Passive cocaine exposure can alter NAcb AMPAR function, but on a different time course than in the VTA. While potentiation of AMPAR-mediated activity in VTA DA neurons was observed as early as 3 hrs after a single cocaine exposure (Argilli et al. 2008); modulation of NAcb AMPAR function was unaffected by a single cocaine injection. Instead, changes in Nacb glutamate function occur only following repeated cocaine injections (Kourrich et al., 2007; Thomas et al., 2001). In sharp contrast to the VTA, alterations in glutamatergic transmission in the NAcb exhibited a biphasic effect. Ex vivo electrophysiological analysis reveals depressed AMPAR function in the shell but not the core of the NAcb in early withdrawal from repeated non-contingent cocaine injections (24 hrs after last exposure) (Kourrich et al., 2007), consistent with a decreased AMPAR-mediated response of NAcb neurons observed in vivo (White 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
