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This Article Full Text Full Text (PDF) All Versions of this Article: 554/3/687    most recent jphysiol.2003.052571v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Parsons, S. P. Articles by Bolton, T. B. Search for Related Content PubMed PubMed Citation Articles by Parsons, S. P. Articles by Bolton, T. B.

Pharmacology and Clinical Pharmacology, Department of Basic Medical Sciences, St Georges Hospital Medical School, Cranmer Terrace, London, SW17 ORE, UK

After enzymatic dispersion of the muscle of the guinea-pig gastric fundus, single elongated cells were observed which differed from archetypal smooth muscle cells due to their knurled, tuberose or otherwise irregular surface morphology. These, but not archetypal smooth muscle cells, consistently displayed spontaneous localized (i.e. non-propagating) intracellular calcium ([Ca²⁺]_i) release events. Such calcium events were novel in their magnitude and kinetic profiles. They included short transient events, plateau events and events which coalesced spatially or temporally (compound events). Quantitative analysis of the events with an automatic detection programme showed that their spatio-temporal characteristics (full width and full duration at half-maximum amplitude) were approximately exponentially distributed. Their amplitude distribution suggested the presence of two release modes. Carbachol application caused an initial cell-wide calcium transient followed by an increase in localized calcium release events. Pharmacological analysis suggested that localized calcium release was largely dependent on external calcium entry acting on both inositol trisphosphate receptors (IP₃Rs) and ryanodine receptors (RyRs) to release stored calcium. Nominally calcium-free external solution immediately and reversibly abolished all localized calcium release without blocking the initial transient calcium release response to carbachol. This was inhibited by 2-APB (100 µM), ryanodine (10 or 50 µM) or U-73122 (1 µM). 2-APB (100 µM), xestospongin C (XeC, 10 µM) or U-73122 (1 µM) blocked both spontaneous localized calcium release and localized release stimulated by 10 µM carbachol. Ryanodine (50 µM) also inhibited spontaneous release, but enhanced localized release in response to carbachol. This study represents the first characterization of localized calcium release events in cells from the gastric fundus.

(Received 1 August 2003; accepted after revision 5 November 2003; first published online 7 November 2003)
Corresponding author T. B. Bolton: Pharmacology and Clinical Pharmacology, Department of Basic Medical Sciences, St Georges Hospital Medical School, Cranmer Terrace, London, SW17 ORE, UK. Email: t.bolton{at}sghms.ac.uk

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