Motor Deficits in Homozygous and Heterozygous P/Q-type Calcium Channel Mutants.
From: Department of Neurobiology, Stanford University, 299 W. Campus Drive, Stanford, CA 94305-5125, USA.
Journal of neurophysiology
- Publish Date: Feb 2007
- ISSN: 0022-3077
- Volume: 97
- Issue: 2
- Pages: 1280-7
- Medium: Print
- Language: English
- Citation (JAMA): Katoh Akira, Jindal Jenelle A, Raymond Jennifer L, et al. Motor Deficits in Homozygous and Heterozygous P/Q-type Calcium Channel Mutants.. J. Neurophysiol. Feb 2007;97:1280-7
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.
Mesh Headings (Keywords): Animals, Calcium Channels, P-Type, Calcium Channels, Q-Type, Gait Ataxia, Heterozygote, Homozygote, Mice, Mice, Inbred C57BL, Mice, Knockout, Oculomotor Muscles, Oculomotor Nerve, Phenotype, Psychomotor Performance
Check for Full Text / PubMed Unique Identifier (PMID): 17005620
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