Increased motor drive and sleep loss in mice lacking Kv3-type potassium channels

F. Espinosa, G. Marks, N. Heintz, R. H. Joho

Research output: Contribution to journalArticlepeer-review

78 Scopus citations


The voltage-gated potassium channels Kv3.1 and Kv3.3 are widely expressed in the brain, including areas implicated in the control of motor activity and in areas thought to regulate arousal states. Although Kv3.1 and Kv3.3-single mutants show some physiological changes, previous studies revealed relatively subtle behavioral alterations suggesting that Kv3.1 and Kv3.3 Kv13 subunits may be encoded by a pair of redundant genes. In agreement with this hypothesis, Kv3.1/Kv3.3-deficient 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 Kv3.1/Kv3.3-deficient 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 Kv3.1-single mutants but not in Kv3.3-single mutants. These findings indicate that the absence of Kv3.1-channel subunits is primarily responsible for the increased motor drive and the reduction in sleep time.

Original languageEnglish (US)
Pages (from-to)90-100
Number of pages11
JournalGenes, Brain and Behavior
Issue number2
StatePublished - Apr 2004


  • Hyperactivity
  • Mouse mutants
  • Myoclonus
  • Potassium channels
  • Sleep disorder

ASJC Scopus subject areas

  • Genetics
  • Neurology
  • Behavioral Neuroscience


Dive into the research topics of 'Increased motor drive and sleep loss in mice lacking Kv3-type potassium channels'. Together they form a unique fingerprint.

Cite this