ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Differential stability of PNS and CNS nodal complexes when neuronal neurofascin is lost.
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 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Potassium channel clustering: mechanisms shaping axonal excitability.Frontiers in cellular neuroscience · 2025Review
- Schwann cell nodal membrane disruption triggers bystander axonal degeneration in a Guillain-Barré syndrome mouse model.The Journal of clinical investigation · 2022Article
- Chondroitin Sulphate Proteoglycan Axonal Coats in the Human Mediodorsal Thalamic Nucleus.Frontiers in integrative neuroscience · 2022Article
- From PNS to CNS: characteristics of anti-neurofascin 186 neuropathy in 16 cases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Article
- Distinguish CIDP with autoantibody from that without autoantibody: pathogenesis, histopathology, and clinical features.Journal of neurology · 2021Review
- An iPSC model of hereditary sensory neuropathy-1 reveals L-serine-responsive deficits in neuronal ganglioside composition and axoglial interactions.Cell reports. Medicine · 2021Article
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- Neuron-Oligodendrocyte Communication in Myelination of Cortical GABAergic Cells.Life (Basel, Switzerland) · 2021Review
- Mechanisms of node of Ranvier assembly.Nature reviews. Neuroscience · 2021Review
- Anti-Neurofascin 155 Antibody-Positive Chronic Inflammatory Demyelinating Polyneuropathy/Combined Central and Peripheral Demyelination: Strategies for Diagnosis and Treatment Based on the Disease Mechanism.Frontiers in neurology · 2021Review
- Review
- Anti-Neurofascin-155 IgG4 antibodies prevent paranodal complex formation in vivo.The Journal of clinical investigation · 2019Article
- Glial Sulfatides and Neuronal Complex Gangliosides Are Functionally Interdependent in Maintaining Myelinating Axon Integrity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Nodal Dynamics afterThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Ataxia in Patients With Bi-AllelicFrontiers in genetics · 2019Article
- Glial βII Spectrin Contributes to Paranode Formation and Maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
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- The Axonal Cytoskeleton and the Assembly of Nodes of Ranvier.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2018Review
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Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Fast, saltatory conduction in myelinated nerves requires the clustering of voltage-gated sodium channels (Nav) at nodes of Ranvier in a nodal complex. The Neurofascin (Nfasc) gene encodes neuronal Neurofascin 186 (Nfasc186) at the node and glial Neurofascin 155 at the paranode, and these proteins play a key role in node assembly. However, their role in the maintenance and stability of the node is less well understood. Here we show that by inducible ablation of Nfasc in neurons in adult mice, Nfasc186 expression is reduced by >99% and 94% at PNS and CNS nodes, respectively. Gliomedin and NrCAM at PNS and brevican at CNS nodes are largely lost with neuronal neurofascin; however, Nav at nodes of Ranvier persist, albeit with ∼40% reduction in expression levels. βIV Spectrin, ankyrin G, and, to a lesser extent, the β1 subunit of the sodium channel, are less affected at the PNS node than in the CNS. Nevertheless, there is a 38% reduction in PNS conduction velocity. Loss of Nfasc186 provokes CNS paranodal disorganization, but this does not contribute to loss of Nav. These results show that Nav at PNS nodes are still maintained in a nodal complex when neuronal neurofascin is depleted, whereas the retention of nodal Nav in the CNS, despite more extensive dissolution of the complex, suggests a supportive role for the partially disrupted paranodal axoglial junction in selectively maintaining Nav at the CNS node.
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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.