Altered cerebellar function in mice lacking CaV2.3 Ca2+ channel

Makoto Osanai, Hironao Saegusa, An a. Kazuno, Shin Nagayama, Qiuping Hu, Shuqin Zong, Takayuki Murakoshi, Tsutomu Tanabe

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


Voltage-dependent Ca2+ channels play important roles in cerebellar functions including motor coordination and learning. Since abundant expression of CaV2.3 Ca2+ channel gene in the cerebellum was detected, we searched for possible deficits in the cerebellar functions in the CaV2.3 mutant mice. Behavioral analysis detected in delayed motor learning in rotarod tests in mice heterozygous and homozygous for the CaV2.3 gene disruption (CaV2.3+/- and CaV2.3-/-, respectively). Electrophysiological analysis of mutant mice revealed perplexing results: deficit in long-term depression (LTD) at the parallel fiber Purkinje cell synapse in CaV2.3+/- mice but apparently normal LTD in CaV2.3-/- mice. On the other hand, the number of spikes evoked by current injection in Purkinje cells under the current-clamp mode decreased in CaV2.3 mutant mice in a gene dosage-dependent manner, suggesting that CaV2.3 channel contributed to spike generation in Purkinje cells. Thus, CaV2.3 channel seems to play some roles in cerebellar functions.

Original languageEnglish
Pages (from-to)920-925
Number of pages6
JournalBiochemical and biophysical research communications
Issue number3
Publication statusPublished - 2006 Jun 9
Externally publishedYes


  • Ca2.3 channel
  • Discharge property
  • Knock-out mouse
  • Long-term depression
  • R-type Ca channel
  • Rotarod
  • Voltage-dependent Ca channel

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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