Differential Control of Clustering of the Sodium Channels Nav1.2 and Nav1.6 at Developing CNS Nodes of Ranvier
Open accessAbstract
Na(v)1.6 is the main sodium channel isoform at adult nodes of Ranvier. Here, we show that Na(v)1.2 and its beta2 subunit, but not Na(v)1.6 or beta1, are clustered in developing central nervous system nodes and that clustering of Na(v)1.2 and Na(v)1.6 is differentially controlled. Oligodendrocyte-conditioned medium is sufficient to induce clustering of Na(v)1.2 alpha and beta2 subunits along central nervous system axons in vitro. This clustering is regulated by electrical activity and requires an intact actin cytoskeleton and synthesis of a non-sodium channel protein. Neither soluble- or contact-mediated glial signals induce clustering of Na(v)1.6 or beta1 in a nonmyelinating culture system. These data reveal that the sequential clustering of Na(v)1.2 and Na(v)1.6 channels is differentially controlled and suggest that myelination induces Na(v)1.6 clustering.
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Deficits in myelination and oligodendrocyte maturation can lead to impaired formation of the nodes of Ranvier.
“Deficits in myelination and oligodendrocyte maturation can also lead to impaired formation of the nodes of Ranvier (Kaplan et al., 2001; Rasband et al., 1999; Tanaka et al., 2009).”
From Down Syndrome Developmental Brain Transcriptome Reveals Defective Oligodendrocyte Differentiation and Myelination (2016) · cites this paper as Kaplan et al., 2001
The Results report that oligodendrocytes must mature before they effectively induce sodium-channel clustering, a step in developing nodes of Ranvier. The paper also suggests that myelination may be necessary for later Nav1.6 clustering, but does not establish that myelination deficits impair node formation as a whole. No page numbers are available in our copy. (LLM, conf=0.84)
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- Authors
- Kaplan, M. R., Cho, M.-H., Ullian, E. M., Isom, L. L., Levinson, S. R., & Barres, B. A.
- Affiliations
- Stanford Medicine (US)
- University of Michigan (US)
- University of Colorado Health (US)
- Corresponding author
- Barres, Ben A
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2001-04
- Volume
- 30
- Issue
- 1
- Pages
- 105-119
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2115628640
- Cited by
- 304
- References
- 4
- Citations by year
- 2026: 2 · 2025: 13 · 2024: 6 · 2023: 5 · 2022: 6 · 2021: 14 · 2020: 9 · 2019: 15 · 2018: 11 · 2017: 12 · 2016: 8 · 2015: 8 · 2014: 13 · 2013: 6 · 2012: 11
- FWCI
- 6.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Michigan
- Regeneron Pharmaceuticals
- National Institutes of Health (5t32ns007280-35)
- National Institute of Neurological Disorders and Stroke (NS07280)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Nav1.2 sodium channel, Nav1.6 sodium channel, sodium channel clustering, nodes of Ranvier, myelination, actin cytoskeleton, electrical activity, central nervous system development, axons, glial signaling
- MeSH terms
- Animals, Biological Assay, Cell Differentiation, Cell Membrane, Cells, Cultured, Central Nervous System, Cytoskeleton, Membrane Potentials, Nerve Tissue Proteins, Neurons, Oligodendroglia, Optic Nerve, Ranvier's Nodes, Sodium Channels, Gene Expression Regulation, Developmental, Protein Isoforms, Protein Transport, Rats
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