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1 Neurobiology, Stanford University, Stanford, California, United States
* To whom correspondence should be addressed. E-mail: jenr{at}stanford.edu.
P/Q-type voltage-dependent Ca2+ channels (VDCCs) are highly expressed in the cerebellum, and mutations of these channels are associated with disrupted motor function. Several allelic variants of the 
1A pore-forming subunit of P/Q-type VDCCs have been described, and mice homozygous for these mutations exhibit gait ataxia, as do 1A knockout mice. Here we report that heterozygous 1A mutants also have a motor phenotype. Mice heterozygous for the leaner and 1A knockout mutations exhibit impaired motor learning in the vestibulo-ocular reflex (VOR), suggesting that subtle disruption of P/Q Ca2+ currents is sufficient to disrupt motor function. Basal VOR and optokinetic reflex (OKR) performance were normal in the heterozygotes but severely impaired in the leaner and 1A knockout homozygotes.
This article has been cited by other articles:
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  S. Liu and D. D. Friel Impact of the leaner P/Q-type Ca2+ channel mutation on excitatory synaptic transmission in cerebellar Purkinje cells J. Physiol., September 15, 2008; 586(18): 4501 - 4515. [Abstract] [Full Text] [PDF]
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 R. R. Kimpo and J. L. Raymond Impaired Motor Learning in the Vestibulo-Ocular Reflex in Mice with Multiple Climbing Fiber Input to Cerebellar Purkinje Cells J. Neurosci., May 23, 2007; 27(21): 5672 - 5682. [Abstract] [Full Text] [PDF]
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