Alterations in subunit assembly could induce alterations in the functional properties of GABAA receptors without alterations in the total number of receptors (Devaud et al. 1995; Kumar et al. 2009; Morrow et al. 1992). The expression of GABAA receptors involves a highly regulated process of synthesis, assembly, endocytosis, and recycling or degradation. Changes in the expression and composition of various GABAA receptors could result from selective endocytosis, recycling, and/or trafficking of newly synthesized receptors to the cell surface. GABAA receptor trafficking on the cell surface following EtOH consumption is thought to contribute to the development of EtOH-dependence (Kumar et al. 2004). It has been reported by Kumar et al. (2003) that chronic EtOH exposure selectively increases the internalization of α1 GABAA receptors with no change in the internalization of α4 GABAA receptors into clathrin coated vesicles of the cerebral cortex. There is also a decrease in α1 GABAA receptors and a significant increase in α4 subunit peptide in the synaptic fraction following chronic EtOH exposure. These results suggest that the regulation of intracellular trafficking following chronic EtOH administration may alter
