Alcohol is the most common drug of abuse in Western societies. Chronic, excessive alcohol consumption may lead to changes in behavior, addiction and cognitive dysfunction (Jernigan et al., 1991; Harper, 1998; Harris et al., 2008; Spanagel, 2009). Acute exposure to ethanol modulates the ion channel function of both glutamate and GABA-A receptors. NMDA receptors are inhibited by ethanol in a concentration-dependent manner over a range of concentrations that produce intoxication (Lovinger et al., 1989; Gass and Olive, 2008). AMPA and kainate receptors are inhibited by high concentrations of alcohol (Gass and Olive, 2008; Moykkynen and Korpi, 2012) and ethanol inhibits several forms of neuronal plasticity, including long-term potentiation (LTP) (Blitzer et al., 1990; Morrisett and Swartzwelder, 1993; Givens and McMahon, 1995; Gass and Olive, 2008). In contrast to the effect on the glutamate transmission, ethanol, if anything, enhances the synaptic 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
