Delayed reward discounting tasks are very similar in human and non-human animals, making this an ideal translational endophenotype [70]. In findings that mirror the human literature, P mice were more impulsive than NP mice in a delayed reward discounting task [102]. Outbred mice that more steeply discounted delayed rewards also displayed more sensitivity to the stimulant effects of ethanol after repeated exposures [103], suggesting that delayed reward discounting and ethanol sensitization (one component of the differentiator model discussed above) may share underlying predispositions to AUD. We note that this translational literature is not entirely consistent. In one study there were no differences in delayed reward discounting between mice that were bred to either consume high or low amounts of ethanol [104], and there is also some evidence that mice bred to be less sensitive to the reinforcing effects of drugs exhibited greater delay discounting compared to mice that were more sensitive to these reinforcing effects [105]. These differences may be attributable to mouse strain differences, and highlight the difficulties in identifying the appropriate model system for translational studies of candidate endophenotypes.
