Our laboratory has a general interest in the relationship between CNS mechanisms that regulate ingestive behavior and drug abuse, with a particular interest in neuroadaptations induced by food restriction that increase the reward magnitude of abused drugs and predispose subjects to binge-eating. In recent years we have established that unconditioned reward-related effects of numerous drugs of abuse and dopamine receptor agonists are increased by food restriction. In tissue preparations, we have identified a variety of dorsal and ventral striatal neuroadaptations that are hypothesized to mediate increased reward sensitivity and synaptic plasticity during chronic food restriction, including upregulation of D-1 dopamine receptor-mediated phosphorylation of NMDA receptor NR1 and AMPA receptor GluR1 subunits, and increased ERK 1/2 MAP kinase and CaM kinase II signaling. Current research is focused on striatal AMPA receptor trafficking and MAP kinase activation in response to palatable food and drugs of abuse, and their potential roles in the genesis of enduring maladaptive reward-directed behavior.