Given its pivotal role in mediating neuroendocrine and brain (outside the HPA axis) responses to stress, it is not surprising that a large number of studies have examined the effect of chronic alcohol on CRF activity in relation to alcohol drinking. The non-selective peptide CRF antagonist (D-Phe-CRF12-41) reduced excessive drinking in dependent animals when administered into the brain ventricles (Finn et al., 2007; Valdez et al., 2002) or into the CeA (Funk et al., 2006). Systemic administration of CRF1 receptor-selective antagonists reduced up-regulated drinking in dependent mice (Chu et al., 2007) and rats (Funk et al., 2007; Gehlert et al., 2007; Gilpin et al., 2008b; Richardson et al., 2008b; Roberto et al., 2010; Sabino et al., 2006; Sommer et al., 2008).
