ArticleThe Journal of cell biology2009
Pro-BDNF-induced synaptic depression and retraction at developing neuromuscular synapses.
Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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Who cites it
62 citing papers in PubMed, 127 citations in OpenAlex.
- p75 neurotrophin receptor preserves neuromuscular synapse stability and muscle strength during aging.npj aging · 2026Article
- Ciliary neurotrophic factor slows axonal transport of signalling endosomes.Brain communications · 2026Article
- Inhibiting proBDNF to mature BDNF conversion leads to ASD-like phenotypes in vivo.Molecular psychiatry · 2024Article
- NgfrNature communications · 2024Article
- Molecular Adaptations of BDNF/NT-4 Neurotrophic and Muscarinic Pathways in Ageing Neuromuscular Synapses.International journal of molecular sciences · 2024Article
- Prelimbic proBDNF Facilitates Retrieval-Dependent Fear Memory Destabilization by Regulation of Synaptic and Neural Functions in Juvenile Rats.Molecular neurobiology · 2022Article
- Aluminium oxide nanoparticles compromise spatial memory performance and proBDNF-mediated neuronal function in the hippocampus of rats.Particle and fibre toxicology · 2022Article
- Recent Advances in the Molecular and Cellular Mechanisms of gp120-Mediated Neurotoxicity.Cells · 2022Review
- Maternal immune activation-induced proBDNF-mediated neural information processing dysfunction at hippocampal CA3-CA1 synapses associated with memory deficits in offspring.Frontiers in cell and developmental biology · 2022Article
- ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses.Frontiers in cellular neuroscience · 2022Article
- HDACi protects against vascular cognitive impairment from CCH injury via induction of BDNF-related AMPA receptor activation.Journal of cellular and molecular medicine · 2021Article
- Stress-primed secretory autophagy promotes extracellular BDNF maturation by enhancing MMP9 secretion.Nature communications · 2021Article
- Running and Swimming Differently Adapt the BDNF/TrkB Pathway to a Slow Molecular Pattern at the NMJ.International journal of molecular sciences · 2021Article
- Injection of Anti-proBDNF Attenuates Hippocampal-Dependent Learning and Memory Dysfunction in Mice With Sepsis-Associated Encephalopathy.Frontiers in neuroscience · 2021Article
- Requirements of Postnatal proBDNF in the Hippocampus for Spatial Memory Consolidation and Neural Function.Frontiers in cell and developmental biology · 2021Article
- Metabolic regulation of aging and age-related disease.Ageing research reviews · 2020Review
- Dorsolateral Striatal proBDNF Improves Reversal Learning by Enhancing Coordination of Neural Activity in Rats.Molecular neurobiology · 2020Article
- Deletion of Fmr1 from Forebrain Excitatory Neurons Triggers Abnormal Cellular, EEG, and Behavioral Phenotypes in the Auditory Cortex of a Mouse Model of Fragile X Syndrome.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- The Neuromuscular Junction in Health and Disease: Molecular Mechanisms Governing Synaptic Formation and Homeostasis.Frontiers in molecular neuroscience · 2020Review
- Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Postsynaptic cells generate positive and negative signals that retrogradely modulate presynaptic function. At developing neuromuscular synapses, prolonged stimulation of muscle cells induces sustained synaptic depression. We provide evidence that pro-brain-derived neurotrophic factor (BDNF) is a negative retrograde signal that can be converted into a positive signal by metalloproteases at the synaptic junctions. Application of pro-BDNF induces a dramatic decrease in synaptic efficacy followed by a retraction of presynaptic terminals, and these effects are mediated by presynaptic pan-neurotrophin receptor p75 (p75(NTR)), the pro-BDNF receptor. A brief stimulation of myocytes expressing cleavable or uncleavable pro-BDNF elicits synaptic potentiation or depression, respectively. Extracellular application of metalloprotease inhibitors, which inhibits the cleavage of endogenous pro-BDNF, facilitates the muscle stimulation-induced synaptic depression. Inhibition of presynaptic p75(NTR) or postsynaptic BDNF expression also blocks the activity-dependent synaptic depression and retraction. These results support a model in which postsynaptic secretion of a single molecule, pro-BDNF, may stabilize or eliminate presynaptic terminals depending on its proteolytic conversion at the synapses.
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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.