Clearly, experimental approaches are more feasible when employing nontraumatic levels of stress in humans. Indeed, some of the largest individual differences in alcohol sensitivity associated with family history of alcoholism are in the domain of autonomic stress reactivity (e.g., Finn, Zeitouni, & Pihl, 1990; Levenson, Oyama, & Meek, 1987). Additionally, there are a number of paradigms for assessing negative affect/stress that translate across human and mammalian species for examining stress reactivity using psychophysiological measures (e.g., affect-potentiated startle) and behavioral measures (e.g., passive avoidance) that have been shown to be alcohol sensitive (e.g., Donohue, Curtin, & Lang, 2007; Sher, 1987; Sher & Grekin, 2005). Moreover, human laboratory models of acute exposure to stress (e.g., Sinha, 2001; Sinha et al., 2006) and the examination of genetic variation that may interact with acute stress (see Clarke & Schumann, 2009) has proven valuable in the study of relapse and clinical alcohol dependence. Given that there is some controversy over the role of stress in the progression of alcohol dependence, translational models that bridge the animal and human work are sorely needed to develop a better understanding of stress and genetic factors that may interact with exposure to stress.
