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    Proc Natl Acad Sci U S A. 2007 Nov 6;104(45):17819-24. Epub 2007 Oct 29.

    Gamma-band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice.

    Llinás RR, Choi S, Urbano FJ, Shin HS.

    Source

    Department of Physiology and Neuroscience, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA. llinar01@med.nyu.edu

    Abstract

    Thalamocortical in vivo and in vitro function was studied in mice lacking P/Q-type calcium channels (Cav2.1), in which N-type calcium channels (Cav2.2) supported central synaptic transmission. Unexpectedly, in vitro patch recordings from thalamic neurons demonstrated no gamma-band subthreshold oscillation, and voltage-sensitive dye imaging demonstrated an absence of cortical gamma-band-dependent columnar activation involving cortical inhibitory interneuron activity. In vivo electroencephalogram recordings showed persistent absence status and a dramatic reduction of gamma-band activity. Pharmacological block of T-type calcium channels (Cav3), although not noticeably affecting normal control animals, left the knockout mice in a coma-like state. Hence, although N-type calcium channels can rescue P/Q-dependent synaptic transmission, P/Q calcium channels are essential in the generation of gamma-band activity and resultant cognitive function.

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    PMID:
    17968008
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2077027
    Free PMC Article

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