ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
The interaction between tropomyosin-related kinase B receptors and presynaptic muscarinic receptors modulates transmitter release in adult rodent motor nerve terminals.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 64 citations in OpenAlex.
- 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
- Exploring the Comprehensive Neuroprotective and Anticancer Potential of Afzelin.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Purinergic Tuning of the Tripartite Neuromuscular Synapse.Molecular neurobiology · 2023Review
- Electrophysiological effects of BDNF and TrkB signaling at type-identified diaphragm neuromuscular junctions.Journal of neurophysiology · 2023Article
- Synaptic retrograde regulation of the PKA-induced SNAP-25 and Synapsin-1 phosphorylation.Cellular & molecular biology letters · 2023Article
- Muscarinic Receptors in Developmental Axonal Competition at the Neuromuscular Junction.Molecular neurobiology · 2023Article
- Article
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Review
- The Molecular Effects of BDNF Synthesis on Skeletal Muscle: A Mini-Review.Frontiers in physiology · 2022Review
- TrkB signaling is correlated with muscular fatigue resistance and less vulnerability to neurodegeneration.Frontiers in molecular neuroscience · 2022Article
- Brain derived neurotrophic factor/tropomyosin related kinase B signaling impacts diaphragm neuromuscular transmission in a novel rat chemogenetic model.Frontiers in cellular neuroscience · 2022Article
- Running and Swimming Differently Adapt the BDNF/TrkB Pathway to a Slow Molecular Pattern at the NMJ.International journal of molecular sciences · 2021Article
- TrkB signaling contributes to transdiaphragmatic pressure generation in aged mice.Journal of neurophysiology · 2021Article
- Inhibition of TrkB kinase activity impairs transdiaphragmatic pressure generation.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Review
- Article
- The p75Acta neuropathologica communications · 2019Article
- 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
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neurotrophin brain-derived neurotrophic factor (BDNF), neurotrophin-4 (NT-4) and the receptors tropomyosin-related kinase B (trkB) and p75(NTR) are present in the nerve terminals on the neuromuscular junctions (NMJs) of the levator auris longus muscle of the adult mouse. Exogenously added BDNF or NT-4 increased evoked ACh release after 3 h. This presynaptic effect (the size of the spontaneous potentials is not affected) is specific because it is not produced by neurotrophin-3 (NT-3) and is prevented by preincubation with trkB-IgG chimera or by pharmacological block of trkB [K-252a (C₂₇H₂₁N₃O₅)] or p75(NTR) [Pep5 (C₈₆H₁₁₁N₂₅O₁₉S₂] signaling. The effect of BDNF depends on the M₁ and M₂ muscarinic acetylcholine autoreceptors (mAChRs) because it is prevented by atropine, pirenzepine and methoctramine. We found that K-252a incubation reduces ACh release (~50%) in a short time (1 h), but the p75(NTR) signaling inhibitor Pep5 does not have this effect. The specificity of the K-252a blocking effect on trkB was confirmed with the anti-trkB antibody 47/trkB, which reduces evoked ACh release, like K-252a, whereas the nonpermeant tyrosine kinase blocker K-252b does not. Neither does incubation with the fusion protein trkB-IgG (to chelate endogenous BDNF/NT-4), anti-BDNF or anti-NT-4 change ACh release. Thus, the trkB receptor normally seems to be coupled to ACh release when there is no short-term local effect of neurotrophins at the NMJ. The normal function of the mAChR mechanism is a permissive prerequisite for the trkB pathway to couple to ACh release. Reciprocally, the normal function of trkB modulates M₁- and M₂-subtype muscarinic pathways.
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