ArticleJournal of neurochemistry2022
Selective activation and down-regulation of Trk receptors by neurotrophins in human neurons co-expressing TrkB and TrkC.
Article in Journal of neurochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Neurotrophin System as a Complex Set of Potential Biomarkers in Psychiatric Disorders and Therapy-Overview of Recent Advances.International journal of molecular sciences · 2026Review
- Structural insights into the specificity of adaptor proteins Dok5 and Dok6 Docking to Trk receptors.Cell communication and signaling : CCS · 2026Article
- Discovery of a sulfotyrosine-motif in the human TrkB extracellular domain required for agonist activation.bioRxiv : the preprint server for biology · 2026Article
- Safety and biodistribution of intrathecal administration of mesenchymal stem cells (MSCs) and neurotrophin-releasing nanoparticles in a porcine CSF-guided delivery model for amyotrophic lateral sclerosis (ALS) drug discovery.Scientific reports · 2026Article
- Review
- Candidate Key Proteins in Thalamo-Amygdala Signaling in Tinnitus: A Bioinformatics Study.International journal of molecular sciences · 2026Article
- Candidate Key Proteins in Tinnitus-A Bioinformatic Study of Synaptic Transmission in the Inferior Colliculus.International journal of molecular sciences · 2025Article
- Genetics of constant and severe pain in the NAPS2 cohort of recurrent acute and chronic pancreatitis patients.The journal of pain · 2025Article
- Calcium-sensing receptors promoted Homer1 expression and osteogenic differentiation in bone marrow mesenchymal stem cells.Open life sciences · 2025Article
- New BDNF and NT-3 Cyclic Mimetics Concur with Copper to Activate Trophic Signaling Pathways as Potential Molecular Entities to Protect Old Brains from Neurodegeneration.Biomolecules · 2024Article
- Candidate Key Proteins in Tinnitus-A Bioinformatic Study of Synaptic Transmission in the Cochlear Nucleus.Biomedicines · 2024Article
- Review
- The amygdala NT3-TrkC pathway underlies inter-individual differences in fear extinction and related synaptic plasticity.Molecular psychiatry · 2024Article
- BDNF as a biomarker for neuropathic pain: Consideration of mechanisms of action and associated measurement challenges.Brain and behavior · 2023Review
- Closing the Gap between the Auditory Nerve and Cochlear Implant Electrodes: Which Neurotrophin Cocktail Performs Best for Axonal Outgrowth and Is Electrical Stimulation Beneficial?International journal of molecular sciences · 2023Article
- Neurotrophin signalling in the human nervous system.Frontiers in molecular neuroscience · 2023Review
- Basophils in pruritic skin diseases.Frontiers in immunology · 2023Review
- Brain-derived neurotrophic factor released from blood platelets prevents dendritic atrophy of lesioned adult central nervous system neurons.Brain communications · 2023Article
- Selective activation and down-regulation of Trk receptors by neurotrophins in human neurons co-expressing TrkB and TrkC.Journal of neurochemistry · 2022Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
In the central nervous system, most neurons co-express TrkB and TrkC, the tyrosine kinase receptors for brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3). As NT3 can also activate TrkB, it has been difficult to understand how NT3 and TrkC can exert unique roles in the assembly of neuronal circuits. Using neurons differentiated from human embryonic stem cells expressing both TrkB and TrkC, we compared Trk activation by BDNF and NT3. To avoid the complications resulting from TrkB activation by NT3, we also generated neurons from stem cells engineered to lack TrkB. We found that NT3 activates TrkC at concentrations lower than those of BDNF needed to activate TrkB. Downstream of Trk activation, the changes in gene expression caused by TrkC activation were found to be similar to those resulting from TrkB activation by BDNF, including a number of genes involved in synaptic plasticity. At high NT3 concentrations, receptor selectivity was lost as a result of TrkB activation. In addition, TrkC was down-regulated, as was also the case with TrkB at high BDNF concentrations. By contrast, receptor selectivity as well as reactivation were preserved when neurons were exposed to low neurotrophin concentrations. These results indicate that the selectivity of NT3/TrkC signalling can be explained by the ability of NT3 to activate TrkC at concentrations lower than those needed to activate TrkB. They also suggest that in a therapeutic perspective, the dosage of Trk receptor agonists will need to be taken into account if prolonged receptor activation is to be achieved.
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