Prolonged excessive alcohol consumption constitutes a potent stressor to the organism, setting in motion a host of neuroadaptive changes within brain reward and stress systems (Becker, 2012; Hansson et al., 2008; Koob, 2013; Koob and Le Moal, 2008; Vengeliene et al., 2008). Stress associated with chronic alcohol exposure and withdrawal experience continually challenges the organism through progressive dysregulation of brain reward and stress systems beyond normal homeostatic limits (Koob, 2003). These neuroadaptive changes are postulated to impact neural and physiological systems integral to the motivational effects of alcohol and, consequently, contribute to escalation of drinking and maintenance of sustained excessive alcohol consumption associated with dependence (Becker, 2012, 2013; Heilig et al., 2010; Koob, 2013). In this vein, alcohol dependence may be viewed as a persistent dysfunctional (allostatic) state, with the organism rendered ill-equipped to exert appropriate behavioral control over alcohol consumption, as well as appropriately respond to other (additional) stressful events that may provoke return to excessive drinking.
