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Cytoplasmic Ca2+ oscillations evoked by acetylcholine or intracellular infusion of inositol trisphosphate or Ca2+ can be inhibited by internal Ca2+

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In single internally perfused mouse pancreatic acinar cells, changes in the free intracellular Ca2+ concentration ([Ca2+]i) were monitored by measuring the Ca2+‐dependent transmembrane Cl− current under voltage‐clamp conditions. Cytoplasmic Ca2+ 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 Ca2+ infusion. Such [Ca2+]i oscillations could be rapidly inhibited by external application of the Ca2+ ionophore ionomycin (10–100 nM). Cytoplasmic Ca2+ oscillations could also be evoked by external caffeine (1 mM) application when the internal perfusion solution did not contain any Ca2+ chelator. In such cases intracellular Ca2+ infusion transiently abolished the [Ca2+]i oscillations. We conclude that although Ca2+‐induced Ca2+ release is the cause of the ACh‐evoked [Ca2+]i oscillations, there is also a negative feed‐back since Ca2+ can inhibit Ca2+ release initiated by Ca2+.
Title: Cytoplasmic Ca2+ oscillations evoked by acetylcholine or intracellular infusion of inositol trisphosphate or Ca2+ can be inhibited by internal Ca2+
Description:
In single internally perfused mouse pancreatic acinar cells, changes in the free intracellular Ca2+ concentration ([Ca2+]i) were monitored by measuring the Ca2+‐dependent transmembrane Cl− current under voltage‐clamp conditions.
Cytoplasmic Ca2+ 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 Ca2+ infusion.
Such [Ca2+]i oscillations could be rapidly inhibited by external application of the Ca2+ ionophore ionomycin (10–100 nM).
Cytoplasmic Ca2+ oscillations could also be evoked by external caffeine (1 mM) application when the internal perfusion solution did not contain any Ca2+ chelator.
In such cases intracellular Ca2+ infusion transiently abolished the [Ca2+]i oscillations.
We conclude that although Ca2+‐induced Ca2+ release is the cause of the ACh‐evoked [Ca2+]i oscillations, there is also a negative feed‐back since Ca2+ can inhibit Ca2+ release initiated by Ca2+.

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