Not only can immediate responses to ethanol affect neuronal excitability, predisposition to AUD itself has also been associated with altered excitability. Electroencephalogram (EEG) studies conducted by the Collaborative Studies on the Genetics of Alcoholism (COGA) identified neurophysiological features commonly observed among subjects diagnosed with AUD, long-term abstinent individuals, as well as individuals at risk for AUD. Multiple studies report an association between AUD and time-locked as well as resting-state EEG responses, including lower P300 amplitude in oddball tasks, lower event-related oscillation (ERO) power during reward processing, particularly frontal theta power, and increased resting state beta power (Meyers et al., 2023). This indicates a higher-level imbalance in the ratio of excitation/inhibition as an index of neural hyper excitability or disinhibition in individuals with AUD and at-risk family members, both in the presence of alcohol usage and among non-users at risk. This predicts a bi-directional interaction between altered excitability and alcohol use.