The basal ganglia play an important role in voluntary movement and substance dependence. Excitatory glutamatergic corticostriatal projections from the cerebral cortex innervate the basal ganglia at the striatal medium spiny neuron, which also receives modulatory dopamine projections from midbrain nuclei. Both dopamine and glutamate have been implicated in numerous neuropsychiatric disorders including Parkinson's disease, Huntington's disease and substance dependence. We have recently shown that dopamine depresses the release of glutamate from a subset of cortical terminals providing filtering of cortical information to the striatum and that alterations in striatal dopamine release lead to long-term changes in striatal excitation mediated by dopamine receptor hypersensitivity and neuroplasticity. Using mouse models for dopamine depletion and dopamine excess, we study the effect of altered dopamine availability on striatal synaptic plasticity. We define the mechanisms underlying these neuroplastic alterations and we determine if drug-induced behaviors are determined by such adaptations. We utilize a newly developed imaging technique that allows direct visualization of release from corticostriatal presynaptic terminals in murine striatal slice preparations.