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* The Neuroscience Group, School of Biomedical Sciences, Faculty of Health, The University of Newcastle, Callaghan NSW 2308, Australia; Department of Pharmacology and Molecular Therapeutics, College of Medicine, University of South Florida, Tampa, Florida, 33612-4799 USA; and Department of Civil and Environmental Engineering, The University of Melbourne, Victoria 3010, Australia
Correspondence: Address reprint requests to Mohammad S. Imtiaz, Tel.: 61-2-49215626; Fax: 61-2-49217406; E-mail: Mohammad.Imtiaz{at}newcastle.edu.au.
Slow waves are rhythmic depolarizations that underlie mechanical activity of many smooth muscles. Slow waves result through rhythmic Ca2+ release from intracellular Ca2+ stores through inositol 1,4,5-trisphosphate (IP3) sensitive receptors and Ca2+-induced Ca2+ release. Ca2+ oscillations are transformed into membrane depolarizations by generation of a Ca2+-activated inward current. Importantly, the store Ca2+ oscillations that underlie slow waves are entrained across many cells over large distances. It has been shown that IP3 receptor-mediated Ca2+ release is enhanced by membrane depolarization. Previous studies have implicated diffusion of Ca2+ or the second messenger IP3 across gap junctions in synchronization of Ca2+ oscillations. In this study, a novel mechanism of Ca2+ store entrainment through depolarization-induced IP3 receptor-mediated Ca2+ release is investigated. This mechanism is significantly different from chemical coupling-based mechanisms, as membrane potential has a coupling effect over distances several orders of magnitude greater than either diffusion of Ca2+ or IP3 through gap junctions. It is shown that electrical coupling acting through voltage-dependent modulation of store Ca2+ release is able to synchronize oscillations of cells even when cells are widely separated and have different intrinsic frequencies of oscillation.
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