Alcohol use disorder (AUD) alters decision-making control over actions, but disruptions to the responsible neural circuit mechanisms are unclear. Premotor corticostriatal circuits are implicated in balancing goal-directed and habitual control over actions and show disruption in disorders with compulsive, inflexible behaviors, including AUD. However, whether there is a causal link between disrupted premotor activity and altered action control is unknown. Here, we find that mice chronically exposed to alcohol (chronic intermittent ethanol CIE) showed impaired ability to use recent action information to guide subsequent actions. Prior CIE exposure resulted in aberrant increases in the calcium activity of premotor cortex (M2) neurons that project to the dorsal medial striatum (M2-DMS) during action control. Chemogenetic reduction of this CIE-induced hyperactivity in M2-DMS neurons rescued goal-directed action control. This suggests a direct, causal relationship between chronic alcohol disruption to premotor circuits and decision-making strategy and provides mechanistic support for targeting activity of human premotor regions as a potential treatment in AUD. Display omitted •Chronic alcohol disrupts action control•Chronic alcohol induces hyperactive M2-DMS during action control•Chemogenetic suppression of M2-DMS hyperactivity rescues action control Appropriate action control relies on learning from recent experiences. Using a rodent model, Schreiner et al. find evidence that chronic alcohol exposure disrupts action control by inducing aberrant hyperactivity in premotor corticostriatal circuits. These findings support the targeting of premotor cortex activity for therapeutic treatment in alcohol use disorder.