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Cytoplasmic Ca 2+ oscillations evoked by acetylcholine or intracellular infusion of inositol trisphosphate or Ca 2+ can be inhibited by internal Ca 2+
Author(s) -
Wakui M.,
Petersen O.H.
Publication year - 1990
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(90)81374-w
Subject(s) - ionomycin , inositol , intracellular , ionophore , chemistry , biophysics , calcium , acetylcholine , cytoplasm , inositol trisphosphate , extracellular , endocrinology , biochemistry , biology , receptor , organic chemistry
In single internally perfused mouse pancreatic acinar cells, changes in the free intracellular Ca 2+ concentration ([Ca 2+ ] i ) were monitored by measuring the Ca 2+ ‐dependent transmembrane Cl − current under voltage‐clamp conditions. Cytoplasmic Ca 2+ oscillations were induced by external acetylcholine (ACh) application, internal infusion of inositol (1,4,5) trisphosphate or its non‐metabolizable analogue inositol trisphosphorothioate or by intracellular Ca 2+ infusion. Such [Ca 2+ ] i oscillations could be rapidly inhibited by external application of the Ca 2+ ionophore ionomycin (10–100 nM). Cytoplasmic Ca 2+ oscillations could also be evoked by external caffeine (1 mM) application when the internal perfusion solution did not contain any Ca 2+ chelator. In such cases intracellular Ca 2+ infusion transiently abolished the [Ca 2+ ] i oscillations. We conclude that although Ca 2+ ‐induced Ca 2+ release is the cause of the ACh‐evoked [Ca 2+ ] i oscillations, there is also a negative feed‐back since Ca 2+ can inhibit Ca 2+ release initiated by Ca 2+ .