organelles, respectively, while PKCε localization remains unaltered (Buchner et al. 1999; Etoh et al. 1991). Therefore, interactions of NMDA and GABAA receptors via intracellular signaling pathways may play a vital role in GABAA receptor adaptation following chronic ethanol administration. In addition, both NMDA and GABAA receptor activation, as well as ethanol administration, alter brain-derived neurotrophic factor (BDNF) expression in neurons (MacLennan et al. 1995; Obrietan et al. 2002; Tapia-Arancibia et al. 2001; Zafra et al. 1991). BDNF has been shown to alter GABAA receptor function and expression. For example, addition of BDNF in cortical cell cultures increases internalization of GABAA receptor α2, β2, β3, and γ2 subunits (Brünig et al. 2001). In contrast, chronic application of BDNF increases expression of GABAA receptor α6 subunit in cerebellar granular cells that is blocked by concomitant application of ethanol (Ericson et al. 2003). Therefore, it is possible that ethanol-induced altered trafficking and expression of GABAA receptors are partially mediated by BDNF. Future studies on interactions of BDNF and GABAA receptor following chronic ethanol exposure are needed to clarify the role of BDNF on ethanol-induced adaptations of GABAA receptors.
