ArticleJournal of applied physiology (Bethesda, Md. : 1985)2014
TrkB kinase activity maintains synaptic function and structural integrity at adult neuromuscular junctions.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 60 citations in OpenAlex.
- Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Motor Neuron Size-Dependent Differences in mRNA Expression of Tropomyosin-Related Kinase Receptor B in Adult Rats.Journal of neurochemistry · 2026Article
- Activity-dependent muscarinic signalling regulates presynaptic PKC pathway and neurotransmission machinery at the neuromuscular junction.Cell communication and signaling : CCS · 2025Article
- Mechanisms Underlying Muscle-Related Diseases and Aging: Insights into Pathophysiology and Therapeutic Strategies.Muscles (Basel, Switzerland) · 2025Review
- Chloroquine Causes Aging-like Changes in Diaphragm Neuromuscular Junction Morphology in Mice.Cells · 2025Article
- Article
- Inhibition of TrkB kinase activity impairs autophagy in cervical motor neurons of young but not old mice.Experimental physiology · 2025Article
- Molecular Adaptations of BDNF/NT-4 Neurotrophic and Muscarinic Pathways in Ageing Neuromuscular Synapses.International journal of molecular sciences · 2024Article
- BDNF/TrkB signalling, in cooperation with muscarinic signalling, retrogradely regulates PKA pathway to phosphorylate SNAP-25 and Synapsin-1 at the neuromuscular junction.Cell communication and signaling : CCS · 2024Article
- Postnatal survival of phrenic motor neurons is promoted by BDNF/TrkB.FL signaling.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Chemogenetic inhibition of TrkB signalling reduces phrenic motor neuron survival and size.Molecular and cellular neurosciences · 2023Article
- Article
- Electrophysiological effects of BDNF and TrkB signaling at type-identified diaphragm neuromuscular junctions.Journal of neurophysiology · 2023Article
- Neurotrophic factors in the physiology of motor neurons and their role in the pathobiology and therapeutic approach to amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2023Review
- Article
- Neuromuscular recruitment strategies of the vastus lateralis according to sex.Acta physiologica (Oxford, England) · 2022Article
- Neuromuscular Junction Dysfunction in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2022Review
- Brain derived neurotrophic factor/tropomyosin related kinase B signaling impacts diaphragm neuromuscular transmission in a novel rat chemogenetic model.Frontiers in cellular neuroscience · 2022Article
- TrkB signaling is correlated with muscular fatigue resistance and less vulnerability to neurodegeneration.Frontiers in molecular neuroscience · 2022Article
- Engineering skeletal muscle tissues with advanced maturity improves synapse formation with human induced pluripotent stem cell-derived motor neurons.APL bioengineering · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Activation of the tropomyosin-related kinase receptor B (TrkB) by brain-derived neurotrophic factor acutely regulates synaptic transmission at adult neuromuscular junctions (NMJs). The role of TrkB kinase activity in the maintenance of NMJ function and structure at diaphragm muscle NMJs was explored using a chemical-genetic approach that permits reversible inactivation of TrkB kinase activity in TrkB(F616A) mice by 1NMPP1. Inhibiting TrkB kinase activity for 7 days resulted in significant, yet reversible, impairments in neuromuscular transmission at diaphragm NMJs. Neuromuscular transmission failure following 2 min of repetitive phrenic nerve stimulation increased from 42% in control to 59% in 1NMPP1-treated TrkB(F616A) mice (P = 0.010). Recovery of TrkB kinase activity following withdrawal of 1NMPP1 treatment improved neuromuscular transmission (P = 0.006). Electrophysiological measurements at individual diaphragm NMJs documented lack of differences in quantal content in control and 1NMPP1-treated mice (P = 0.845). Morphological changes at diaphragm NMJs were modest following inhibition and recovery of TrkB kinase activity. Three-dimensional reconstructions of diaphragm NMJs revealed no differences in volume at motor end plates (labeled by α-bungarotoxin; P = 0.982) or presynaptic terminals (labeled by synaptophysin; P = 0.515). Inhibition of TrkB kinase activity by 1NMPP1 resulted in more compact NMJs, with increased apposition of presynaptic terminals and motor end plates (P = 0.017) and reduced fragmentation of motor end plates (P = 0.005). Recovery of TrkB kinase activity following withdrawal of 1NMPP1 treatment resulted in postsynaptic remodeling likely reflecting increased gutter depth (P = 0.007), without significant presynaptic changes. These results support an essential role for TrkB kinase activity in maintaining synaptic function and structural integrity at NMJs in the adult mouse diaphragm muscle.
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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.