experience stimulant-like or sedative-like effects of alcohol under normal conditions. In healthy males given the Trier Social Stress Test, production of salivary cortisol was inhibited when ethanol was administered intravenously after a stressor to achieve a breath alcohol concentration of 40mg/dL (Childs, O'Connor et al. 2011). Similarly, acute ethanol consumption in healthy men blocked activation of the HPA axis by naloxone (at the level of the hypothalamus or above) (Cami, de la Torre et al. 1988), blunted the ACTH and cortisol response to corticotropin-releasing hormone (CRH; at the level of the pituitary) but not ACTH (level of the adrenal) (Waltman, Blevins et al. 1993). Therefore, although acute alcohol consumption can activate the HPA axis in non-dependent subjects, studies indicate that it interferes with the HPA responses to other stressors potentially through a negative feedback loop. Studies show altered expression of steroidogenic enzymes necessary for metabolism of steroid hormones from their precursors with both acute (Kim, Ha et al. 2003) as 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
