Project Summary/Abstract Response inhibition, or the ability to stop an action, is essential for successfully navigating everyday life, and loss of this control is a hallmark in many neurological disorders, such as alcohol use disorder. A major unanswered question for those experiencing alcohol use disorder is why they are unable to stop drinking: 1) after periods of abstinence that lead to relapse, 2) in situations that can lead to risk or themselves are inherently risky, and 3) to excessive amounts or binging once they have initiated drinking, all of which coalesce around action control as a key differentiator between healthy and disordered outcomes. It is known that brain regions responsible for action control, like the globus pallidus (GPe) are altered due to alcohol use. However, which underlying mechanisms, cell-types, neural circuits and subsequently their spatial organization are altered by alcohol and play key roles in controlling behaviors implicated in disordered alcohol use remain to be fully elucidated. This proposal leverages new genetic marker technologies, sophisticated electrophysiological and biosensing approaches, and advanced animal behavioral assays paired with in-vivo imaging. The proposed experiments will define, characterize, and modulate principal GPe neurons and those that form connections with them, to further resolve the neural basis of action selection in relation to stopping alcohol use. This study will generate new knowledge that helps further detail the complexity of the GPe and its role in balancing the promotion and inhibition of actions in relation to alcohol use. In the long term, this research will advance research on the neural correlates that drive key features of alcohol use disorder, identifying novel therapeutic targets and knowledge in the process. This research is particularly timely given the lack of information relevant to the recent surge in “high-intensity” binge drinking, and hyperkatifeia-motivated relapse, two phenomena that lead to excessive, avoidable harm that are highly dependent on response inhibition.