ArticleProceedings of the National Academy of Sciences of the United States of America1998
Characteristics of acute and chronic kainate excitotoxic damage to the optic nerve.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 124 citations in OpenAlex.
- Glutamate signaling and transport around nodes of Ranvier and internodal myelin regions.Histology and histopathology · 2026Review
- Prospero-related homeobox protein 1 (Prox1) enhances myelin sheath regeneration in injured sciatic nerve.IBRO neuroscience reports · 2025Article
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- Developmental exposure to domoic acid targets reticulospinal neurons and leads to aberrant myelination in the spinal cord.Scientific reports · 2023Article
- Targeting N-type calcium channels in young-onset of some neurological diseases.Frontiers in cell and developmental biology · 2022Review
- Myelin sheath structure and regeneration in peripheral nerve injury repair.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Excitotoxins, Mitochondrial and Redox Disturbances in Multiple Sclerosis.International journal of molecular sciences · 2017Review
- Alteration of synaptic connectivity of oligodendrocyte precursor cells following demyelination.Frontiers in cellular neuroscience · 2015Article
- Ionic regulation of cell volume changes and cell death after ischemic stroke.Translational stroke research · 2014Review
- Pathophysiological processes in multiple sclerosis: focus on nuclear factor erythroid-2-related factor 2 and emerging pathways.Clinical pharmacology : advances and applications · 2014Review
- Demyelination in multiple sclerosis.Handbook of clinical neurology · 2014Review
- Optic neuritis in neuromyelitis optica.Progress in retinal and eye research · 2013Article
- Ectopic vesicular glutamate release at the optic nerve head and axon loss in mouse experimental glaucoma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Chronic excitotoxin-induced axon degeneration in a compartmented neuronal culture model.ASN neuro · 2012Article
- Therapeutic potential of kainate receptors.CNS neuroscience & therapeutics · 2011Review
- Glutamate and ATP signalling in white matter pathology.Journal of anatomy · 2011Review
- Increased expression of cystine/glutamate antiporter in multiple sclerosis.Journal of neuroinflammation · 2011Article
- Dual-specific phosphatase-6 (Dusp6) and ERK mediate AMPA receptor-induced oligodendrocyte death.The Journal of biological chemistry · 2011Article
- Bax and calpain mediate excitotoxic oligodendrocyte death induced by activation of both AMPA and kainate receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Kainate-mediated excitotoxicity induces neuronal death in the rat spinal cord in vitro via a PARP-1 dependent cell death pathway (Parthanatos).Cellular and molecular neurobiology · 2010Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macroglial cells express ionotropic glutamate receptors. In the adult optic nerve, reverse transcription-PCR showed that the native receptors are formed by subunits belonging to the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate classes. Because activation of AMPA and kainate receptors can be toxic to oligodendrocytes in vitro, I examined the nature of the damage caused by kainate, an agonist of both receptor classes, applied directly onto the optic nerve. Acute infusion or chronic slow delivery of the agonist caused massive nerve damage that was more extensive in the latter. Interestingly, chronic delivery also produced inflammation and demyelination in well circumscribed areas of the nerve, together with other pathological features that closely resemble those observed in multiple sclerosis patients. Acute and chronic kainate lesions were both prevented by the non-N-methyl-D-aspartate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. However, GYKI53655, a specific AMPA receptor antagonist, did not significantly reduce the size of the lesion, suggesting that the kainate toxicity was mainly mediated through activation of kainate-preferring glutamate receptors. These observations suggest that alterations in glutamate signaling may be detrimental to oligodendrocytes and may be involved in the pathogenesis of multiple sclerosis and other demyelinating diseases.
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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.