Significance Alcoholism is characterized by a progressive degradation of executive control and an increase in compulsive alcohol seeking that is hypothesized to involve a shift from prefrontal cortex to dorsal striatal (DLS) control over behavior. Here, we show that mice exposed to chronic intermittent alcohol exhibited expansion of dendritic material in DLS neurons, coupled with loss of endocannabinoid CB1 receptor signaling and CB1-mediated long-term depression in the DLS. Behaviorally, chronic alcohol exposure facilitated various forms of DLS-dependent learning and augmented in vivo DLS neuronal activity as correct learned choices were made. These findings support a model in which chronic ethanol causes DLS neuroadaptations that prime for greater striatal control over behavior, potentially contributing to the progression of alcoholism.