well as chronic intermittent ethanol consumption (Cagetti, Pinna et al. 2004), but systematic, dose-dependent studies are lacking. One mechanism by which alcohol could alter HPA activity is via modulation of glutamatergic and GABAergic input on parvocellular neurons of the PVN of the hypothalamus. These cells produce CRH and arginine vasopressin (AVP), peptides essential for the stress response, and ACTH release from the anterior pituitary (Rivier and Vale 1983). Additional studies are needed to better understand alcohol-induced alterations in the HPA response and the hyporesponsiveness to stress observed in those with AUD.
