Evidence map›Paper›PMID 19893614›Full record

ArticlePloS one2009

TRPV1 and TRPA1 mediate peripheral nitric oxide-induced nociception in mice.

Takashi Miyamoto, Adrienne E Dubin, Matt J Petrus, Ardem Patapoutian

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

102 citing papers in PubMed, 220 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Peptide-Based Approaches for Pain Relief and Healing in Wounds.International journal of molecular sciences · 2026
    Review
  6. BH4 Oxidation-Derived HJournal of neurochemistry · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Cross-species RNAi therapy via AAV delivery alleviates neuropathic pain by targeting GCH1.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  11. Article
  12. Review
  13. Molecular Mechanisms of Migraine: Nitric Oxide Synthase and Neuropeptides.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

42 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Takashi MiyamotoDepartment of Cell Biology, The Scripps Research Institute, La Jolla, California, USA.
Adrienne E Dubin
Matt J Petrus
Ardem Patapoutian
Genomics Institute of the Novartis Research Foundation · USScripps Research Institute · US

Funding

Temperature-activated TRP channels and thermosensationR01NS049104 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI PATAPOUTIAN, ARDEM · 2005 to 2009
$2.1M
NINDS NIH HHS R01 NS049104NINDS NIH HHS R01NS049104
6 · The paper itself

Abstract

Nitric oxide (NO) can induce acute pain in humans and plays an important role in pain sensitization caused by inflammation and injury in animal models. There is evidence that NO acts both in the central nervous system via a cyclic GMP pathway and in the periphery on sensory neurons through unknown mechanisms. It has recently been suggested that TRPV1 and TRPA1, two polymodal ion channels that sense noxious stimuli impinging on peripheral nociceptors, are activated by NO in heterologous systems. Here, we investigate the relevance of this activation. We demonstrate that NO donors directly activate TRPV1 and TRPA1 in isolated inside-out patch recordings. Cultured primary sensory neurons display both TRPV1- and TRPA1-dependent responses to NO donors. BH4, an essential co-factor for NO production, causes activation of a subset of DRG neurons as assayed by calcium imaging, and this activation is at least partly dependent on nitric oxide synthase activity. We show that BH4-induced calcium influx is ablated in DRG neurons from TRPA1/TRPV1 double knockout mice, suggesting that production of endogenous levels of NO can activate these ion channels. In behavioral assays, peripheral NO-induced nociception is compromised when TRPV1 and TRPA1 are both ablated. These results provide genetic evidence that the peripheral nociceptive action of NO is mediated by both TRPV1 and TRPA1.

Indexed as

AnimalsBehavior, AnimalCell LineCHO CellsCricetinaeCricetulusGanglia, SpinalHumansMaleMiceMice, KnockoutNeuronsNitric OxideNociceptorsPainTransient Receptor Potential ChannelsNitric OxideTransient Receptor Potential ChannelsTRPA1 Cation ChannelTrpa1 protein, mouseTRPV1 protein, mouseTRPV Cation Channels

Identifiers

PMID19893614
PMCPMC2764051
OpenAlexW2087077009

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.