This review will refer to studies employing either operant or passive drug-exposure models to probe AMPAR-mediated plasticity. Importantly, the extinction-reinstatement model has been used to demonstrate a central role of NAcb AMPAR (Cornish et al., 1999; Cornish and Kalivas, 2000; Di Ciano and Everitt, 2001; McFarland and Kalivas, 2001; McFarland et al., 2004) and glutamate released from prefrontal afferents into the NAcb (McFarland et al., 2003; Park et al., 2002) for cue-primed (Backstrom and Hyytia, 2007; Di Ciano and Everitt, 2001), stress-primed (McFarland et al., 2004), and cocaine-primed (Bachtell et al., 2008; Cornish and Kalivas, 2000; Ping et al., 2008) reinstatement. In general, striatal AMPAR antagonism prevents relapse while AMPAR activation promotes it (Cornish et al., 1999; Cornish and Kalivas, 2000; Di Ciano and Everitt, 2001; McFarland et al., 2004; Suto et al., 2004; Vanderschuren et al., 2005), but this may be an oversimplified hypothesis (Bachtell et al., 2008).
