Acute and chronic ethanol-induced changes in plasticity have also been extensively studied in the NAc, a region implicated in the rewarding effects of ethanol (reviewed in Renteria et al., 2016), and will only be briefly summarized here. Acute ethanol inhibits NMDAR-dependent LTD in the NAc shell in an MSN-sub-type-specific manner (Jeanes et al., 2014). In the NAc core, acute ethanol impairs LTP via effects on mGluRs (Mishra et al., 2012). Following chronic ethanol exposure, LTD is altered such that D1-negative MSNs show LTD while D1-positive MSNs lose LTD, and sometimes show LTP (Jeanes et al., 2014; Renteria et al., 2017) (Figure 3O). These effects were lost after 2 weeks of withdrawal. Another study found impaired expression of NMDAR-LTD in the NAc core, but not shell, of mice that showed robust locomotor sensitization to ethanol after 2 weeks of withdrawal from chronic ethanol treatment (Abrahao et al., 2013) (Figure 3P). Thus, plasticity deficits in the NAc and hippocampus may contribute to behavioral adaptations to chronic ethanol (Coune et al., 2017).
