Chronic, heavy consumption of alcohol by humans has been shown to lead to impairment of executive and cognitive functions that require normal prefrontal cortical function (Goldstein et al., 2004; Crego et al., 2010). We have previously shown in post-mortem samples from alcoholics that the mRNA expression levels of glutamate and GABA-A receptors in the dorsal-lateral prefrontal cortex (DL-PFC) are not altered from that of normal controls (Jin et al., 2014b). This is in contrast to the present study where mRNA expression of specific glutamate and GABA receptor subunits were altered in the caudate of the alcoholics. Imaging studies have demonstrated connectivity and significant co-activation between caudate and higher level cognitive areas like the DL-PFC, rostral anterior cingulate and inferior frontal gyri (Strafella et al., 2003; Postuma and Dagher, 2006; Grahn et al., 2008). In contrast, the putamen links more to the primary cortical motor areas (Postuma and Dagher, 2006; Grahn et al., 2008). Recent neurobiological ideas of alcoholism (Depoy et al., 2013) suggest that there may be diminished executive effects on alcohol seeking and behavior and, rather, a shift to
