Twin and adoption studies have shown that the heritability of alcoholism may be as high as 50-60% (Kendler et al., 1997, Prescott & Kendler, 1999). The neuropathophysiology of alcoholism and its underlying genetic architecture is complex and remains largely elusive. In recent years, progress in the identification of genetic risk has occurred through the use of intermediate phenotypes for alcohol use disorders (Ducci & Goldman, 2008, Hines et al., 2005), including the effects of alcohol on the neural pathways of stress. The corticotropin releasing factor (CRF) is critical to the stress response through its activation of the corticotropin-releasing hormone type I receptor (CRHR1), as CRF stimulates the synthesis and release of adrenocorticotropic hormone (ACTH) by the pituitary which in turn stimulates the synthesis and release of cortisol by the adrenal cortex. Hypothalamic-pituitary-adrenal (HPA) axis dysregulation can develop in response to childhood trauma, which permanently alters the stress response to acute stressors into adulthood (Nemeroff, 2004). Further, dysregulation of the extra hypothalamic CRF system is associated with the development and maintenance of alcoholism in both preclinical (Koob, 2008, Koob, 2010) and
