It is important to briefly discuss the concentrations of alcohol employed in most studies aiming to model AUDs using animal models. Although alcohol is not a particularly potent drug, it exerts dramatic depressive effects on the CNS which do not manifest until an individual’s blood alcohol concentration is rather high (5–10 mM) (Katzung, 2001). Furthermore, mutations in enzymes responsible for alcohol breakdown can explain inter-individual variability in alcohol concentration and metabolism in the blood (Edenberg, 2007). Thus, it is nearly impossible to precisely model the variable drinking habits and changing blood alcohol concentrations of an AUD individual (Dolganiuc & Szabo, 2009) and in animal models. The majority of studies performed in rodent models use a 50 mM alcohol concentration (Lieberman, Levine, Kranzler, Abreu, & Covault, 2012), which in more practical terms corresponds to a blood alcohol concentration of 0.24 g/L. With the normal legal driving limit for blood alcohol concentration being 0.08 g/L a dose of 50 mM alcohol would equate to ~ 3× the legal limit for operating a vehicle in the United States (Lieberman, Kranzler, Levine, & Covault,
