| Drug-induced conditioned place preference (CPP) requires the formation of an association between environmental cues and the affective state produced by treatment. However, the neurobiology of the stimulus-reward learning processes involved in CPP behavior is not well understood. The present study investigated the effects of both reversible inactivation and glutamatergic NMDA receptor function within the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) on extinction underlying an amphetamine CPP. Following training and testing for acquisition of a CPP, adult male Long-Evans rats were given extinction trials consisting of confinement to the pairing compartments of the CPP apparatus in the absence of amphetamine injections. Prior to each daily extinction trial, rats received pre-trial intra-mPFC or intra-BLA infusions of bupivacaine, APV, or saline. Following extinction training, rats were given a test session during which the amount of time spent in each of the compartments was recorded. Intra-mPFC and intra-BLA infusions of bupivacaine or APV blocked extinction of an amphetamine CPP. Consistent with prior studies using irreversible lesions, pre-training or pre-retention intra-BLA bupivacaine infusions blocked acquisition and expression of an amphetamine CPP, respectively, and pre-training intra-BLA APV infusions also blocked acquisition. Taken together with previous findings, these results suggest a common neural basis involving the BLA in the mediation of acquisition and extinction of amphetamine CPP behavior, but also a distinct neural basis involving the mPFC in the development of inhibitory learning characterized by extinction. |
