ArticleProceedings of the National Academy of Sciences of the United States of America1999
Neurotrophins regulate agrin-induced postsynaptic differentiation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 80 citations in OpenAlex.
- NMJ-associated transcriptomic remodeling correlates with disease severity in juvenile dermatomyositis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Localized release of muscle-generated BDNF regulates the initial formation of postsynaptic apparatus at neuromuscular synapses.Cell death and differentiation · 2025Article
- Skeletal muscle reprogramming enhances reinnervation after peripheral nerve injury.Nature communications · 2024Article
- Skeletal muscle reprogramming enhances reinnervation after peripheral nerve injury.Research square · 2024Article
- Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024Article
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- hiPSC-Derived Schwann Cells Influence Myogenic Differentiation in Neuromuscular Cocultures.Cells · 2021Article
- BDNF is a mediator of glycolytic fiber-type specification in mouse skeletal muscle.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Disease AffectsInternational journal of molecular sciences · 2019Article
- Brain-derived neurotrophic factor in urinary continence and incontinence.Nature reviews. Urology · 2014Review
- Stress incontinence in the era of regenerative medicine: reviewing the importance of the pudendal nerve.The Journal of urology · 2013Review
- Neurotrophin therapy improves recovery of the neuromuscular continence mechanism following simulated birth injury in rats.Neurourology and urodynamics · 2013Article
- Emerging roles for MAP kinases in agrin signaling.Communicative & integrative biology · 2011Article
- The recent understanding of the neurotrophin's role in skeletal muscle adaptation.Journal of biomedicine & biotechnology · 2011Review
- Secreted factors as synaptic organizers.The European journal of neuroscience · 2010Review
- Dual simulated childbirth injuries result in slowed recovery of pudendal nerve and urethral function.Neurourology and urodynamics · 2009Article
- The role of Wnt/beta-catenin signaling in postsynaptic differentiation.Communicative & integrative biology · 2008Article
- Multifunctional role of protein kinase C in regulating the formation and maturation of specific synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Bioengineered nerve regeneration and muscle reinnervation.Journal of anatomy · 2006Review
- BDNF is expressed in skeletal muscle satellite cells and inhibits myogenic differentiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The precise orchestration of synaptic differentiation is critical for efficient information exchange in the nervous system. The nerve-muscle synapse forms in response to agrin, which is secreted from the motor nerve terminal and induces the clustering of acetylcholine receptors (AChRs) and other elements of the postsynaptic apparatus on the subjacent muscle cell surface. In view of the highly restricted spatial localization and the plasticity of neuromuscular junctions, it seems likely that synapse formation and maintenance are regulated by additional, as-yet-unidentified factors. Here, we tested whether neurotrophins modulate the agrin-induced differentiation of postsynaptic specializations. We show that both brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4) inhibit agrin-induced AChR clustering on cultured myotubes. Nerve growth factor and NT-3 are without effect. Muscle cells express full-length TrkB, the cognate receptor for BDNF and NT-4. Direct activation of this receptor by anti-TrkB antibodies mimicked the BDNF/NT-4 inhibition of agrin-induced AChR clustering. This BDNF/NT-4 inhibition is likely to be an intrinsic mechanism for regulating AChR clustering, because neutralization of endogenous TrkB ligands resulted in elevated levels of AChR clustering even in the absence of added agrin. Finally, high concentrations of agrin can occlude the BDNF/NT-4 inhibition of AChR clustering. These results indicate that an interplay between agrin and neurotrophins can regulate the formation of postsynaptic specializations. They also suggest a mechanism for the suppression of postsynaptic specializations at nonjunctional regions.
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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.