Unlike the effects of non-contingent infusions of cocaine, the effects of voluntary cocaine self-administration on glutamatergic function in the NAcb are generally similar to that observed in the VTA. One difference from the VTA is that self-administration of cocaine also elicits a biphasic response in AMPAR function during abstinence. In early abstinence, a depression of AMPAR function was observed in NAcb shell (Schramm-Sapyta et al., 2006), but after a longer period of abstinence, an increase in AMPAR-mediated response was observed in both the shell (Anderson et al., 2008) and the core (Conrad et al., 2008). In these studies, enhanced AMPA function was attributed to a shift in AMPAR subunit composition, leading to greater channel conductance. Anderson and colleagues (2008) observed an increase in cell-surface expression of GluA1-containing AMPARs, while Conrad et al. (2008) saw an increase in GluA2-lacking AMPARs (Conrad et al., 2008). The increase in GluA2-lacking AMPAR appears to play an important role in facilitating the incubation of cocaine craving (Figure 2B; Conrad et al., 2008), and promoting GluA2 surface expression in either the NAcb core or shell attenuated
