Mitochondrial calcium spiking: A transduction mechanism based on calcium‐induced permeability transition involved in cell calcium signalling
- 11 July 1994
- journal article
- Published by Wiley in FEBS Letters
- Vol. 348 (2) , 211-215
- https://doi.org/10.1016/0014-5793(94)00615-6
Abstract
We report reversible Ca(2+)-induced Ca2+ release from mitochondria, which takes the form of Ca2+ spikes. Mitochondrial Ca2+ spiking is an all-or-none process with a threshold dependence on both the frequency and the amplitude of the Ca2+ pulses used as stimuli. This spiking relies on the transient operation of the mitochondrial permeability transition pore, and is initiated--in a threshold-dependent manner--with inositol-triphosphate-mediated Ca2+ responses on permeabilized cells. Evidence that mitochondrial Ca(2+)-induced Ca2+ release contributes to inositol-triphosphate-mediated Ca2+ responses in intact cells is also reported.Keywords
This publication has 12 references indexed in Scilit:
- The Ca2+-induced permeability transition pore is involved in Ca2+-induced mitochondrial oscillationsCell Calcium, 1994
- Microdomains with High Ca 2+ Close to IP 3 -Sensitive Channels that Are Sensed by Neighboring MitochondriaScience, 1993
- Evidence that stimulation of plasma-membrane Ca2+ inflow is an early action of glucagon and dibutyryl cyclic AMP in rat hepatocytesBiochemical Journal, 1993
- Modulation of the mitochondrial cyclosporin A-sensitive permeability transition pore. II. The minimal requirements for pore induction underscore a key role for transmembrane electrical potential, matrix pH, and matrix Ca2+.Journal of Biological Chemistry, 1993
- Inositol trisphosphate and calcium signallingNature, 1993
- Molecular mechanisms of intracellular calcium excitability in X. laevis oocytesCell, 1992
- The mitochondrial megachannel is the permeability transition poreJournal of Bioenergetics and Biomembranes, 1992
- Inositol phosphates and cell signallingNature, 1989
- Extracellular ATP activates polyphosphoinositide breakdown and Ca2+ mobilization in Ehrlich ascites tumor cellsArchives of Biochemistry and Biophysics, 1986
- Cytosolic Ca2+ homeostasis in Ehrlich and Yoshida carcinomas. A new, membrane-permeant chelator of heavy metals reveals that these ascites tumor cell lines have normal cytosolic free Ca2+.Journal of Biological Chemistry, 1985