ArticleDevelopment (Cambridge, England)1999
Expression of Trk receptors in the developing mouse trigeminal ganglion: in vivo evidence for NT-3 activation of TrkA and TrkB in addition to TrkC.
Article in Development (Cambridge, England), 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 157 citations in OpenAlex.
- Multiple glycoforms of TrkA interact with N-cadherin during trigeminal ganglion neurodevelopment.Journal of cell science · 2026Article
- AAV1.NT3 gene therapy mitigates the severity of autoimmune encephalomyelitis in the mouse model for multiple sclerosis.Gene therapy · 2025Article
- Study of the Pharmacological Activity Spectrum of the New Original NT-3 Mimetic Dipeptide GTS-302.Doklady. Biochemistry and biophysics · 2025Article
- Role of Neurotrophins in Orofacial Pain Modulation: A Review of the Latest Discoveries.International journal of molecular sciences · 2023Review
- Influencers in the Somatosensory System: Extrinsic Control of Sensory Neuron Phenotypes.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2023Review
- CMT1A current gene therapy approaches and promising biomarkers.Neural regeneration research · 2023Review
- Loss of Elp1 disrupts trigeminal ganglion neurodevelopment in a model of familial dysautonomia.eLife · 2022Article
- Age Related Response of Neonatal Rat Retinal Ganglion Cells to Reduced TrkB SignalingFrontiers in cell and developmental biology · 2021Article
- Suckling, Feeding, and Swallowing: Behaviors, Circuits, and Targets for Neurodevelopmental Pathology.Annual review of neuroscience · 2020Review
- Neurogenesis From Neural Crest Cells: Molecular Mechanisms in the Formation of Cranial Nerves and Ganglia.Frontiers in cell and developmental biology · 2020Review
- Enhancing the Therapeutic Potential of Olfactory Ensheathing Cells in Spinal Cord Repair Using Neurotrophins.Cell transplantation · 2018Review
- Molecular basis of tactile specialization in the duck bill.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Dabbling with Piezo2 for mechanosensation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- AAV1.NT-3 gene therapy attenuates spontaneous autoimmune peripheral polyneuropathy.Gene therapy · 2016Article
- HBpF-proBDNF: A New Tool for the Analysis of Pro-Brain Derived Neurotrophic Factor Receptor Signaling and Cell Biology.PloS one · 2016Article
- Sensory and spinal inhibitory dorsal midline crossing is independent of Robo3.Frontiers in neural circuits · 2015Article
- Loss of neurotrophin-3 from smooth muscle disrupts vagal gastrointestinal afferent signaling and satiation.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- NeuroD regulates neuronal migration.Molecules and cells · 2013Article
- Protein tyrosine phosphatase receptor type O inhibits trigeminal axon growth and branching by repressing TrkB and Ret signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Brn3a and Islet1 act epistatically to regulate the gene expression program of sensory differentiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Animals lacking neurotrophin-3 (NT-3) are born with deficits in almost all sensory ganglia. Among these, the trigeminal ganglion is missing 70% of the normal number of neurons, a deficit which develops during the major period of neurogenesis between embryonic stages (E) 10.5 and E13.5. In order to identify the mechanisms for this deficit, we used antisera specific for TrkA, TrkB, and TrkC to characterize and compare the expression patterns of each Trk receptor in trigeminal ganglia of wild type and NT-3 mutants between E10.5 and E15.5. Strikingly, TrkA, TrkB, and TrkC proteins appear to be exclusively associated with neurons, not precursors. While some neurons show limited co-expression of Trk receptors at E11.5, by E13. 5 each neuron expresses only one Trk receptor. Neuronal birth dating and cell counts show that in wild-type animals all TrkB- and TrkC-expressing neurons are generated before E11.5, while the majority of TrkA-expressing neurons are generated between E11.5 and E13.5. In mice lacking NT-3, the initial formation of the ganglion, as assessed at E10.5, is similar to that in wild-type animals. At E11.5, however, the number of TrkC-expressing neurons is dramatically reduced and the number of TrkC-immunopositive apoptotic profiles is markedly elevated. By E13.5, TrkC-expressing neurons are virtually eliminated. At E11.5, compared to wild type, the number of TrkB-expressing neurons is also reduced and the number of TrkB immunoreactive apoptotic profiles is increased. TrkA neurons are also reduced in the NT-3 mutants, but the major deficit develops between E12.5 and E13.5 when elevated numbers of TrkA-immunoreactive apoptotic profiles are detected. Normal numbers of TrkA- and TrkB-expressing neurons are seen in a TrkC-deficient mutant. Therefore, our data provide evidence that NT-3 supports the survival of TrkA-, TrkB- and TrkC-expressing neurons in the trigeminal ganglion by activating directly each of these receptors in vivo.
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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.