| First Author | Osanai M | Year | 2006 |
| Journal | Biochem Biophys Res Commun | Volume | 344 |
| Issue | 3 | Pages | 920-5 |
| PubMed ID | 16631598 | Mgi Jnum | J:108529 |
| Mgi Id | MGI:3624207 | Doi | 10.1016/j.bbrc.2006.03.206 |
| Citation | Osanai M, et al. (2006) Altered cerebellar function in mice lacking CaV2.3 Ca2+ channel. Biochem Biophys Res Commun 344(3):920-5 |
| abstractText | Voltage-dependent Ca(2+) channels play important roles in cerebellar functions including motor coordination and learning. Since abundant expression of Ca(V)2.3 Ca(2+) channel gene in the cerebellum was detected, we searched for possible deficits in the cerebellar functions in the Ca(V)2.3 mutant mice. Behavioral analysis detected in delayed motor learning in rotarod tests in mice heterozygous and homozygous for the Ca(V)2.3 gene disruption (Ca(V)2.3+/- and Ca(V)2.3-/-, respectively). Electrophysiological analysis of mutant mice revealed perplexing results: deficit in long-term depression (LTD) at the parallel fiber Purkinje cell synapse in Ca(V)2.3+/- mice but apparently normal LTD in Ca(V)2.3-/- mice. On the other hand, the number of spikes evoked by current injection in Purkinje cells under the current-clamp mode decreased in Ca(V)2.3 mutant mice in a gene dosage-dependent manner, suggesting that Ca(V)2.3 channel contributed to spike generation in Purkinje cells. Thus, Ca(V)2.3 channel seems to play some roles in cerebellar functions. |
