Abstract:
:P/Q-type voltage-dependent Ca(2+) channels (VDCCs) are highly expressed in the cerebellum, and mutations of these channels are associated with disrupted motor function. Several allelic variants of the alpha1A pore-forming subunit of P/Q-type VDCCs have been described, and mice homozygous for these mutations exhibit gait ataxia, as do alpha1A knockout mice. Here we report that heterozygous alpha1A mutants also have a motor phenotype. Mice heterozygous for the leaner and alpha1A knockout mutations exhibit impaired motor learning in the vestibulo-ocular reflex (VOR), suggesting that subtle disruption of P/Q Ca(2+) currents is sufficient to disrupt motor function. Basal VOR and optokinetic reflex performance were normal in the heterozygotes but severely impaired in the leaner and alpha1A knockout homozygotes.
journal_name
J Neurophysioljournal_title
Journal of neurophysiologyauthors
Katoh A,Jindal JA,Raymond JLdoi
10.1152/jn.00322.2006subject
Has Abstractpub_date
2007-02-01 00:00:00pages
1280-7issue
2eissn
0022-3077issn
1522-1598pii
00322.2006journal_volume
97pub_type
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