ArticleNeurochemical research2009
Ca(2+) buffering capacity of mitochondria after oxygen-glucose deprivation in hippocampal neurons.
Article in Neurochemical research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- A multimodal electrochemical approach to measure the effect of zinc on vesicular content and exocytosis in a single cell model of ischemia.QRB discovery · 2021Article
- Knocking down TRPM2 expression reduces cell injury and NLRP3 inflammasome activation in PC12 cells subjected to oxygen-glucose deprivation.Neural regeneration research · 2020Article
- Sirt3 protects cortical neurons against oxidative stress via regulating mitochondrial Ca2+ and mitochondrial biogenesis.International journal of molecular sciences · 2014Article
- The physiological behaviour of IMR-32 neuroblastoma cells is affected by a 12-h hypoxia/24-h reoxygenation period.Neurochemical research · 2010Article
- Hypoxia-inducible factor-1alpha suppresses the expression of macrophage scavenger receptor 1.Pflugers Archiv : European journal of physiology · 2009Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In an earlier study, we showed that mitochondria hyperpolarized after short periods of oxygen-glucose deprivation (OGD), and this response appeared to be associated with subsequent apoptosis or survival. Here, we demonstrated that hyperpolarization following short periods of OGD (30 min; 30OGD group) increased the cytosolic Ca(2+) ([Ca(2+)](c)) buffering capacity in mitochondria. After graded OGD (0 min (control), 30 min, 120 min), rat cultured hippocampal neurons were exposed to glutamate, evoking Ca(2+)influx. The [Ca(2+)](c) level increased sharply, followed by a rapid increase in mitochondrial Ca(2+) [Ca(2+)](m). The increase in the [Ca(2+)](m) level accompanied a reduction in the [Ca(2+)](c) level. After reaching a peak, the [Ca(2+)](c) level decreased more rapidly in the 30OGD group than in the control group. This buffering reaction was pronounced in the 30OGD group, but not in the 120OGD group. The enhanced buffering capacity of the mitochondria may be linked to preconditioning after short-term ischemic episodes.
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Registered trials
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