Abstract
We report Ca2(+)-induced release of Ca2+ from mitochondria (mCICR) dependent on transitory opening of the permeability transition pore (PTP) operating in a low conductance mode. The Ca2+ fluxes taking place during mCICR are a direct consequence of the mitochondrial depolarization spike (mDPS) caused by PTP opening. Both mDPS and mCICR can propagate from one mitochondrion to another in vitro, generating traveling depolarization and Ca2+ waves. Mitochondria thus appear to be excitable organelles capable of generating and conveying electrical and Ca2+ signals. In living cells, mDPS/mCICR is triggered during IP3-induced Ca2+ mobilization and results in the amplification of the Ca2+ signals primarily emitted from the endoplasmic reticulum.
Keywords
MeSH Terms
Affiliated Institutions
Related Publications
The Permeability Transition Pore Complex: A Target for Apoptosis Regulation by Caspases and Bcl-2–related Proteins
Early in programmed cell death (apoptosis), mitochondrial membrane permeability increases. This is at least in part due to opening of the permeability transition (PT) pore, a mu...
Origin of eukaryotic programmed cell death: A consequence of aerobic metabolism?
Abstract A marked feature of eukaryotic programmed cell death is an early drop in mitochondrial transmembrane potential. This results from the opening of permeability transition...
Arachidonic acid induces both Na<sup>+</sup> and Ca<sup>2+</sup> entry resulting in apoptosis
Abstract Marked accumulation of arachidonic acid (AA) and intracellular Ca 2+ and Na + overloads are seen during brain ischemia. In this study, we show that, in neurons, AA indu...
Publication Info
- Year
- 1997
- Type
- article
- Volume
- 89
- Issue
- 7
- Pages
- 1145-1153
- Citations
- 743
- Access
- Closed
External Links
Social Impact
Social media, news, blog, policy document mentions
Citation Metrics
Cite This
Identifiers
- DOI
- 10.1016/s0092-8674(00)80301-3
- PMID
- 9215636