ArticleNeuron glia biology2004
Oligodendrocytes assist in the maintenance of sodium channel clusters independent of the myelin sheath.
Article in Neuron glia biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 68 citations in OpenAlex.
- Astroglial modulation of synaptic function in the non-demyelinated cerebellar cortex is dependent on MyD88 signaling in a model of toxic demyelination.Journal of neuroinflammation · 2025Article
- Incomplete remyelination via therapeutically enhanced oligodendrogenesis is sufficient to recover visual cortical function.Nature communications · 2025Article
- VEP Latency Delay Reflects Demyelination Beyond the Optic Nerve in the Cuprizone Model.Investigative ophthalmology & visual science · 2024Article
- Article
- Higher throughput workflow with sensitive, reliable and automatic quantification of myelination in vitro suitable for drug screening.Scientific reports · 2023Article
- Utilizing hiPSC-derived oligodendrocytes to study myelin pathophysiology in neuropsychiatric and neurodegenerative disorders.Frontiers in cellular neuroscience · 2023Review
- Parvalbumin basket cell myelination accumulates axonal mitochondria to internodes.Nature communications · 2022Article
- Revealing nanostructures in brain tissue via protein decrowding by iterative expansion microscopy.Nature biomedical engineering · 2022Article
- Cuprizone Intoxication Results in Myelin Vacuole Formation.Frontiers in cellular neuroscience · 2022Article
- Neuron-Oligodendrocyte Interactions in the Structure and Integrity of Axons.Frontiers in cell and developmental biology · 2021Review
- Nodes of Ranvier during development and repair in the CNS.Nature reviews. Neurology · 2020Review
- Article
- Microglial process convergence on axonal segments in health and disease.Neuroimmunology and neuroinflammation · 2020Article
- Structural adaption of axons during de- and remyelination in the Cuprizone mouse model.Brain pathology (Zurich, Switzerland) · 2019Article
- Progressive ataxia of Charolais cattle highlights a role of KIF1C in sustainable myelination.PLoS genetics · 2018Article
- Glial Cells in the Genesis and Regulation of Circadian Rhythms.Frontiers in physiology · 2018Review
- Cuprizone-Containing Pellets Are Less Potent to Induce Consistent Demyelination in the Corpus Callosum of C57BL/6 Mice.Journal of molecular neuroscience : MN · 2017Article
- Neuroprotection by central nervous system remyelination: Molecular, cellular, and functional considerations.Journal of neuroscience research · 2016Review
- Functional and structural properties of ion channels at the nerve terminal depends on compact myelin.The Journal of physiology · 2016Article
- Myelin loss and axonal ion channel adaptations associated with gray matter neuronal hyperexcitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
Abstract
To ensure rapid and efficient impulse conduction, myelinated axons establish and maintain specific protein domains. For instance, sodium (Na+) channels accumulate in the node of Ranvier; potassium (K+) channels aggregate in the juxtaparanode and neurexin/caspr/paranodin clusters in the paranode. Our understanding of the mechanisms that control the initial clustering of these proteins is limited and less is known about domain maintenance. Correlative data indicate that myelin formation and/or mature myelin-forming cells mediate formation of all three domains. Here, we test whether myelin is required for maintaining Na+ channel domains in the nodal gap by employing two demyelinating murine models: (1) cuprizone ingestion, which induces complete demyelination through oligodendrocyte toxicity; and (2) ceramide galactosyltransferase deficient mice, which undergo spontaneous adult-onset demyelination without oligodendrocyte death. Our data indicate that the myelin sheath is essential for long-term maintenance of sodium channel domains; however, oligodendrocytes, independent of myelin, provide a partial protective influence on the maintenance of nodal Na+ channel clusters. Thus, we propose that multiple mechanisms regulate the maintenance of nodal protein organization. Finally, we present evidence that following the loss of Na+ channel clusters the chronological progression of expression and reclustering of Na+ channel isoforms during the course of CNS remyelination recapitulates development.
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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.