Additional research will be necessary to clarify which gene or genes are responsible for these protective effects. Animal studies (Le et al. 2000; Shaham et al. 2000; Funk et al. 2003; Hansson et al. 2006; Sommer et al. 2008; Heilig & Koob, 2007; Pastor et al. 2008; Funk et al. 2003) published to date provide evidence that alterations in CRHR1 expression are involved in important facets of alcohol consumption, dependence, and relapse. Marchigian-Sardinian Preferring (msP) rats, selectively bred for high alcohol preference, have a CRHR1 promoter polymorphism that results in increased CRHR1 expression in limbic regions (Hansson et al. 2006). Alcohol self-administration by non-dependent msP rats is suppressed by CRF1 antagonists; similar effects are not seen in unselected Wistar (control) rats. msP rats also display greater sensitivity to inhibition of foot-shock-induced ethanol reinstatement by a CRF1 antagonist than do control rats.(Hansson et al. 2006) Rodents (not limited to those bred for ethanol preference) experience a prolonged period of increased anxiety and stress responsivity when withdrawn from ethanol after having been made dependent, symptoms that can be blocked by administration of
