We previously tested the hypothesis that noradrenergic activation promotes and maintains alcohol drinking by assessing whether alcohol drinking in rats is decreased by prazosin treatment. Prazosin is a drug that is centrally active when administered peripherally and that decreases brain noradrenergic signaling by blocking postsynaptic α1-adrenergic receptors. Prazosin dose-dependently reduced withdrawal-induced operant self-administration of alcohol in alcohol-dependent Wistar rats (Walker, Rasmussen, Raskind, & Koob, 2008). Prazosin also suppressed voluntary alcohol drinking by rats selectively bred for alcohol preference (P line) when administered either acutely (Rasmussen, Alexander, Raskind, & Froehlich, 2009) or chronically (Froehlich, Hausauer, Federoff, Fischer, & Rasmussen, 2013; Froehlich, Hausauer, & Rasmussen, 2013). The ability of prazosin to reduce alcohol drinking has been confirmed in humans; Simpson and colleagues (2009) reported that prazosin decreased relapse alcohol drinking in treatment-seeking alcohol-dependent men. These results from both rodents and humans provide compelling evidence that noradrenergic activation plays an important role in mediating alcohol drinking and alcohol relapse.
