dependence (Eckardt et al. 1998; Grobin et al. 1998). Chronic EtOH exposure often results in the development of tolerance to many GABAergic effects of the drug including the anxiolytic, sedative, ataxic, and positive reinforcing effects (Kumar et al. 2004, 2009). Substantial evidence suggests that these behavioral and neural adaptations involve marked changes in the expression profile of specific GABAA receptor subunits (Grobin et al. 1998) and in the pharmacological properties of GABAA receptors (Kang et al. 1998b) (Fig. 1).
