ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Long-term maintenance of Na+ channels at nodes of Ranvier depends on glial contact mediated by gliomedin and NrCAM.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- Chronic Inflammatory Demyelinating Polyneuropathy (CIDP): A Comprehensive Review of Types, Pathophysiology, and Treatment Approaches.Brain and behavior · 2026Review
- Modulating Schwann cell behavior via functional nerve guidance conduits for enhanced peripheral nerve regeneration.NPJ Regenerative medicine · 2025Review
- Abnormal Innervation, Demyelination, and Degeneration of Spiral Ganglion Neurons as Well as Disruption of Heminodes are Involved in the Onset of Deafness in Cx26 Null Mice.Neuroscience bulletin · 2024Article
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- Compromised Myelin and Axonal Molecular Organization Following Adult-Onset Sulfatide Depletion.Biomedicines · 2023Article
- Bi-allelic loss of function variant in the NRCAM gene is associated with motor-predominant axonal polyneuropathy; the second report.Molecular genetics & genomic medicine · 2023Article
- The structure of sensory afferent compartments in health and disease.Journal of anatomy · 2022Review
- Concussion leads to widespread axonal sodium channel loss and disruption of the node of Ranvier.Acta neuropathologica · 2022Article
- Clinical and diagnostic features of anti-neurofascin-155 antibody-positive neuropathy in Han Chinese.Annals of clinical and translational neurology · 2022Article
- Two distinct types of nodes of Ranvier support auditory nerve function in the mouse cochlea.Glia · 2022Article
- Bi-allelic variants in neuronal cell adhesion molecule cause a neurodevelopmental disorder characterized by developmental delay, hypotonia, neuropathy/spasticity.American journal of human genetics · 2022Article
- Paranodal Axoglial Junctions, an Essential Component in Axonal Homeostasis.Frontiers in cell and developmental biology · 2022Review
- Nodal β spectrins are required to maintain NaeLife · 2020Article
- Schwann cell transcript biomarkers for hereditary neuropathy skin biopsies.Annals of neurology · 2019Article
- Gene replacement therapy in a model of Charcot-Marie-Tooth 4C neuropathy.Brain : a journal of neurology · 2019Article
- Anti-Neurofascin-155 IgG4 antibodies prevent paranodal complex formation in vivo.The Journal of clinical investigation · 2019Article
- Nodal Dynamics afterThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Expression and Function of Neuron-Glia-Related Cell Adhesion Molecule (NrCAM) in the Amygdalar Pathway.Frontiers in cell and developmental biology · 2019Article
- Glial βII Spectrin Contributes to Paranode Formation and Maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Clustering of Na(+) channels at the nodes of Ranvier is coordinated by myelinating glia. In the peripheral nervous system, axoglial contact at the nodes is mediated by the binding of gliomedin and glial NrCAM to axonal neurofascin 186 (NF186). This interaction is crucial for the initial clustering of Na(+) channels at heminodes. As a result, it is not clear whether continued axon-glial contact at nodes of Ranvier is required to maintain these channels at the nodal axolemma. Here, we report that, in contrast to mice that lack either gliomedin or NrCAM, absence of both molecules (and hence the glial clustering signal) resulted in a gradual loss of Na(+) channels and other axonal components from the nodes, the formation of binary nodes, and dysregulation of nodal gap length. Therefore, these mice exhibit neurological abnormalities and slower nerve conduction. Disintegration of the nodes occurred in an orderly manner, starting with the disappearance of neurofascin 186, followed by the loss of Na(+) channels and ankyrin G, and then βIV spectrin, a sequence that reflects the assembly of nodes during development. Finally, the absence of gliomedin and NrCAM led to the invasion of the outermost layer of the Schwann cell membrane beyond the nodal area and the formation of paranodal-like junctions at the nodal gap. Our results reveal that axon-glial contact mediated by gliomedin, NrCAM, and NF186 not only plays a role in Na(+) channel clustering during development, but also contributes to the long-term maintenance of Na(+) channels at nodes of Ranvier.
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