EtOH potentiation of GABAergic synaptic inhibition is now known to result from both pre and postsynaptic actions. As discussed in the section on LGICs, the postsynaptic effects result from potentiation of GABAA/anion channels. Recent studies indicate that EtOH also acts to enhance GABA release from presynaptic terminals, and this action contributes to enhanced synaptic inhibition (reviewed in Siggins et al. 2005) (Fig. 1). Increases in fast GABAergic synaptic transmission during EtOH treatment have been observed in cerebellum, hippocampus, ventral tegmental area (VTA), hypoglossal nucleus, and amygdala, both basolateral and central nuclei (Ariwodola and Weiner 2004; Ming et al. 2006; Kelm et al. 2007; Theile et al. 2008; Zhu and Lovinger 2006; Roberto et al. 2003; Sebe et al. 2003; Ziskind-Conhaim et al. 2003). These studies have been carried out mostly in brain slices and isolated brain neurons. Examination of spontaneous and miniature GABAergic IPSCs allows investigators to determine whether the frequency of synaptic events is altered (a likely presynaptic change), or whether the amplitude is affected (likely a postsynaptic change). Such analyses have consistently shown that sISPC and mIPSC frequencies
