An additional strength of this model is that HAP mice express other neurobehavioral phenotypes consistent with the clinical AUD description, thus increasing its translational validity. HAP mice exhibit a greater basal pharmacodynamic, but not pharmacokinetic, alcohol tolerance capacity relative to LAP mice and will drink alcohol to the point of both pharmacodynamic and pharmacokinetic tolerance development (Fritz & Boehm II 2014; Fritz et al. 2013). In addition, HAP mice are more impulsive than LAP mice (Oberlin & Grahame 2009), develop sensitization to alcohol’s psychomotor stimulating effects (Grahame et al. 2000), and demonstrate binge-like alcohol consumption (Linsenbardt & Boehm 2015). Collectively, these data strongly support the use of HAP and LAP mice as divergent genetic risk models for AUD development.
