increased motor drive and sleep loss in mice lacking kv3type potassium channels the voltagegated potassium channels kv31 and kv33 are widely expressed in the brain including areas implicated in the control of motor activity and in areas thought to regulate arousal states although kv31 and kv33single mutants show some physiological changes previous studies revealed relatively subtle behavioral alterations suggesting that kv31 and kv33 channel subunits may be encoded by a pair of redundant genes in agreement with this hypothesis kv31kv33deficient mice display a strong mutant phenotype that includes motor dysfunction ataxia myoclonus tremor and hyperactivity when exposed to a novel environment in this paper we report that kv31kv33deficient mice are also constitutively hyperactive compared to wildtype mice double mutants display restlessness that is particularly prominent during the light period when mice are normally at rest characterized by more than a doubling of ambulatory and stereotypic activity and accompanied by a 40 sleep reduction when we reinvestigated both single mutants we observed constitutive increases of ambulatory and stereotypic activity in conjunction with sleep loss in kv31single mutants but not in kv33single mutants these findings indicate that the absence of kv31channel subunits is primarily responsible for the increased motor drive and the reduction in sleep time