and tonic GABA transmission in neurons (Mihic et al., 1997; Sundstrom-Poromaa et al., 2002; Wallner et al., 2003; Wei et al., 2004; Borghese et al., 2006; Korpi et al., 2007; Baur et al., 2009). At low concentrations of ethanol (3–30 mM), tonic GABA-A receptor currents may be enhanced but as the alcohol concentration is raised (> 60 mM), GABA-A receptor-mediated synaptic transmission is also facilitated. In many brain regions, the main effect of ethanol on GABA signaling is enhancement of presynaptic release (Siggins et al., 2005). During chronic alcohol exposure, NMDA receptors are generally up-regulated and GABA-A receptors down-regulated in rodent models (Uusi-Oukari and Korpi, 2010; Lovinger and Roberto, 2013).
