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 the capacity of cocaine to reinstate extinguished drug-seeking behavior (Famous et al., 2008). Moreover, GluA1 and GluA2 trafficking increased during the extinction of cocaine-seeking behavior (Ghasemzadeh et al., 2009), and the extent of extinction was correlated with the upregulation of GluA1 (Sutton et al., 2003).
