It has been suggested that excessive noradrenergic activation which accompanies anxiety and hyperarousal may contribute to increased alcohol drinking in an effort to self-medicate, since alcohol is sympatho-suppressive, anxiolytic, and sedating (Edwards, Chandler, Hensman, & Peto, 1972; Koob & LeMoal, 1997; Kushner, Sher, & Beitman, 1990; Kushner, Sher, & Erickson, 1999; Shirao et al., 1988). Numerous lines of evidence support this view: a) anxiety is associated with increased brain noradrenergic and associated sympathoadrenal activation (Kopin, 1984; Sullivan, Coplan, Kent, & Gorman, 1999), b) “anxious” rats consume more alcohol than “non-anxious” rats (Spanagel et al., 1995), c) blocking norepinephrine biosynthesis decreases alcohol self-administration by rodents (Amit, Brown, Levitan, & Ogren, 1977; Brown, Amit, Levitan, Ogren, & Sutherland, 1977; Davis, Smith, & Werner, 1978), d) alcoholics commonly state that relief of anxiety is an important reason for drinking (e.g., Edwards et al., 1972), e) alcoholism co-occurs at high rates with anxiety disorders (Kushner et al., 1990), suggesting that the two disorders represent manifestations of similar underlying mechanisms (Merikangas, Risch, & Weissman, 1994; Merikangas et al., 1998; Sinha, Robinson, & O'Malley, 1998), f)
