ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Delayed mitochondrial dysfunction in excitotoxic neuron death: cytochrome c release and a secondary increase in superoxide production.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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Who cites it
69 citing papers in PubMed, 231 citations in OpenAlex.
- The Design Strategies and Applications of Engineered Nanoparticles for Traumatic Brain Injury.International journal of nanomedicine · 2026Review
- Temporal Changes in Mitochondria-Centric Excitotoxic Responses Following Severe Penetrating Traumatic Brain Injury.Biomedicines · 2025Article
- Reduction of the CaFrontiers in cellular neuroscience · 2025Review
- Article
- ACTA1 H40Y mutant iPSC-derived skeletal myocytes display mitochondrial defects in an in vitro model of nemaline myopathy.Experimental cell research · 2023Article
- A review of stress-induced hyperglycaemia in the context of acute ischaemic stroke: Definition, underlying mechanisms, and the status of insulin therapy.Frontiers in neurology · 2023Review
- Targeting Estrogen Signaling in the Radiation-induced Neurodegeneration: A Possible Role of Phytoestrogens.Current neuropharmacology · 2023Review
- Engineered Neutral Phosphorous Dendrimers Protect Mouse Cortical Neurons and Brain Organoids from Excitotoxic Death.International journal of molecular sciences · 2022Article
- Computational analysis of cortical neuronal excitotoxicity in a large animal model of neonatal brain injury.Journal of neurodevelopmental disorders · 2022Article
- Regulation of Superoxide by BAP31 through Its Effect on p22Oxidative medicine and cellular longevity · 2021Article
- Isolinderalactone Induces Cell Death via Mitochondrial Superoxide- and STAT3-Mediated Pathways in Human Ovarian Cancer Cells.International journal of molecular sciences · 2020Article
- Going the Extra (Synaptic) Mile: Excitotoxicity as the Road Toward Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2020Review
- Mitochondrial quality control and neurodegenerative diseases.Neuronal signaling · 2018Review
- PQQ ameliorates D-galactose induced cognitive impairments by reducing glutamate neurotoxicity via the GSK-3β/Akt signaling pathway in mouse.Scientific reports · 2018Article
- Inhibition of Bcl-xL prevents pro-death actions of ΔN-Bcl-xL at the mitochondrial inner membrane during glutamate excitotoxicity.Cell death and differentiation · 2017Article
- Tangeretin inhibits neurodegeneration and attenuates inflammatory responses and behavioural deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease dementia in rats.Inflammopharmacology · 2017Article
- Bioenergetics and redox adaptations of astrocytes to neuronal activity.Journal of neurochemistry · 2016Review
- The Chemical Molecule B355252 is Neuroprotective in an In Vitro Model of Parkinson's Disease.Cellular and molecular neurobiology · 2016Article
- The metabolic response to excitotoxicity - lessons from single-cell imaging.Journal of bioenergetics and biomembranes · 2015Review
- Bax regulates neuronal Ca2+ homeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An increased production of superoxide has been shown to mediate glutamate-induced neuron death. We monitored intracellular superoxide production of hippocampal neurons during and after exposure to the glutamate receptor agonist NMDA (300 microm). During a 30 min NMDA exposure, intracellular superoxide production increased significantly and remained elevated for several hours after wash-out of NMDA. After a 5 min exposure, superoxide production remained elevated for 10 min, but then rapidly returned to baseline. Mitochondrial membrane potential also recovered after wash-out of NMDA. However, recovery of mitochondria was transient and followed by delayed mitochondrial depolarization, loss of cytochrome c, and a secondary rise in superoxide production 4-8 hr after NMDA exposure. Treatment with a superoxide dismutase mimetic before the secondary rise conferred the same protection against cell death as a treatment before the first. The secondary rise could be inhibited by the complex I inhibitor rotenone (in combination with oligomycin) and mimicked by the complex III inhibitor antimycin A. To investigate the relationship between cytochrome c release and superoxide production, human D283 medulloblastoma cells deficient in mitochondrial respiration (rho(-) cells) were exposed to the apoptosis-inducing agent staurosporine. Treatment with staurosporine induced mitochondrial release of cytochrome c, caspase activation, and cell death in control and rho(-) cells. However, a delayed increase in superoxide production was only observed in control cells. Our data suggest that the delayed superoxide production in excitotoxicity and apoptosis occurs secondary to a defect in mitochondrial electron transport and that mitochondrial cytochrome c release occurs upstream of this defect.
Indexed as
Identifiers
10908611PMC6772544W1938199221What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.