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 long-term facilitation is mediated through Fyn-mediated phosphorylation of GluN2B subunits [83]. More recent findings show that washout after acute EtOH and repeated systemic administration of EtOH followed by acute withdrawal facilitated LTP in the dorsal striatum in a GluN2B dependent manner [87]. More notable is that the induction of LTP is mediated by the synaptic localization of AMPARs in the dorsomedial striatum [87]. Few studies have investigated whether protracted consumption of EtOH affects synaptic transmission and plasticity in the dorsal striatum. A recent study used the intermittent-access two bottle choice alcohol drinking procedure and measured synaptic transmission in the dorsal striatum 24 hours after the last drinking session. They demonstrated that the intermittent-access procedure produced unregulated EtOH consumption, and that repeated cycles of unregulated EtOH consumption altered neurotransmission in the dorsomedial striatum, evident as strengthening of glutamatergic transmission in direct pathway neurons [91]. In addition, months of EtOH consumption leads to opposing effects on synaptic transmission in the dorsomedial versus
