Periods of abstinence (i.e., withdrawal) are characterized by elevated glucocorticoid levels that reflect increased HPA axis activity. This, along with increased activity of the sympathetic division of the autonomic nervous system, mediate an array of physiological symptoms of acute alcohol withdrawal (e.g., tachycardia, elevated blood pressure, diaphoresis, body temperature dysregulation) (Becker, 2000; Heilig et al., 2010). While heightened HPA axis activation associated with withdrawal usually resolves within a few days (Kakihana, 1979; Tabakoff et al., 1978), blunted HPA axis responsiveness appears to persist for a protracted period of time (Rasmussen et al., 2000; Zorrilla et al., 2001). In some cases, this may be accompanied by reduced basal levels of circulating corticosteroids (Rasmussen et al., 2000; Richardson et al., 2008a; Zorrilla et al., 2001). These perturbations in HPA axis function align with findings reported in abstinent human alcoholics (Adinoff et al., 1990; Adinoff et al., 1991; Costa et al., 1996; Lovallo et al., 2000; Willenbring et al., 1984). Dysregulation of HPA axis function that extends into protracted phases of withdrawal is thought to contribute to dysphoria and negative affect associated with
