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1 Laboratoire de Physiologie Générale, Unité Mixte de Recherche 6018 du Centre National de la Recherche Scientifique, Faculté des Sciences et des Techniques, Université de Nantes, F-44322 Nantes, Cedex 03; and 2 Laboratoire des Gènes et des Protéines Musculaires, Ecole Polytechnique, Centre National de la Recherche Scientifique 1088, Université Paris-Sud, 91405 Orsay, Cedex, France
The present study was designed to examine whether changes in Ca2+ release by inositol-1,4,5-trisphosphate (IP3) in 8-, 15-, and 30-day-old rat skeletal muscles could be associated with the expression of IP3 receptors. Experiments were conducted in slow-twitch muscle in which both IP3-induced Ca2+ release and IP3-receptor (IP3R) expression have been shown to be larger than in fast-twitch muscle. In saponin-skinned fibers, IP3 induced transient contractile responses in which the amplitude was dependent on the Ca2+-loading period with the maximal IP3 contracture being at 20 min of loading. The IP3 tension decreased during postnatal development, was partially inhibited by ryanodine (100 µM), and was blocked by heparin (20-400 µg/ml). Amplification of the DNA sequence encoding for IP3R isoforms (using the RT-PCR technique) showed that in slow-twitch muscle, the type 2 isoform is mainly expressed, and its level decreases during postnatal development in parallel with changes in IP3 responses in immature fibers. IP3-induced Ca2+ release would then have greater participation in excitation-contraction coupling in developing fibers than in mature muscle.
sarcoplasmic reticulum Ca2+ release; inositol-1,4,5-trisphosphate; skinned slow-twitch fibers; mammalian muscles
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J. K. Foskett, C. White, K.-H. Cheung, and D.-O. D. Mak Inositol Trisphosphate Receptor Ca2+ Release Channels Physiol Rev, April 1, 2007; 87(2): 593 - 658. [Abstract] [Full Text] [PDF] |
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