Literature DB >> 8791284

Evidence that quantal Ca2+ release in HSG cells is not due to 'all-or-none' release from discrete Ca2+ stores with differing sensitivities to IP3.

A Moran1, R J Turner.   

Abstract

We demonstrate that the application of the muscarinic agonist carbachol to the human salivary epithelial cell line HSG elicits the now well-known phenomenon of 'quantal' Ca2+ release; namely, that the application of a submaximal concentration of agonist results in the release of only a portion of the agonist-sensitive intracellular Ca2+ pool. One explanation that has been proposed to account for this effect is that there are multiple intracellular Ca2+ stores, each with a different agonist sensitivity, which release Ca2+ in an 'all-or-none' fashion. We test this hypothesis in intact HSG cells with an experimental protocol designed to preferentially load less-agonist-sensitive stores with 40Ca2+ and more-agonist-sensitive stores with 45Ca2+. However, contrary to the expectations of the above explanation, these cells do not preferentially release 45Ca2+ in response to low concentrations of agonist. Thus our data suggest that quantal Ca2+ release must arise from some other property of the stores or their Ca2+ release channels.

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Year:  1996        PMID: 8791284     DOI: 10.1007/bf00225882

Source DB:  PubMed          Journal:  Mol Cell Biochem        ISSN: 0300-8177            Impact factor:   3.396


  19 in total

1.  Do submaximal InsP3 concentrations only induce the partial discharge of permeabilized hepatocyte calcium pools because of the concomitant reduction of intraluminal Ca2+ concentration?

Authors:  L Combettes; M Claret; P Champeil
Journal:  FEBS Lett       Date:  1992-04-27       Impact factor: 4.124

Review 2.  'Quantal' Ca2+ release and the control of Ca2+ entry by inositol phosphates--a possible mechanism.

Authors:  R F Irvine
Journal:  FEBS Lett       Date:  1990-04-09       Impact factor: 4.124

3.  Hormone-evoked calcium release from intracellular stores is a quantal process.

Authors:  S Muallem; S J Pandol; T G Beeker
Journal:  J Biol Chem       Date:  1989-01-05       Impact factor: 5.157

4.  Imaging of inositol 1,4,5-trisphosphate-induced Ca2+ fluxes in single permeabilized hepatocytes. Demonstration of both quantal and nonquantal patterns of Ca2+ release.

Authors:  D C Renard-Rooney; G Hajnóczky; M B Seitz; T G Schneider; A P Thomas
Journal:  J Biol Chem       Date:  1993-11-05       Impact factor: 5.157

Review 5.  Quantal Ca2+ release from InsP3-sensitive intracellular Ca2+ stores.

Authors:  M D Bootman
Journal:  Mol Cell Endocrinol       Date:  1994-01       Impact factor: 4.102

Review 6.  Partial calcium release in response to submaximal inositol 1,4,5-trisphosphate receptor activation.

Authors:  L Missiaen; J B Parys; H De Smedt; M Oike; R Casteels
Journal:  Mol Cell Endocrinol       Date:  1994-01       Impact factor: 4.102

7.  Ca2+ release induced by inositol 1,4,5-trisphosphate is a steady-state phenomenon controlled by luminal Ca2+ in permeabilized cells.

Authors:  L Missiaen; H De Smedt; G Droogmans; R Casteels
Journal:  Nature       Date:  1992-06-18       Impact factor: 49.962

8.  Functional homogeneity of the non-mitochondrial Ca2+ pool in intact mouse lacrimal acinar cells.

Authors:  G J Bird; J F Obie; J W Putney
Journal:  J Biol Chem       Date:  1992-09-15       Impact factor: 5.157

9.  Loading dependence of inositol 1,4,5-trisphosphate-induced Ca2+ release in the clonal cell line A7r5. Implications for the mechanism of quantal Ca2+ release.

Authors:  J B Parys; L Missiaen; H De Smedt; R Casteels
Journal:  J Biol Chem       Date:  1993-11-25       Impact factor: 5.157

10.  Luminal communication between intracellular calcium stores modulated by GTP and the cytoskeleton.

Authors:  G Hajnóczky; C Lin; A P Thomas
Journal:  J Biol Chem       Date:  1994-04-08       Impact factor: 5.157

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