The task of identifying the correct phenotypes to be used in humans and animals is not straightforward, as alcohol-related concepts are often operationalized in a different manner in animal and human studies. Most obviously, clinical studies often times rely on diagnoses or symptom counts as primary phenotypes whereas animal models have adopted a more quantitative assessment of behavioral traits. For example, in mice, the severity of behavioral convulsions is commonly used as the primary measure of the alcohol withdrawal syndrome (Buck et al., 1997, 2002; Crabbe, 1998). Other withdrawal signs that are more common in humans (e.g., tremors, tachycardia, diaphoreses) are less studied in animals (Kosobud and Crabbe, 1986; Belknap et al., 1987, Philibin et al, 2008). Similarly, while level of response to alcohol in animals is measured using a variety of behaviors including the duration of the loss of righting reflex, in humans a self-report measure of the number of drinks needed to achieve a subjective “effect” the first five times an individual drank alcohol is often used (Schuckit et al., 2001). Such differences in phenotype definitions may contribute
