The striatal complex critically integrates a variety of inputs to regulate the motivation to perform, and the performance of, discrete action sequences executed under goal-directed and habitual strategies. Drugs of abuse such as alcohol target the striatal complex, strengthening associations between rewards and external cues and, over time, shifting intake from being goal-oriented toward compulsively automated. Our work herein examines alcohol targeting of the striatal complex under two different conditions: under the first condition, we ultimately aim to determine if and how alcohol alters the firing of a GABAergic cellular population called fast-spiking interneurons (FSIs) known to regulate striatal output to mediate habitual behaviors. To that end, we uncover a novel mechanism mediating FSI synchronous firing. Under the second condition, we examine how acute alcohol exposure influences the experience of reward. Alcohol strengthens a form of inhibitory plasticity in the NAc that is mediated by brain derived neurotrophic factor (BDNF) signaling, but whether this interaction regulates alcohol reward is unknown. We here discover the sources of BDNF that drive this form of plasticity and further find that simulating BDNF-releasing afferents in vivo is rewarding to mice. We also find that alcohol and BDNF may interact in vivo to mediate reward. As such, these findings point to a novel mechanism for alcohol reward: BDNF signaling at inhibitory synapses in the NAc.