Several studies demonstrated GABAB receptor involvement in the effects of EtOH. For instance, GABAB receptor antagonists enhance the ability of acute EtOH to facilitate GABA transmission in the hippocampus (Ariwodola and Weiner 2004; Wan et al. 1996; Wu and Saggau 1994) and NAc (Nie et al. 2000). Ariwodola and Weiner (2004) suggested that the effect of EtOH to facilitate GABA transmission is limited because of GABA feedback on presynaptic GABAB receptors (Fig. 1). The presence of GABAB receptors accounted for the difference in sensitivity to EtOH influences on GABA transmission in specific subfields of the hippocampus (Weiner et al. 1997). On the other hand, GABAB receptors did not influence GABA release from neurons in the CeA (Roberto et al. 2003). Thus, the involvement of GABAB receptors on GABA release in various brain regions may not be universal, suggesting that the presence or absence of presynaptic GABAB receptors may be an important determinant for the regional specificity of EtOH to affect GABA transmission (Ariwodola and Weiner 2004).
