A functional role for EWcp-Ucn1 neurons in alcohol consumption is supported by findings that electrolytic lesions of the mouse EWcp decreased alcohol preference in a Ucn1-dependent manner (Giardino et al., 2011a). This issue has, however, been complicated by findings in which exogenous administration of urocortins decreased alcohol intake in non-dependent mice (Lowery et al., 2010; Ryabinin et al., 2008; Sharpe and Phillips, 2009). It was recently shown that genetic deletion of Ucn1 blunts alcohol preference and alcohol-induced reward, but does not influence alcohol-induced aversion (Giardino et al., 2011a). In non-dependent animals, the net effect of endogenous Ucn1 activity is to promote alcohol consumption, but this seems to be mediated through appetitive rather than aversive, stress-related mechanisms.
