IP3 receptors and associated Ca2+ signals localize to satellite cells and to components of the neuromuscular junction in skeletal muscle. - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue Journal of Neuroscience Année : 2003

IP3 receptors and associated Ca2+ signals localize to satellite cells and to components of the neuromuscular junction in skeletal muscle.

Résumé

Recently, we described an inositol 1,4,5-trisphosphate (IP3) signaling system in cultured rodent skeletal muscle, triggered by high K+ and affecting gene transcription (Powell et al., 2001). Now, in a study of adult rodent skeletal muscle, using immunocytology and confocal microscopy, we have found a high level of IP3 receptor (IP3R) staining in satellite cells, which have been shown recently to contribute to nuclei in adult fibers after muscle exercise. These IP3R staining cells are positively identified as satellite cells by their position, morphology and staining with satellite-cell-specific antibodies such as desmin and neural cell adhesion molecule. IP3Rs are also localized to postsynaptic components of the neuromuscular junction (NMJ), in areas surrounding the nuclei of the motor end plate, and in perisynaptic Schwann cells, and localized close to nicotinic acetylcholine receptors of the endplate gutters. Ca2+ imaging experiments show calcium release at the motor endplate upon K+ depolarization precisely in these IP3R-rich regions. We suggest that electrical activity stimulates IP3-associated Ca2+ signals that may be involved in gene regulation in satellite cells and in elements of the NMJ, contributing both to muscle fiber growth and stabilization of the NMJ.
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Dates et versions

hal-00188162 , version 1 (15-11-2007)

Identifiants

  • HAL Id : hal-00188162 , version 1
  • PUBMED : 12967979

Citer

Jeanne A Powell, Jordi Molgó, Dany S Adams, Cesare Colasante, Aislinn Williams, et al.. IP3 receptors and associated Ca2+ signals localize to satellite cells and to components of the neuromuscular junction in skeletal muscle.. Journal of Neuroscience, 2003, 23 (23), pp.8185-92. ⟨hal-00188162⟩

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