Cytoplasmic Ca2+ oscillations evoked by acetylcholine or intracellular infusion of inositol trisphosphate or Ca2+ can be inhibited by internal Ca2+.
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+.
Wakui
M
M
MRC Secretory Control Research Group, University of Liverpool, England.
Petersen
O H
OH
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000502:physiology; D003593:Cytoplasm / Q000378:metabolism*; D005246:Feedback; D066298:In Vitro Techniques; D015544:Inositol 1,4,5-Trisphosphate / Q000494:pharmacology*; D015759:Ionomycin / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D010179:Pancreas / Q000378:metabolism
D002110:Caffeine; D015759:Ionomycin; D015544:Inositol 1,4,5-Trisphosphate; D000109:Acetylcholine; D002118:Calcium