ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Loss of glial neurofascin155 delays developmental synapse elimination at the neuromuscular junction.
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 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Neural Circuit Remodeling: Mechanistic Insights from Invertebrates.Journal of developmental biology · 2024Review
- Muscarinic Receptors in Developmental Axonal Competition at the Neuromuscular Junction.Molecular neurobiology · 2023Article
- A method to identify, dissect and stain equine neuromuscular junctions for morphological analysis.Journal of anatomy · 2022Article
- Synaptic proteomics reveal distinct molecular signatures of cognitive change and C9ORF72 repeat expansion in the human ALS cortex.Acta neuropathologica communications · 2022Article
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Blockage of neuromuscular glutamate receptors impairs reinnervation following nerve crush in adult mice.Frontiers in cellular neuroscience · 2022Article
- iPSC-derived myelinoids to study myelin biology of humans.Developmental cell · 2021Article
- Completion of neuronal remodeling prompts myelination along developing motor axon branches.The Journal of cell biology · 2021Article
- Engulfed by Glia: Glial Pruning in Development, Function, and Injury across Species.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- Focal loss of the paranodal domain protein Neurofascin155 in the internal capsule impairs cortically induced muscle activity in vivo.Molecular brain · 2020Article
- Developmental neuromuscular synapse elimination: Activity-dependence and potential downstream effector mechanisms.Neuroscience letters · 2020Review
- The Neuromuscular Junction in Health and Disease: Molecular Mechanisms Governing Synaptic Formation and Homeostasis.Frontiers in molecular neuroscience · 2020Review
- Tumor necrosis factor alpha mediates neuromuscular synapse elimination.Cell discovery · 2020Article
- Differences in the constituent fiber types contribute to the intermuscular variation in the timing of the developmental synapse elimination.Scientific reports · 2019Article
- Oligodendroglial Lineage Cells in Thyroid Hormone-Deprived Conditions.Stem cells international · 2019Review
- Homozygous mutation in the Neurofascin gene affecting the glial isoform of Neurofascin causes severe neurodevelopment disorder with hypotonia, amimia and areflexia.Human molecular genetics · 2018Article
- Axonal domain disorganization in Caspr1 and Caspr2 mutant myelinated axons affects neuromuscular junction integrity, leading to muscle atrophy.Journal of neuroscience research · 2017Article
- The Scaffolding Protein, Grb2-associated Binder-1, in Skeletal Muscles and Terminal Schwann Cells Regulates Postnatal Neuromuscular Synapse Maturation.Experimental neurobiology · 2017Article
- Identification of a novel CNTNAP1 mutation causing arthrogryposis multiplex congenita with cerebral and cerebellar atrophy.European journal of medical genetics · 2017Article
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Postnatal synapse elimination plays a critical role in sculpting and refining neural connectivity throughout the central and peripheral nervous systems, including the removal of supernumerary axonal inputs from neuromuscular junctions (NMJs). Here, we reveal a novel and important role for myelinating glia in regulating synapse elimination at the mouse NMJ, where loss of a single glial cell protein, the glial isoform of neurofascin (Nfasc155), was sufficient to disrupt postnatal remodeling of synaptic circuitry. Neuromuscular synapses were formed normally in mice lacking Nfasc155, including the establishment of robust neuromuscular synaptic transmission. However, loss of Nfasc155 was sufficient to cause a robust delay in postnatal synapse elimination at the NMJ across all muscle groups examined. Nfasc155 regulated neuronal remodeling independently of its canonical role in forming paranodal axo-glial junctions, as synapse elimination occurred normally in mice lacking the axonal paranodal protein Caspr. Rather, high-resolution proteomic screens revealed that loss of Nfasc155 from glial cells was sufficient to disrupt neuronal cytoskeletal organization and trafficking pathways, resulting in reduced levels of neurofilament light (NF-L) protein in distal axons and motor nerve terminals. Mice lacking NF-L recapitulated the delayed synapse elimination phenotype observed in mice lacking Nfasc155, suggesting that glial cells regulate synapse elimination, at least in part, through modulation of the axonal cytoskeleton. Together, our study reveals a glial cell-dependent pathway regulating the sculpting of neuronal connectivity and synaptic circuitry in the peripheral nervous system.
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