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    Cerebellum. 2009 Sep;8(3):222-30. Epub 2009 May 30.

    The ataxic Cacna1a-mutant mouse rolling nagoya: an overview of neuromorphological and electrophysiological findings.

    Plomp JJ, van den Maagdenberg AM, Kaja S.

    Source

    Department of Neurology, Leiden University Medical Centre, 2300 RC Leiden, The Netherlands. j.j.plomp@lumc.nl

    Abstract

    Homozygous rolling Nagoya natural mutant mice display a severe ataxic gait and frequently roll over to their side or back. The causative mutation resides in the Cacna1a gene, encoding the pore-forming alpha(1) subunit of Ca(v)2.1 type voltage-gated Ca(2+) channels. These channels are crucially involved in neuronal Ca(2+) signaling and in neurotransmitter release at many central synapses and, in the periphery, at the neuromuscular junction. We here review the behavioral, histological, biochemical, and neurophysiological studies on this mouse mutant and discuss its usefulness as a model of human neurological diseases associated with Ca(v)2.1 dysfunction.

    PMID:
    19484318
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2734259
    Free PMC Article

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