Although mechanisms of excessive alcohol consumption have been explored using brain gene expression profiling, a causal link between changes in expression of specific genes or gene networks and ethanol consumption has not been established (Spanagel, 2009). Even in the larger realm of behavioral neuroscience, there are only a few studies that have validated microarray targets with subsequent behavioral analysis (Kong et al., 2010; Flint and Mott, 2008). Other examples include the role of glyoxalase-1 and glutathione reductase 1 in anxiety (Hovatta et al., 2005), prodynorphin and FK506bp in morphine withdrawal (McClung et al., 2005) and Cdk5 in adaptation to cocaine (Bibb et al., 2001).
