ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Schwann cells inhibit ectopic clustering of axonal sodium channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 52 citations in OpenAlex.
- Adhesion G-Protein Coupled Receptors in Neurological and Psychiatric Disorders.Journal of psychiatry and brain science · 2025Article
- Recent Advances in Biomolecular Patho-Mechanistic Pathways behind the Development and Progression of Diabetic Neuropathy.Biomedicines · 2024Review
- Article
- Mechanosensitive channel of large conductance enhances the mechanical stretching-induced upregulation of glycolysis and oxidative metabolism in Schwann cells.Cell communication and signaling : CCS · 2024Article
- Role of Extracellular Vesicles in Glia-Neuron Intercellular Communication.Frontiers in molecular neuroscience · 2022Review
- Phagocytosis by Peripheral Glia: Importance for Nervous System Functions and Implications in Injury and Disease.Frontiers in cell and developmental biology · 2021Review
- Effects of Pacap on Schwann Cells: Focus on Nerve Injury.International journal of molecular sciences · 2020Review
- Modulation of Small RNA Signatures in Schwann-Cell-Derived Extracellular Vesicles by the p75 Neurotrophin Receptor and Sortilin.Biomedicines · 2020Article
- Oligodendrocyte Neurofascin Independently Regulates Both Myelin Targeting and Sheath Growth in the CNS.Developmental cell · 2019Article
- Peripheral Glial Cells in the Development of Diabetic Neuropathy.Frontiers in neurology · 2018Review
- Motor Exit Point (MEP) Glia: Novel Myelinating Glia That Bridge CNS and PNS Myelin.Frontiers in cellular neuroscience · 2018Review
- Neuronal Ndrg4 Is Essential for Nodes of Ranvier Organization in Zebrafish.PLoS genetics · 2016Article
- Schwann Cell Exosomes Mediate Neuron-Glia Communication and Enhance Axonal Regeneration.Cellular and molecular neurobiology · 2016Review
- Mechanisms of sodium channel clustering and its influence on axonal impulse conduction.Cellular and molecular life sciences : CMLS · 2016Review
- Glial cell development and function in zebrafish.Cold Spring Harbor perspectives in biology · 2014Review
- Mutation of sec63 in zebrafish causes defects in myelinated axons and liver pathology.Disease models & mechanisms · 2013Article
- Unmyelinated nerve fibers in the human dental pulp express markers for myelinated fibers and show sodium channel accumulations.BMC neuroscience · 2012Article
- Neuronal Neuregulin 1 type III directs Schwann cell migration.Development (Cambridge, England) · 2011Article
- New insights into signaling during myelination in zebrafish.Current topics in developmental biology · 2011Review
- Schwann cells reposition a peripheral nerve to isolate it from postembryonic remodeling of its targets.Development (Cambridge, England) · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The clustering of voltage-gated sodium channels at the axon initial segment (AIS) and nodes of Ranvier is essential for the initiation and propagation of action potentials in myelinated axons. Sodium channels localize to the AIS through an axon-intrinsic mechanism driven by ankyrin G, while clustering at the nodes requires cues from myelinating glia that interact with axonal neurofascin186 (Sherman et al., 2005; Dzhashiashvili et al., 2007; Yang et al., 2007). Here, we report that in zebrafish mutants lacking Schwann cells in peripheral nerves (erbb2, erbb3, and sox10/colorless), axons form numerous aberrant sodium channel clusters throughout their length. Morpholino knockdown of ankyrin G, but not neurofascin, reduces the number of sodium channel clusters in Schwann cell-deficient mutants, suggesting that these aberrant clusters form by an axon-intrinsic mechanism. We also find that gpr126 mutants, in which Schwann cells are arrested at the promyelinating stage (Monk et al., 2009), are deficient in the clustering of neurofascin at the nodes of Ranvier. When Schwann cell migration in gpr126 mutants is blocked, there is an increase in the number of neurofascin clusters in peripheral axons. Our results suggest that Schwann cells inhibit the ability of ankyrin G to cluster sodium channels at ectopic locations, restricting its activity to the AIS and nodes of Ranvier.
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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.