et al., 1995) and in biochemical experiments (Boudreau et al., 2007). However, after a longer abstinence period (>10 days), AMPAR function is enhanced (Boudreau et al., 2007; Kourrich et al., 2007). Interestingly, re-exposure to cocaine during abstinence reverses the potentiated AMPAR function to a decreased AMPAR function (Kourich et al. 2007). This rapid, cocaine-induced reversal in AMPAR function is mirrored by a decrease in AMPAR surface expression (Boudreau et al., 2007) and decreased efficacy of intra-NAcb AMPAR to modulate locomotion (Bachtell et al., 2008) following cocaine exposure. In addition, repeated amphetamine administration did not alter GluA1 or GluR2 surface expression in the NAcb (Nelson and Killcross, 2006), but did upregulate the flip isoform of GluA2 (Yu et al., 2005), which can dramatically alter fast channel kinetics (Mosbacher et al., 1994).
