The results we obtained largely reveal an association between severe AUD and increased PAC than in the unaffected controls, however it remains unclear how these effects might reflect the underlying neurophysiology of AUD. The task of interpreting these results is complicated by the absence of any previous studies of putative roles PAC might play in AUD etiology. A review of earlier studies of how PAC strength changes under different experimental conditions can provide helpful context for how to interpret our results.
