Animal models have been successfully used in developing treatments for both medical and psychiatric disorders (Griffin, 2002; McKinney, 2001). An animal model allows an experimenter to control an animal’s genetic background, environmental factors and prior drug experience. In addition, it allows for the examination of neurobehavioral, neurochemical and neurophysiological correlates associated with the behavioral, physiological or neurological state that is modeled, in the present case alcohol abuse and dependence. These correlates can, in turn, facilitate the development of pharmacological and/or behavioral treatments for these disorders. There have been reservations as to whether a valid animal model of alcoholism could be developed (Cicero, 1979). These concerns stemmed from the fact that, in general, heterogeneous stock rats consume only modest levels of ethanol, such that blood alcohol concentrations (BACs) achieved are minimal. Thus, experimental manipulations such as fluid deprivation (Sandi et al., 1990), schedule-induced polydipsia (Meisch, 1976), scheduled availability (Holloway et al., 1984), sucrose-fading (Samson, 1986) and forced induction of dependence (Deutsch and Eisner, 1977; Roberts et al., 2000) are generally required to induce appreciable levels of ethanol intake or self-administration which
