ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996
Mitochondrial depolarization in glutamate-stimulated neurons: an early signal specific to excitotoxin exposure.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.
What it found
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Who cites it
153 citing papers in PubMed, 596 citations in OpenAlex.
- The Bright and Dark Sides of Nitric Oxide in Neurodegenerative Diseases.Journal of personalized medicine · 2026Review
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- The role of mitochondrial uncoupling in the regulation of mitostasis after traumatic brain injury.Neurochemistry international · 2024Article
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- Plasticity of perisynaptic astroglia during ischemia-induced spreading depolarization.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation.Frontiers in molecular neuroscience · 2023Review
- Modulation and Pharmacology of the Mitochondrial Permeability Transition: A Journey from F-ATP Synthase to ANT.Molecules (Basel, Switzerland) · 2021Review
- The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction.Biomedicines · 2021Review
- Different Roles of Mitochondria in Cell Death and Inflammation: Focusing on Mitochondrial Quality Control in Ischemic Stroke and Reperfusion.Biomedicines · 2021Review
- Glial Cell-Based Vascular Mechanisms and Transplantation Therapies in Brain Vessel and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Review
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- Deletion of the Mitochondrial Matrix Protein CyclophilinD Prevents Parvalbumin Interneuron Dysfunctionand Cognitive Deficits in a Mouse Model of NMDA Hypofunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- The bimodal mechanism of interaction between dopamine and mitochondria as reflected in Parkinson's disease and in schizophrenia.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Neuronal Parasitism, Early Myenteric Neurons Depopulation and Continuous Axonal Networking Damage as Underlying Mechanisms of the Experimental Intestinal Chagas' Disease.Frontiers in cellular and infection microbiology · 2020Article
- Miro proteins prime mitochondria for Parkin translocation and mitophagy.The EMBO journal · 2019Article
- Deletion of mitochondrial calcium uniporter incompletely inhibits calcium uptake and induction of the permeability transition pore in brain mitochondria.The Journal of biological chemistry · 2018Article
- Avenues to molecular imaging of dying cells: Focus on cancer.Medicinal research reviews · 2018Review
- Calcium uptake and cytochrome c release from normal and ischemic brain mitochondria.Neurochemistry international · 2018Article
- Diffuse Axonal Injury and Oxidative Stress: A Comprehensive Review.International journal of molecular sciences · 2017Review
- Differential Molecular Targets for Neuroprotective Effect of Chlorogenic Acid and its Related Compounds Against Glutamate Induced Excitotoxicity and Oxidative Stress in Rat Cortical Neurons.Neurochemical research · 2017Article
93 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A brief exposure to high concentrations of glutamate kills cultured forebrain neurons by an excitotoxic process that is dependent on Ca2+ influx through the NMDA receptor. In this study, we have measured striking changes in mitochondrial function during and immediately after intense glutamate receptor activation. Using indo-1 microfluorometry and a specific inhibitor of the mitochondrial Na+/Ca2+ exchanger, CGP-37157, we have demonstrated that mitochondria accumulate large quantities of Ca2+ during a toxic glutamate stimulus and further that Ca2+ efflux from mitochondria contributes to the prolonged [Ca2+]i elevation after glutamate removal. We then used JC-1 (5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine+ ++ iodide), a ratiometric indicator of mitochondrial membrane potential (delta psi), to show that Ca2+ accumulation within the organelle dissipates delta psi. The abrupt loss of delta psi after glutamate stimulation did not occur in the presence of MK801 or in the absence of extracellular Ca2+. The mitochondrial depolarization was also cyclosporin A-sensitive, indicating a probable role for the permeability transition pore. Hence mitochondrial Ca2+ accumulation and the subsequent permeability transition may be a critical early event specific to the NMDA receptor-mediated excitotoxic cascade.
Indexed as
Identifiers
8795624PMC6578963W1550986239What 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.