GABAergic activity is also involved in mediating the effects of chronic alcohol exposure, and becomes altered with the development of alcohol tolerance and dependence, and during withdrawal. Administration of GABA agonists increases alcohol consumption, and administration of GABA antagonists decreases alcohol consumption (Boyle et al., 1993); but while acute alcohol exposure enhances GABA activity, GABAA receptors down-regulate with chronic exposure to ethanol, resulting in diminished efficacy of alcohol (Grobin et al., 1998). Further, GABA agonists block the behavioral symptoms of alcohol withdrawal, while GABA antagonists exacerbate them (Koob, 2006). Chronic alcohol exposure also affects the expression and brain region localization of separate GABAA receptor subunits each differently, as well altering the subunit composition of the completed receptor (Enoch, 2008).
