ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Transient receptor potential canonical 3 (TRPC3) is required for IgG immune complex-induced excitation of the rat dorsal root ganglion 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 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 66 citations in OpenAlex.
- TRPM2 is a direct pain transducer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The neuro-immune insights of itch: peripheral mechanisms and central glial contributions.Cellular & molecular biology letters · 2026Review
- Fc gamma receptor IIa signaling from spinal cord astrocytes promotes neuropathic pain in rats.The journal of pain · 2025Article
- Spinal TRPC3 promotes neuropathic pain and coordinates phospholipase C-induced mechanical hypersensitivity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- TRPC3/6 Channels Mediate Mechanical Pain Hypersensitivity via Enhancement of Nociceptor Excitability and of Spinal Synaptic Transmission.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- B cells drive neuropathic pain-related behaviors in mice through IgG-Fc gamma receptor signaling.Science translational medicine · 2024Article
- Pain Hypersensitivity in SLURP1 and SLURP2 Knock-out Mouse Models of Hereditary Palmoplantar Keratoderma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Neuronal C-Reactive Protein/FcγRI Positive Feedback Proinflammatory Signaling Contributes to Nerve Injury Induced Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The transient receptor potential channels in rheumatoid arthritis: Need to pay more attention.Frontiers in immunology · 2023Review
- Emerging Roles of Type-I Interferons in Neuroinflammation, Neurological Diseases, and Long-Haul COVID.International journal of molecular sciences · 2022Review
- TRPC3 Antagonizes Pruritus in a Mouse Contact Dermatitis Model.The Journal of investigative dermatology · 2022Article
- Neuronal FcεRIα directly mediates ocular itch via IgE-immune complex in a mouse model of allergic conjunctivitis.Journal of neuroinflammation · 2022Article
- Targeting the high affinity receptor, FcγRI, in autoimmune disease, neuropathy, and cancer.Immunotherapy advances · 2022Review
- FcεR1-expressing nociceptors trigger allergic airway inflammation.The Journal of allergy and clinical immunology · 2021Article
- The Neuroimmunology of Chronic Pain: From Rodents to Humans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- Autoimmune regulation of chronic pain.Pain reports · 2021Review
- Characterizing the Mechanical Properties of Ectopic Axonal Receptive Fields in Inflamed Nerves and Following Axonal Transport Disruption.Neuroscience · 2020Article
- Elevated myocardial SORBS2 and the underlying implications in left ventricular noncompaction cardiomyopathy.EBioMedicine · 2020Article
- Canonical Transient Receptor Potential (TRPC) Channels in Nociception and Pathological Pain.Neural plasticity · 2020Review
- Cartilage-binding antibodies induce pain through immune complex-mediated activation of neurons.The Journal of experimental medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 3 countries.
Funding
Abstract
Chronic pain may accompany immune-related disorders with an elevated level of serum IgG immune complex (IgG-IC), but the underlying mechanisms are obscure. We previously demonstrated that IgG-IC directly excited a subpopulation of dorsal root ganglion (DRG) neurons through the neuronal Fc-gamma receptor I (FcγRI). This might be a mechanism linking IgG-IC to pain and hyperalgesia. The purpose of this study was to investigate the signaling pathways and transduction channels activated downstream of IgG-IC and FcγRI. In whole-cell recordings, IgG-IC induced a nonselective cation current (I(IC)) in the rat DRG neurons, carried by Ca(2+) and Na(+). The I(IC) was potentiated or attenuated by, respectively, lowering or increasing the intracellular Ca(2+) buffering capacity, suggesting that this current was regulated by intracellular calcium. Single-cell RT-PCR revealed that transient receptor potential canonical 3 (TRPC3) mRNA was always coexpressed with FcγRI mRNA in the same DRG neuron. Moreover, ruthenium red (a general TRP channel blocker), BTP2 (a general TRPC channel inhibitor), and pyrazole-3 (a selective TRPC3 blocker) each potently inhibited the I(IC). Specific knockdown of TRPC3 using small interfering RNA attenuated the IgG-IC-induced Ca(2+) response and the I(IC). Additionally, the I(IC) was blocked by the tyrosine kinase Syk inhibitor OXSI-2, the phospholipase C (PLC) inhibitor neomycin, and either the inositol triphosphate (IP(3)) receptor antagonist 2-aminoethyldiphenylborinate or heparin. These results indicated that the activation of neuronal FcγRI triggers TRPC channels through the Syk-PLC-IP(3) pathway and that TRPC3 is a key molecular target for the excitatory effect of IgG-IC on DRG neurons.
Indexed as
Identifiers
What OpenQuestion holds
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.