ArticleJournal of neuroscience research2009
Spatiotemporal ablation of myelinating glia-specific neurofascin (Nfasc NF155) in mice reveals gradual loss of paranodal axoglial junctions and concomitant disorganization of axonal domains.
Article in Journal of neuroscience research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 1 of them a synthesis that pooled it.
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Who cites it
121 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.
- Association of neurofascin IgG4 and atypical chronic inflammatory demyelinating polyneuropathy: A systematic review and meta-analysis.Brain and behavior · 2018Pooled it
- Specific effects of Pulsed Field Ablation on the cardiac tissue, the nervous system and the conduction system in experimental and clinical studies.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026Review
- Myelin dysfunction in autism spectrum disorder: insights into core symptoms and mechanisms of brain development.Molecular psychiatry · 2026Review
- Neurofascin Antibodies in a Large Cohort of Inflammatory Neuropathies from India.Annals of Indian Academy of Neurology · 2026Article
- Human CNTNAP1 Variants Associated With Severe Neurological Deficits: Additional Cases and Literature Review.Muscle & nerve · 2026Review
- Clinical utility of human leukocyte antigen genotyping and immunoglobulin G4 autoantibody testing in autoimmune neurological diseases: A focused minireview.World journal of biological chemistry · 2026Review
- Purkinje cell-specific loss of Neurofascin and Ankyrin G causes disruption of axon initial segments, neurodegeneration, and cerebellar ataxia.Frontiers in cellular neuroscience · 2026Article
- Clinical characteristics of anti-neurofascin 155 antibody-positive autoimmune nodopathy in children.Pediatric investigation · 2025Article
- Review
- A Novel Mutation in CNTNAP1 Gene Causes Disorganization of Axonal Domains, Hypomyelination and Severe Neurological Deficits.Journal of neuroscience research · 2025Article
- Age-dependent regulation of axoglial interactions and behavior by oligodendrocyte AnkyrinG.Nature communications · 2024Article
- Identification of novel genetic loci related to dromedary camel (Camelus dromedarius) morphometrics, biomechanics, and behavior by genome-wide association studies.BMC veterinary research · 2024Article
- Age-dependent regulation of axoglial interactions and behavior by oligodendrocyte AnkyrinG.bioRxiv : the preprint server for biology · 2024Article
- Clinical characteristics of patients with autoimmune nodopathy with anti-neurofascin155 antibodies.Frontiers in immunology · 2024Article
- Mouse models of human CNTNAP1-associated congenital hypomyelinating neuropathy and genetic restoration of murine neurological deficits.Cell reports · 2023Article
- Adult-onset depletion of sulfatide leads to axonal degeneration with relative myelin sparing.Glia · 2023Article
- Compromised Myelin and Axonal Molecular Organization Following Adult-Onset Sulfatide Depletion.Biomedicines · 2023Article
- Anti-pan-neurofascin antibodies induce subclass-related complement activation and nodo-paranodal damage.Brain : a journal of neurology · 2023Article
- Growing Spectrum of Autoimmune Nodopathies.Current neurology and neuroscience reports · 2023Review
- Altered plasma membrane abundance of the sulfatide-binding protein NF155 links glycosphingolipid imbalances to demyelination.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
61 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The evolutionary demand for rapid nerve impulse conduction led to the process of myelination-dependent organization of axons into distinct molecular domains. These domains include the node of Ranvier flanked by highly specialized paranodal domains where myelin loops and axolemma orchestrate the axoglial septate junctions. These junctions are formed by interactions between a glial isoform of neurofascin (Nfasc(NF155)) and axonal Caspr and Cont. Here we report the generation of myelinating glia-specific Nfasc(NF155) null mouse mutants. These mice exhibit severe ataxia, motor paresis, and death before the third postnatal week. In the absence of glial Nfasc(NF155), paranodal axoglial junctions fail to form, axonal domains fail to segregate, and myelinated axons undergo degeneration. Electrophysiological measurements of peripheral nerves from Nfasc(NF155) mutants revealed dramatic reductions in nerve conduction velocities. By using inducible PLP-CreER recombinase to ablate Nfasc(NF155) in adult myelinating glia, we demonstrate that paranodal axoglial junctions disorganize gradually as the levels of Nfasc(NF155) protein at the paranodes begin to drop. This coincides with the loss of the paranodal region and concomitant disorganization of the axonal domains. Our results provide the first direct evidence that the maintenance of axonal domains requires the fence function of the paranodal axoglial junctions. Together, our studies establish a central role for paranodal axoglial junctions in both the organization and the maintenance of axonal domains in myelinated axons.
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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.