The central amygdala (CeA) plays a central role in physiological and behavioral responses to fearful stimuli, stressful stimuli, and drug-related stimuli. The CeA receives dense inputs from cortical regions, is the major output region of the amygdala, is primarily GABAergic (inhibitory), and expresses high levels of pro- and anti-stress peptides. The CeA is also a constituent region of a conceptual macrostructure called the extended amygdala that is recruited during the transition to alcohol dependence. In this review, we discuss neurotransmission in the CeA as a potential integrative hub between anxiety disorders and Alcohol Use Disorder (AUD), which are commonly co-occurring in humans. Human imaging work and multi-disciplinary work in animals collectively suggest that CeA structure and function are altered in individuals with anxiety disorders and AUD, the end result of which may be disinhibition of downstream “effector” regions that regulate anxiety- and alcohol-related behaviors.