Expression of a cardiac Ca2+-release channel isoform in mammalian brain

Author:

Lai F A1,Dent M1,Wickenden C1,Xu L2,Kumari G2,Misra M3,Lee H B2,Sar M4,Meissner G2

Affiliation:

1. MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, U.K.

2. Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, U.S.A.

3. Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, U.S.A.

4. Department of Cell Biology and Anatomy, University of North Carolina School of Medicine, Chapel Hill, NC 27599, U.S.A.

Abstract

Mammalian brain possesses ryanodine-sensitive Ca2+ channels, which in muscle cells mediate rapid Ca2+ release from intracellular stores during excitation-contraction coupling. Analysis of bovine brain ryanodine receptor (RyR) channels suggests specific expression of the cardiac-muscle RyR isoform in mammalian brain. Localization using cardiac-muscle RyR-specific antibodies and antisense RNA revealed that brain RyRs were present in dendrites, cell bodies and terminals of rat forebrain, and highly enriched in the hippocampus. Activity of skeletal-muscle RyR channels is coupled to sarcolemmal voltage sensors, in contrast with cardiac-muscle RyR channels, which are known to be Ca(2+)-induced Ca(2+)-release channels. Thus Ca(2+)-induced Ca2+ release from intracellular stores mediated by brain RyR channels may be a major Ca(2+)-signalling pathway in specific regions of mammalian brain, and hence may play a fundamental role in neuronal Ca2+ homoeostasis.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry

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