The World Health Organization (WHO) estimates that there are about 2 billion people worldwide who consume alcoholic beverages (WHO, 2004). Alcohol use is related to a wide range of physical, mental, and social detriments. Additionally, alcohol affects almost every organ in the human body as well as the central nervous system (CNS) (Spanagel, 2009). There are several theories as to how alcohol affects the CNS. They are classified into two main groups depending on the primary target of ethanol. These two groups are lipid and protein theories (Goldstein, 1986). Before the 1990s, different lipid theories postulated that alcohol acted via some perturbation of the membrane lipids in CNS neurons. In particular, the effects on membrane fluidity and the disordering of the bulk lipid phase of membranes were originally attractive hypotheses for alcohol action. However, recently the protein hypothesis has become the predominant theory (Lovinger, 1997). This hypothesis predicts that alcohol acts specifically on membrane proteins such as receptors and ion channels. The main reason for a shift towards the protein theory originates from evidence that alcohol, at concentrations in the 10–20 mM range, directly interferes with the function of several ion channels (K+, Ca2+) and receptors (Lovinger et al., 1989). These ethanol effects are mediated through a number of neural transmitter systems including γ-aminobutyric acid (GABA) and glutamate (Takadera et al., 2008; Murail et al., 2011).