Alcohol use disorder (AUD) is a prevalent condition which affects nearly 14% of the U.S. population during a given year (Grant et al. 2015). Inhibitory gamma aminobutyric acid type-A (GABAA) ionotropic receptors have been implicated in the behavioral effects of alcohol and the pathophysiology of alcohol use disorder (Enoch 2008). GABAA receptors are pentameric structures composed of various combinations of 2α, 2β and 1 non-α/β subunit (19 GABAA subunits have been identified α1-6, β1-3, γ1-3, δ, ε, θ, π, and ρ1-3) that surround a chloride-permeable pore. The subunit stoichiometry of receptors dictates their functional and pharmacological properties (Olsen and Sieghart 2009). Interactions between alcohol and GABAA receptors were first suggested by similarities between the behavioral effects of alcohol and the GABAA allosteric modulators benzodiazepines and barbiturates, the cross tolerance that develops between alcohol and these drugs, and findings in rodent models indicating that the behavioral effects of acute alcohol intoxication can be modified by co-administration of various agonists or antagonists of the GABAA receptor (for detailed reviews, see (Grobin et al. 1998, Weiner and Valenzuela 2006, Kumar et al. 2009).
