ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Both laminin and Schwann cell dystroglycan are necessary for proper clustering of sodium channels at nodes of Ranvier.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 113 citations in OpenAlex.
- Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Roles and therapeutic prospects of the laminin family in disorders of the nervous system.Journal of translational medicine · 2026Review
- Laminin Receptors in Peripheral Tissues: Functions Revealed by Analysis of Knockout Mice.The American journal of pathology · 2025Review
- The STRIPAK complex is required for radial sorting and laminin receptor expression in Schwann cells.Cell reports · 2025Article
- Engineering cell-derived extracellular matrix for peripheral nerve regeneration.Materials today. Bio · 2024Review
- From adhesion complex to signaling hub: the dual role of dystroglycan.Frontiers in molecular biosciences · 2023Review
- Review
- Ninj2 regulates Schwann cells development by interfering laminin-integrin signaling.Theranostics · 2022Article
- Genetic analysis of Pycr1 and Pycr2 in mice.Genetics · 2021Article
- Mechanisms of node of Ranvier assembly.Nature reviews. Neuroscience · 2021Review
- αGlia · 2021Article
- Adult tissue-derived neural crest-like stem cells: Sources, regulatory networks, and translational potential.Stem cells translational medicine · 2020Review
- Brain Dysfunction in LAMA2-Related Congenital Muscular Dystrophy: Lessons From Human Case Reports and Mouse Models.Frontiers in molecular neuroscience · 2020Article
- LAMA2 Neuropathies: Human Findings and Pathomechanisms From Mouse Models.Frontiers in molecular neuroscience · 2020Article
- The Adult Murine Intestine is Dependent on Constitutive Laminin-γ1 Synthesis.Scientific reports · 2019Article
- Schwann cell-derived periostin promotes autoimmune peripheral polyneuropathy via macrophage recruitment.The Journal of clinical investigation · 2018Article
- Sustained Expression of Negative Regulators of Myelination Protects Schwann Cells from Dysmyelination in a Charcot-Marie-Tooth 1B Mouse Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- A dual role for Integrin α6β4 in modulating hereditary neuropathy with liability to pressure palsies.Journal of neurochemistry · 2018Article
- Article
- Laminin 211 inhibits protein kinase A in Schwann cells to modulate neuregulin 1 type III-driven myelination.PLoS biology · 2017Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 8 institutions in 2 countries.
Funding
Abstract
Nodes of Ranvier are specialized axonal domains, at which voltage-gated sodium channels cluster. How axons cluster molecules in discrete domains is mostly unknown. Both axons and glia probably provide constraining mechanisms that contribute to domain formation. Proper sodium channel clustering in peripheral nerves depends on contact from Schwann cell microvilli, where at least one molecule, gliomedin, binds the sodium channel complex and induces its clustering. Furthermore, mice lacking Schwann cell dystroglycan have aberrant microvilli and poorly clustered sodium channels. Dystroglycan could interact at the basal lamina or at the axonglial surface. Because dystroglycan is a laminin receptor, and laminin 2 mutations [merosin-deficient congenital muscular dystrophy (MDC1A)] cause reduced nerve conduction velocity, we asked whether laminins are involved. Here, we show that the composition of both laminins and the dystroglycan complex at nodes differs from that of internodes. Mice defective in laminin 2 have poorly formed microvilli and abnormal sodium clusters. These abnormalities are similar, albeit less severe, than those of mice lacking dystroglycan. However, mice lacking all Schwann cell laminins show severe nodal abnormalities, suggesting that other laminins compensate for the lack of laminin 2. Thus, although laminins are located at a distance from the axoglial junction, they are required for proper clustering of sodium channels. Laminins, through their specific nodal receptors and cytoskeletal linkages, may participate in the formation of mechanisms that constrain clusters at nodes. Finally, abnormal sodium channel clusters are present in a patient with MDC1A, providing a molecular basis for the reduced nerve conduction velocity in this disorder.
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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.