ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
TRPC5 channel is the mediator of neurotrophin-3 in regulating dendritic growth via CaMKIIα in rat hippocampal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. 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, 42 citations in OpenAlex.
- TRPC4 regulates limbic behavior and neuronal development by stabilizing dendrite branches through actomyosin-driven integrin activation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- TRPC4 deletion elicits behavioral defects in sociability by dysregulating expression of microRNA-138-2.iScience · 2024Article
- The odyssey of the TR(i)P journey to the cellular membrane.Frontiers in cell and developmental biology · 2024Review
- Extracellular molecular signals shaping dendrite architecture during brain development.Frontiers in cell and developmental biology · 2023Review
- Wireless neuromodulation in vitro and in vivo by intrinsic TRPC-mediated magnetomechanical stimulation.Communications biology · 2022Article
- Role of Oxidative Stress and CaFrontiers in cell and developmental biology · 2021Review
- Effects of Transient Receptor Potential Cation 5 (TRPC5) Inhibitor, NU6027, on Hippocampal Neuronal Death after Traumatic Brain Injury.International journal of molecular sciences · 2020Article
- CaBritish journal of pharmacology · 2020Review
- TRP Channels Regulation of Rho GTPases in Brain Context and Diseases.Frontiers in cell and developmental biology · 2020Review
- Evidence of a Role for the TRPC Subfamily in Mediating Oxidative Stress in Parkinson's Disease.Frontiers in physiology · 2020Review
- Gq-Coupled Muscarinic Receptor Enhancement of KCNQ2/3 Channels and Activation of TRPC Channels in Multimodal Control of Excitability in Dentate Gyrus Granule Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- AMPA receptor GluA1 Ser831 phosphorylation is critical for nitroglycerin-induced migraine-like pain.Neuropharmacology · 2018Article
- TRPC6 specifically interacts with APP to inhibit its cleavage by γ-secretase and reduce Aβ production.Nature communications · 2015Article
- mRNA and microRNA expression profiles of radioresistant NCI-H520 non-small cell lung cancer cells.Molecular medicine reports · 2015Article
- Ca(2+) signaling initiated by canonical transient receptor potential channels in dendritic development.Neuroscience bulletin · 2015Review
- Increased expression of TRPC5 in cortical lesions of the focal cortical dysplasia.Journal of molecular neuroscience : MN · 2015Article
- The role of canonical transient receptor potential channels in seizure and excitotoxicity.Cells · 2014Article
- Brain-derived neurotrophic factor (BDNF)-induced mitochondrial motility arrest and presynaptic docking contribute to BDNF-enhanced synaptic transmission.The Journal of biological chemistry · 2014Article
- Cocaine self-administration in mice with forebrain knock-down of trpc5 ion channels.F1000Research · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurotrophin-3 (NT-3) plays numerous important roles in the CNS and the elevation of intracellular Ca(2+) ([Ca(2+)](i)) is critical for these functions of NT-3. However, the mechanism by which NT-3 induces [Ca(2+)](i) elevation remains largely unknown. Here, we found that transient receptor potential canonical (TRPC) 5 protein and TrkC, the NT-3 receptor, exhibited a similar temporal expression in rat hippocampus and cellular colocalization in hippocampal neurons. Stimulation of the neurons by NT-3 induced a nonselective cation conductance and PLCγ-dependent [Ca(2+)](i) elevation, which were both blocked when TRPC5, but not TRPC6 channels, were inhibited. Moreover, the Ca(2+) influx through TRPC5 induced by NT-3 inhibited the neuronal dendritic growth through activation of calmodulin-dependent kinase (CaMK) IIα. In contrast, the Ca(2+) influx through TRPC6 induced by NT-4 promoted the dendritic growth. Thus, TRPC5 acts as a novel and specific mediator for NT-3 to regulate dendrite development through CaMKIIα.
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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.