From the preceding review, it is clear that the majority of the early studies characterizing chronic effects of EtOH on GABAergic transmission focused mainly on postsynaptic properties and the subunit composition of the GABAA receptors themselves. Some of the disparity in the findings across laboratories on postsynaptic sites of EtOH action may reflect the differences in the chronic EtOH treatment duration and protocol, brain region examined, and methods of assessing receptor function. Most of these studies were generally in agreement that chronic EtOH exposure and withdrawal did not result in dramatic decreases in the number of GABAA receptors in most brain regions. However, many of these studies reported marked alterations in the expression of specific GABAA receptor subunits and hypothesized that those changes in the subunit composition of the GABAA receptors may account for the physiologic and pharmacologic alterations in GABAergic signaling associated with chronic EtOH administration (Grobin et al. 1998).
