Generally, acute EtOH exposure enhances the function of cys-loop LGICs (Aguayo et al. 2002; Harris 1999; Lovinger 1997; Perkins et al. 2010), but instances of inhibition of the nAChRs and GABAARs have been reported (Aguayo et al. 2002; Cardoso et al. 1999; Davis and De Fiebre 2006; Marszalec et al. 1994; Roberto et al. 2003). The most common EtOH action is to potentiate channel opening in the presence of a low concentration of agonist by increasing the probability of channel opening (Zhou et al. 1998), and/or increasing agonist affinity (Tonner and Miller 1995; Welsh et al. 2009). This potentiating effect can influence both synaptic and extrasynaptic receptors (Sebe et al. 2003; Ye et al. 2001; Eggers and Berger 2004; Ziskind-Conhaim et al. 2003) (Fig. 1). For example, EtOH has been shown to increase the amplitude and/or duration of GABAA and GlyR-mediated inhibitory postsynaptic currents (IPSCs) (Sebe et al. 2003; Ziskind-Conhaim et al. 2003).
