ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Alternative splicing of the TRPC3 ion channel calmodulin/IP3 receptor-binding domain in the hindbrain enhances cation flux.
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 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Functional and structural basis of a hypermorphic TRPC3 variant.Science advances · 2026Article
- Schizophrenia-associated 22q11.2 deletion elevates striatal acetylcholine and disrupts thalamostriatal projections to produce amotivation in mice.bioRxiv : the preprint server for biology · 2025Article
- Heterogeneity in Slow Synaptic Transmission Diversifies Purkinje Cell Timing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- TRPC Channels Activated by G Protein-Coupled Receptors Drive CaTranslational stroke research · 2024Article
- Phenotypical, genotypical and pathological characterization of the moonwalker mouse, a model of ataxia.Neurobiology of disease · 2024Article
- Widespread alternative splicing dysregulation occurs presymptomatically in CAG expansion spinocerebellar ataxias.Brain : a journal of neurology · 2024Article
- Dysregulation of alternative splicing in spinocerebellar ataxia type 1.Human molecular genetics · 2024Article
- Review
- Isoflavones Mediate Dendritogenesis Mainly through Estrogen Receptor α.International journal of molecular sciences · 2023Article
- Inhibition of TRPC3 channels by a novel pyrazole compound confers antiseizure effects.Epilepsia · 2022Article
- TRPC3, but not TRPC1, as a good therapeutic target for standalone or complementary treatment of DMD.Journal of translational medicine · 2021Article
- Human Brain Region-Specific Alternative Splicing of TRPC3, the Type 3 Canonical Transient Receptor Potential Non-Selective Cation Channel.Cerebellum (London, England) · 2019Article
- Focal Ischaemic Infarcts Expand Faster in Cerebellar Cortex than Cerebral Cortex in a Mouse Photothrombotic Stroke Model.Translational stroke research · 2018Article
- Structure-function analyses of the ion channel TRPC3 reveal that its cytoplasmic domain allosterically modulates channel gating.The Journal of biological chemistry · 2018Article
- A Closely Associated Phospholipase C Regulates Cation Channel Function through Phosphoinositide Hydrolysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Alternative splicing and nonsense-mediated mRNA decay enforce neural specific gene expression.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2016Review
- Diacylglycerol-mediated regulation of Aplysia bag cell neuron excitability requires protein kinase C.The Journal of physiology · 2016Article
- TRPC6 is the endothelial calcium channel that regulates leukocyte transendothelial migration during the inflammatory response.The Journal of experimental medicine · 2015Article
- TRPC3-dependent synaptic transmission in central mammalian neurons.Journal of molecular medicine (Berlin, Germany) · 2015Review
- Motor Learning and the Cerebellum.Cold Spring Harbor perspectives in biology · 2015Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Canonical transient receptor potential (TRPC3) nonselective cation channels are effectors of G-protein-coupled receptors (GPCRs), activated via phospholipase C-diacylglycerol signaling. In cerebellar Purkinje cells, TRPC3 channels cause the metabotropic glutamate receptor (mGluR)-mediated slow EPSC (sEPSC). TRPC3 channels also provide negative feedback regulation of cytosolic Ca(2+), mediated by a C terminus "calmodulin and inositol trisphosphate receptor binding" (CIRB) domain. Here we report the alternative splicing of the TRPC3 mRNA transcript (designated TRPC3c), resulting in omission of exon 9 (approximately half of the CIRB domain) in mice, rats, and guinea pigs. TRPC3c expression is brain region specific, with prevalence in the cerebellum and brainstem. The TRPC3c channels expressed in HEK293 cells exhibit increased basal and GPCR-activated channel currents, and increased Ca(2+) fluorescence responses, compared with the previously characterized (TRPC3b) isoform when activated via either the endogenous M3 muscarinic acetylcholine receptor, or via coexpressed mGluR1. GPCR-induced TRPC3c channel opening rate (cell-attached patch) matched the maximum activation achieved with inside-out patches with zero cytosolic Ca(2+), whereas the GPCR-induced TRPC3b activation frequency was significantly less. Both TRPC3 channel isoforms were blocked with 2 mm Ca(2+), attributable to CIRB domain regulation. In addition, genistein blocked Purkinje cell (S)-2-amino-2-(3,5-dihydroxyphenyl) acetic acid (mGluR1)-activated TPRC3 current as for recombinant TRPC3c current. This novel TRPC3c ion channel therefore has enhanced efficacy as a neuronal GPCR-Ca(2+) signaling effector, and is associated with sensorimotor coordination, neuronal development, and brain injury.
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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.