ArticleAmerican journal of physiology. Cell physiology2012
Genetic deletion of trkB.T1 increases neuromuscular function.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- p75 neurotrophin receptor preserves neuromuscular synapse stability and muscle strength during aging.npj aging · 2026Article
- Open-Source Tools for Neuromuscular Electrical Stimulation in Mouse Models: A Methodological Validation Study.Muscles (Basel, Switzerland) · 2026Article
- Motor Neuron Size-Dependent Differences in mRNA Expression of Tropomyosin-Related Kinase Receptor B in Adult Rats.Journal of neurochemistry · 2026Article
- Ciliary neurotrophic factor slows axonal transport of signalling endosomes.Brain communications · 2026Article
- Lycopene Alleviates Depression-Like Behavior in Chronic Social Defeat Stress-Induced Mice by Promoting Synaptic Plasticity via the BDNF-TrkB Pathway.Food science & nutrition · 2025Article
- Aging Skeletal Muscles: What Are the Mechanisms of Age-Related Loss of Strength and Muscle Mass, and Can We Impede Its Development and Progression?International journal of molecular sciences · 2024Review
- 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
- Neurotrophins and Other Growth Factors in the Pathogenesis of Alzheimer's Disease.Life (Basel, Switzerland) · 2023Review
- Review
- The Role of Neurotrophin Signaling in Age-Related Cognitive Decline and Cognitive Diseases.International journal of molecular sciences · 2022Review
- Endothelial cells are an important source of BDNF in rat skeletal muscle.Scientific reports · 2022Article
- The Molecular Effects of BDNF Synthesis on Skeletal Muscle: A Mini-Review.Frontiers in physiology · 2022Review
- Article
- Running and Swimming Differently Adapt the BDNF/TrkB Pathway to a Slow Molecular Pattern at the NMJ.International journal of molecular sciences · 2021Article
- Delayed onset of inherited ALS by deletion of the BDNF receptor TrkB.T1 is non-cell autonomous.Experimental neurology · 2021Article
- The BDNF rs6265 Polymorphism is a Modifier of Cardiomyocyte Contractility and Dilated Cardiomyopathy.International journal of molecular sciences · 2020Article
- Running and swimming prevent the deregulation of the BDNF/TrkB neurotrophic signalling at the neuromuscular junction in mice with amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2020Article
- Review
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Authors and funding
25 authors at 8 institutions in 1 country.
Funding
Abstract
Neurotrophin-dependent activation of the tyrosine kinase receptor trkB.FL modulates neuromuscular synapse maintenance and function; however, it is unclear what role the alternative splice variant, truncated trkB (trkB.T1), may have in the peripheral neuromuscular axis. We examined this question in trkB.T1 null mice and demonstrate that in vivo neuromuscular performance and nerve-evoked muscle tension are significantly increased. In vitro assays indicated that the gain-in-function in trkB.T1(-/-) animals resulted specifically from an increased muscle contractility, and increased electrically evoked calcium release. In the trkB.T1 null muscle, we identified an increase in Akt activation in resting muscle as well as a significant increase in trkB.FL and Akt activation in response to contractile activity. On the basis of these findings, we conclude that the trkB signaling pathway might represent a novel target for intervention across diseases characterized by deficits in neuromuscular function.
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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.