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Multiple, coordinated Ca2+ ‐release events underlie the inositol trisphosphate‐induced local Ca2+ spikes in mouse pancreatic acinar cells.
Author(s) -
Thorn P.,
Moreton R.,
Berridge M.
Publication year - 1996
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1996.tb00436.x
Subject(s) - biology , inositol , inositol trisphosphate , inositol phosphate , microbiology and biotechnology , calcium , inositol trisphosphate receptor , endocrinology , medicine , receptor , biochemistry
Ca2+ wave initiation and non‐propagating Ca2+ spikes occur as a result of localized Ca2+ release from the more sensitive intracellular Ca2+ stores. Using high spatial and temporal Ca2+ ‐imaging techniques we have investigated inositol 1,4,5 triphosphate (InsP3)‐induced local Ca2+ spiking, which occurs at the site of Ca2+ wave initiation in pancreatic acinar cells. The spatial and temporal organization of a single spike suggested discrete hot spots of Ca2+ release. Further analysis of long trains of Ca2+ spikes demonstrated that these hot spots showed regenerative Ca2+ ‐release events which were consistently active from spike to spike. Regions adjacent to these hot spots also showed regenerative Ca2+ ‐release events of similar amplitude but with a much lower frequency of occurrence. We conclude that the InsP3‐induced non‐propagating Ca2+ spikes can be devolved into smaller components of release. Our results are consistent with a model of coordinated activity of pacemaker hot spots of Ca2+ release that recruit and entrain active Ca2+ ‐release events from surrounding regions.