Drugs targeting the noradrenergic system also has been reported to reduce alcohol consumption in a number of preclinical studies. Prazosin reduced alcohol drinking in rats selectively bred for high alcohol preference (Froehlich et al., 2013a; Rasmussen et al., 2009). The drug also was effective in reducing intake in relapse models involving repeated alcohol deprivation periods (Froehlich et al., 2015) and stress-induced reinstatement of alcohol seeking behavior (Le et al., 2011). Prazosin treatment prior to stress (restraint) exposure during repeated deprivation periods prevented increased anxiety-like behaviors during a subsequent deprivation period (Rasmussen et al., 2017). Additionally, several studies found prazosin in combination with naltrexone to be more effective in reducing drinking than either drug given alone (Froehlich et al., 2013b; Rasmussen et al., 2015; Verplaetse and Czachowski, 2015). Studies also have shown prazosin reduces alcohol self-administration in dependent rats (Walker et al., 2008), and a similar effect was obtained with the beta-adrenergic antagonist propranolol (Gilpin and Koob, 2010). Given this preclinical and clinical evidence, there is active interest in the potential for drugs targeting central adrenergic receptors in the treatment of
