ArticleAnnals of neurology2009
Glutamate receptors on myelinated spinal cord axons: II. AMPA and GluR5 receptors.
Article in Annals of neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 104 citations in OpenAlex.
- Glutamate signaling and transport around nodes of Ranvier and internodal myelin regions.Histology and histopathology · 2026Review
- Potential physiological and pathological roles for axonal ryanodine receptors.Neural regeneration research · 2023Review
- Galvanic vestibular stimulation down-regulated NMDA receptors in vestibular nucleus of PD model.Scientific reports · 2022Article
- Review
- IPNeurobiology of disease · 2020Article
- Molecular Mechanisms of Glutamate Toxicity in Parkinson's Disease.Frontiers in neuroscience · 2020Review
- Decoding the intensity of sensory input by two glutamate receptors in one C. elegans interneuron.Nature communications · 2018Article
- Axo-myelinic neurotransmission: a novel mode of cell signalling in the central nervous system.Nature reviews. Neuroscience · 2018Review
- Excitotoxins, Mitochondrial and Redox Disturbances in Multiple Sclerosis.International journal of molecular sciences · 2017Review
- Imaging Axonal Degeneration and Repair in Preclinical Animal Models of Multiple Sclerosis.Frontiers in immunology · 2016Review
- Soluble Tumor Necrosis Factor Alpha Promotes Retinal Ganglion Cell Death in Glaucoma via Calcium-Permeable AMPA Receptor Activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Lactate transport and signaling in the brain: potential therapeutic targets and roles in body-brain interaction.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Review
- The Role of Astrocytes in Multiple Sclerosis Progression.Frontiers in neurology · 2015Review
- Genetic markers of white matter integrity in schizophrenia revealed by parallel ICA.Frontiers in human neuroscience · 2015Article
- The back and forth of axonal injury and repair after stroke.Current opinion in neurology · 2014Review
- In vivo evidence of glutamate toxicity in multiple sclerosis.Annals of neurology · 2014Article
- Relapsing and progressive forms of multiple sclerosis: insights from pathology.Current opinion in neurology · 2014Review
- Ionic regulation of cell volume changes and cell death after ischemic stroke.Translational stroke research · 2014Review
- Neurodegeneration in multiple sclerosis involves multiple pathogenic mechanisms.Degenerative neurological and neuromuscular disease · 2014Review
- Role of calpains in the injury-induced dysfunction and degeneration of the mammalian axon.Neurobiology of disease · 2013Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveGlutamate receptors, which play a major role in the physiology and pathology of central nervous system gray matter, are also involved in the pathophysiology of white matter. However, the cellular and molecular mechanisms responsible for excitotoxic damage to white matter elements are not fully understood. We explored the roles of AMPA and GluR5 kainate receptors in axonal Ca(2+) deregulation.
methodsDorsal column axons were loaded with a Ca(2+) indicator and imaged in vitro using confocal microscopy.
resultsBoth AMPA and a GluR5 kainate receptor agonist increased intraaxonal Ca(2+) in myelinated rat dorsal column fibers. These responses were inhibited by selective antagonists of these receptors. The GluR5-mediated Ca(2+) increase was mediated by both canonical (ie, ionotropic) and noncanonical (metabotropic) signaling, dependent on a pertussis toxin-sensitive G protein/phospholipase C-dependent pathway, promoting Ca(2+) release from inositol triphosphate-dependent stores. In addition, the GluR5 response was reduced by intraaxonal NO scavengers. In contrast, GluR4 AMPA receptors operated via Ca(2+)-induced Ca(2+) release, dependent on ryanodine receptors, and unaffected by NO scavengers. Neither pathway depended on L-type Ca(2+) channels, in contrast with GluR6 kainate receptor action.1 Immunohistochemistry confirmed the presence of GluR4 and GluR5 clustered at the surface of myelinated axons; GluR5 coimmunoprecipitated with nNOS and often colocalized with neuronal nitric oxide synthase clusters on the internodal axon.
interpretationCentral myelinated axons express functional AMPA and GluR5 kainate receptors, and can directly respond to glutamate receptor agonists. These glutamate receptor-dependent signaling pathways promote an increase in intraaxonal Ca(2+) levels potentially contributing to axonal degeneration.
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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.