ArticlePain2011
Nucleotides control the excitability of sensory neurons via two P2Y receptors and a bifurcated signaling cascade.
Article in Pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Nucleotides Cytidine and Uridine Associated with Vitamin B12 vs B-Complex Vitamins in the Treatment of Low Back Pain: The NUBES Study.Journal of pain research · 2020Trial
- Structural insight into the self-activation and G-protein coupling of P2Y2 receptor.Cell discovery · 2025Article
- Gaussian white noise stimulation as an alternative method to excite sensory neurons.Frontiers in pharmacology · 2025Article
- Selective KCNQ2/3 Potassium Channel Opener ICA-069673 Inhibits Excitability in Mouse Vagal Sensory Neurons.The Journal of pharmacology and experimental therapeutics · 2024Article
- The Similar and Distinct Roles of Satellite Glial Cells and Spinal Astrocytes in Neuropathic Pain.Cells · 2023Review
- Peripheral mechanisms of chronic pain.Medical review (2021) · 2022Review
- Article
- Disrupted Association of Sensory Neurons With Enveloping Satellite Glial Cells in Fragile X Mouse Model.Frontiers in molecular neuroscience · 2021Article
- PJournal of pain research · 2020Article
- Corneal pain and experimental model development.Progress in retinal and eye research · 2019Review
- Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019Review
- Article
- P2Y1R is involved in visceral hypersensitivity in rats with experimental irritable bowel syndrome.World journal of gastroenterology · 2017Article
- Control of sensory neuron excitability by serotonin involves 5HT2C receptors and Ca(2+)-activated chloride channels.Neuropharmacology · 2016Article
- Membrane coordination of receptors and channels mediating the inhibition of neuronal ion currents by ADP.Purinergic signalling · 2016Article
- Enhancement of acid-sensing ion channel activity by metabotropic P2Y UTP receptors in primary sensory neurons.Purinergic signalling · 2016Article
- P2Y Receptors Sensitize Mouse and Human Colonic Nociceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Chronic inflammatory pain upregulates expression of P2Y2 receptor in small-diameter sensory neurons.Metabolic brain disease · 2015Article
- Inhibition of G protein-coupled P2Y2 receptor induced analgesia in a rat model of trigeminal neuropathic pain.Molecular pain · 2014Article
- Acid evoked thermal hyperalgesia involves peripheral P2Y1 receptor mediated TRPV1 phosphorylation in a rodent model of thrombus induced ischemic pain.Molecular pain · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Nucleotides contribute to the sensation of acute and chronic pain, but it remained enigmatic which G protein-coupled nucleotide (P2Y) receptors and associated signaling cascades are involved. To resolve this issue, nucleotides were applied to dorsal root ganglion neurons under current- and voltage-clamp. Adenosine triphosphate (ATP), adenosine diphosphate (ADP), and uridine triphosphate (UTP), but not uridine diphosphate (UDP), depolarized the neurons and enhanced action potential firing in response to current injections. The P2Y(2) receptor preferring agonist 2-thio-UTP was equipotent to UTP in eliciting these effects. The selective P2Y(1) receptor antagonist MRS2179 largely attenuated the excitatory effects of ADP, but left those of 2-thio-UTP unaltered. Thus, the excitatory effects of the nucleotides were mediated by 2 different P2Y receptors, P2Y(1) and P2Y(2). Activation of each of these 2 receptors by either ADP or 2-thio-UTP inhibited currents through K(V)7 channels, on one hand, and facilitated currents through TRPV(1) channels, on the other hand. Both effects were abolished by inhibitors of phospholipase C or Ca(2+)-ATPase and by chelation of intracellular Ca(2+). The facilitation of TRPV(1), but not the inhibition K(V)7 channels, was prevented by a protein kinase C inhibitor. Simultaneous blockage of K(V)7 channels and of TRPV(1) channels prevented nucleotide-induced membrane depolarization and action potential firing. Thus, P2Y(1) and P2Y(2) receptors mediate an excitation of dorsal root ganglion neurons by nucleotides through the inhibition of K(V)7 channels and the facilitation of TRPV(1) channels via a common bifurcated signaling pathway relying on an increase in intracellular Ca(2+) and an activation of protein kinase C, respectively.
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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.