ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Mitochondrial membrane potential and glutamate excitotoxicity in cultured cerebellar granule cells.
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 115 papers.
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Who cites it
115 citing papers in PubMed, 306 citations in OpenAlex.
- Review
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- Small-scale protocols to characterize mitochondrial Complex V activity and assembly in peripheral blood mononuclear cells.PloS one · 2025Article
- Calcium signaling in postsynaptic mitochondria: mechanisms, dynamics, and role in ATP production.Frontiers in molecular neuroscience · 2025Review
- NEK10 kinase ablation affects mitochondrial morphology, function and protein phosphorylation status.Proteome science · 2024Article
- Bisbiguanide analogs induce mitochondrial stress to inhibit lung cancer cell invasion.iScience · 2024Article
- The role of mitochondrial uncoupling in the regulation of mitostasis after traumatic brain injury.Neurochemistry international · 2024Article
- The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation.Frontiers in molecular neuroscience · 2023Review
- Fluorescence microscopy imaging of mitochondrial metabolism in cancer cells.Frontiers in oncology · 2023Review
- Apoe4 and Alzheimer's Disease Pathogenesis-Mitochondrial Deregulation and Targeted Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Calpain-Independent Intracellular Protease Activity Is Elevated in Excitotoxic Cortical Neurons Prior to Delayed Calcium Deregulation and Mitochondrial Dysfunction.Biomolecules · 2022Article
- The Role of Mitochondrial Dynamin in Stroke.Oxidative medicine and cellular longevity · 2022Review
- Extracellular ferritin contributes to neuronal injury in an in vitro model of ischemic stroke.Journal of physiology and biochemistry · 2021Article
- From OCR and ECAR to energy: Perspectives on the design and interpretation of bioenergetics studies.The Journal of biological chemistry · 2021Review
- Mitochondrial clearance of calcium facilitated by MICU2 controls insulin secretion.Molecular metabolism · 2021Article
- Curcumin Ameliorates Copper-Induced Neurotoxicity Through Inhibiting Oxidative Stress and Mitochondrial Apoptosis in SH-SY5Y Cells.Neurochemical research · 2021Article
- Aglycemic growth enhances carbohydrate metabolism and induces sensitivity to menadione in cultured tumor-derived cells.Cancer & metabolism · 2021Article
- Quantitative analysis of mitochondrial membrane potential heterogeneity in unsynchronized and synchronized cancer cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Potential protective roles of phytochemicals on glutamate-induced neurotoxicity: A review.Iranian journal of basic medical sciences · 2020Review
55 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The relationship between changes in mitochondrial membrane potential (Deltapsi(m)) and the failure of cytoplasmic Ca(2+) homeostasis, delayed Ca(2+)deregulation (DCD), is investigated for cultured rat cerebellar granule cells exposed to glutamate. To interpret the single-cell fluorescence response of cells loaded with tetramethylrhodamine methyl ester (TMRM(+)) or rhodamine-123, we devised and validated a mathematical simulation with well characterized effectors of Deltapsi(m) and plasma membrane potential (Deltapsi(P)). Glutamate usually caused an immediate decrease in Deltapsi(m) of <10 mV, attributable to Ca(2+) accumulation rather than enhanced ATP demand, and these cells continued to generate ATP by oxidative phosphorylation until DCD. Cells for which the mitochondria showed a larger initial depolarization deregulated more rapidly. The mitochondria in a subpopulation of glutamate-exposed cells that failed to extrude Ca(2+) that was released from the matrix after protonophore addition were bioenergetically competent. The onset of DCD during continuous glutamate exposure in the presence or absence of oligomycin was associated with a slowly developing mitochondrial depolarization, but cause and effect could not be established readily. In contrast, the slowly developing mitochondrial depolarization after transient NMDA receptor activation occurs before cytoplasmic free Ca(2+) ([Ca(2+)](c)) has risen to the set point at which mitochondria retain Ca(2+). In the presence of oligomycin no increase in [Ca(2+)](c) occurs during this depolarization. We conclude that transient Ca(2+) loading of mitochondria as a consequence of NMDA receptor activation initiates oxidative damage to both plasma membrane Ca(2+) extrusion pathways and the inhibition of mitochondrial respiration. Depending on experimental conditions, one of these factors becomes rate-limiting and precipitates DCD.
Indexed as
Identifiers
11007877PMC6772767W2098324936What 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.