The environmental context in which abused drugs are taken contribute to the drug experience and is a powerful and persistent stimulus to elicit memories of that experience even in the abstinent addict. Using amphetamine (AMPH) as the unconditioned stimulus, the present dissertation project compared two popular context-dependent paradigms in rats, conditioned motor sensitization (CMS) and conditioned place preference (CPP), to ascertain if particular brain regions were differentially involved in these behaviors. We determined that receptors for brain derived neurotrophic factor (BDNF), i.e., tyrosine kinase receptors B (TrkB), were uniquely enhanced in the dentate gyrus (DG) of the hippocampus in rats that showed CPP with repeated exposure to i.p. AMPH (0.3mg/kg). A higher AMPH dose (1.0mg/kg) induced both CPP and CMS, and elevated Trk13 in the DG as well as the NAc shell. Verifying that the DG Trk receptor is necessary for both AMPH-induced conditioned behaviors, we revealed that neither CPP nor CMS developed in rats that received intra-DG infusions of the Trk inhibitor K-252a. Furthermore, co-administration of intra-DG BDNF with subthreshold doses of AMPH (0.1mg/kg, i.p.) produced a robust CPP (but not CMS). This indicates that CPP and CMS are induced by different doses of AMPH, and are associated with region specific BDNF/TrkB. We further explored whether Trk13 exerted its effects via ionotropic glutamatergic receptors. Electrophysiological evaluations were performed one day after the CPP test via extracellular recordings of single neurons in the DG of the hippocampus from chloral hydrate anesthetized rats demonstrating AMPH-induced CPP with 0.3 mg/kg AMPH. Results showed that DG neuronal responding to NMDA and AMPA was upregulated by AMPH-induced CPP. Behavioral evaluations revealed that NMDA activation was critical for AMPH-induced associative learning, since the CPP that was induced by intra-DG BDNF co-administered with subthreshold doses of' AMPH (0.1mg/kg, i.p.) was disrupted by intra-hippocampal pretreatments with NMDA receptor antagonist D-AP5. This disruption did not occur with the AMPA receptor antagonist CNQX. These findings suggest that TrkB receptors in the hippocampus mediate neuronal changes necessary for AMPH-induced associative learning through NMDA receptors.