ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Bax and calpain mediate excitotoxic oligodendrocyte death induced by activation of both AMPA and kainate receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 60 citations in OpenAlex.
- Role of Microglia in Stroke.Advances in neurobiology · 2024Review
- The Diversity of Astrocyte Activation during Multiple Sclerosis: Potential Cellular Targets for Novel Disease Modifying Therapeutics.Healthcare (Basel, Switzerland) · 2023Review
- GABA Receptor Agonists Protect From Excitotoxic Damage Induced by AMPA in Oligodendrocytes.Frontiers in pharmacology · 2022Article
- Biomaterials reinforced MSCs transplantation for spinal cord injury repair.Asian journal of pharmaceutical sciences · 2022Review
- Transient astrocyte-like NG2 glia subpopulation emerges solely following permanent brain ischemia.Glia · 2021Article
- The role of Bcl-2 proteins in modulating neuronal CaBiochimica et biophysica acta. Molecular cell research · 2021Review
- Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells.Frontiers in cellular neuroscience · 2020Article
- Glial Cell AMPA Receptors in Nervous System Health, Injury and Disease.International journal of molecular sciences · 2019Review
- Chlorogenic Acid Prevents AMPA-Mediated Excitotoxicity in Optic Nerve Oligodendrocytes Through a PKC and Caspase-Dependent Pathways.Neurotoxicity research · 2018Article
- Article
- Attenuation of Glutamate-Induced Excitotoxicity by Withanolide-A in Neuron-Like Cells: Role for PI3K/Akt/MAPK Signaling Pathway.Molecular neurobiology · 2018Article
- Inhibition of Casein Kinase 2 Protects Oligodendrocytes From Excitotoxicity by Attenuating JNK/p53 Signaling Cascade.Frontiers in molecular neuroscience · 2018Article
- Mitochondrial dysfunction in glial cells: Implications for neuronal homeostasis and survival.Toxicology · 2017Review
- Mitochondrial mechanisms of neuronal rescue by F-68, a hydrophilic Pluronic block co-polymer, following acute substrate deprivation.Neurochemistry international · 2017Review
- Withanone, an Active Constituent from Withania somnifera, Affords Protection Against NMDA-Induced Excitotoxicity in Neuron-Like Cells.Molecular neurobiology · 2017Article
- Astrocytes in Oligodendrocyte Lineage Development and White Matter Pathology.Frontiers in cellular neuroscience · 2016Review
- Novel Stroke Therapeutics: Unraveling Stroke Pathophysiology and Its Impact on Clinical Treatments.Neuron · 2015Review
- Bax regulates neuronal Ca2+ homeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Review
- The challenge of understanding cerebral white matter injury in the premature infant.Neuroscience · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sustained activation of AMPA and kainate receptors in rat oligodendrocytes induces cytosolic calcium overload, mitochondrial depolarization, and an increase of reactive oxygen species, resulting in cell death. Here, we provide evidence that Bax, a proapoptotic member of the Bcl-2 protein family, is involved in excitotoxic apoptotic death of oligodendrocytes and that calpain mediates Bax activation. Cultured Bax(-/-) oligodendrocytes, obtained from the optic nerve of Bax knock-out mice, were resistant to AMPA and kainate receptor-mediated insults. In turn, both mitochondrial calcium uptake and mitochondrial alterations after excitotoxic insults were diminished in Bax-null oligodendrocytes. Moreover, pretreatment with furosemide, a blocker of Bax translocation to mitochondria, significantly protected rat and mouse oligodendrocytes from AMPA- and kainate-induced damage; in contrast, bongkrekic acid, a blocker of the mitochondrial permeability transition pore, had no effect. Finally, we analyzed the participation of calpain, which cleaves Bax and is activated by AMPA and kainate, in oligodendrocyte death. Pretreatment with 3-(4-iodophenyl)-2-mercapto-(Z)-2-propenoic acid (PD150606), a broad cell-permeable calpain inhibitor, and two additional calpain inhibitors diminished Bax activation, inhibited its translocation to mitochondria, and attenuated all apoptotic events resulting from excitotoxic insults to rat oligodendrocytes. Together, these results indicate that Bax and calpain are essential intermediaries of the mitochondria-dependent death pathway, triggered by AMPA and kainate receptor activation in oligodendrocytes.
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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.