An individual's risk for earning a diagnosis of dependence on alcohol (ethanol) has been shown over many years to reflect both genetic and environmental influences to an approximately equal degree (Enoch et al. 2003). Genetic risk is also clearly conditional upon multiple environmental circumstances, making it difficult to estimate any particular individual's specific risk (Johnson et al. 1998). Studies of gene-environment interaction are in theory much easier to perform with suitable animal models, where matings can be arranged and environmental control is relatively easy. So too, are studies whose goal is to identify any of the multiple genes affecting risk. The advantages of rodents for modeling alcohol dependence phenotypes were recognized in the late 1940s, when Jorge Mardones began to selectively breed rat lines with high (UChB) or low (UChA) relative preference for 10% alcohol solutions when water was freely available (Mardones and Segovia-Riquelme 1983). Over the course of several days, animals develop a stable and characteristic intake of ethanol, which can be indexed as either the relative preference for ethanol (the preference ratio, or PR, equals the percentage of
