While the neural substrates of impulsive behavior are commonly studied in humans and preclinical models, the behavioral substrates which contribute to impulsivity are still understudied. Understanding the behavioral underpinnings of impulsive behavior will allow us to better model disorders of impulsive behavior in animals, and also help more clearly define the underlying neural circuits. Our goal here was to explore behavioral correlates and effectors of impulsive behavior, using a mouse model

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... for disordered impulsivity, namely mice lacking the serotonin 1B receptor (5-HT1BR). Our past work, along with others', implicates 5-HT1BR in the regulation of impulsivity, specifically, impulsive action. In mice, the absence of 5-HT1BR expression in adulthood results in a reduced ability to wait or withhold responses. We report here, that in addition to increased impulsive action, mice lacking expression of 5-HT1BR show increased goal-directed responding and motivation, with no differences in extinction, development of habitual behavior, or impulsive choice measured in a delay discounting paradigm. Interestingly, mice lacking 5-HT1BR also show increased hedonic responses to sweet rewards. Finally, using a newly developed paradigm, we report that increasing reward value increases impulsive action on a trial-by-trial basis, showing how changing reward value can directly influence impulsive behavior. Taken together, these data support the hypothesis that the effects of 5-HT1BR on impulsive action reflect enhanced reward sensitivity, and point to potential neural and phenotypic causes for clinically-relevant increases in impulsivity.