The dorsal striatum is a brain region that controls movement, is implicated in mediating the formation of goal-directed responses and behavioral habits, and plays a role in the binge/intoxication phase of the addiction cycle [21, 32, 85]. Recent studies have demonstrated that superfusion of EtOH and alcohol experience leads to disruption of synaptic plasticity in the dorsal striatum [82, 83, 86, 87] and ventral striatum [88, 89]. Mechanistic studies have shown that HFS induced LTD in the dorsal striatum in the presence of EtOH, and that this occurred independent of NMDAR activity, and was however, dependent on dopamine D2 and cannabinoid CB1 receptor activation [82]. With respect to NMDARs, these receptors consist of an obligatory GluN1 subunit and GluN2 (A-D) subunits [90]. GluN2A and GluN2B subunits are expressed in the striatum. A report demonstrates that superfusion of EtOH decreased NMDAR-mediated synaptic transmission in the striatum, indicating that acute EtOH induces immediate depressive effect on NMDAR activity. However, washout after acute EtOH conditions induces long-term facilitation via GluN2B NMDARs, particularly in the dorsal striatum [83]. Furthermore, washout of EtOH’s effect on
