Evidence map›Paper›PMID 17692121›Full record

ArticleMolecular pain2007

Prostaglandin E2 potentiation of P2X3 receptor mediated currents in dorsal root ganglion neurons.

Congying Wang, Guang-Wen Li, Li-Yen Mae Huang

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Action potential-independent spontaneous microdomain CaProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Analyzing the Antinociceptive Effect of Interleukin-31 in Mice.International journal of molecular sciences · 2023
    Article
  8. The Role of ATP Receptors in Pain Signaling.Neurochemical research · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Novel Analgesics with Peripheral Targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020
    Review
  14. Review
  15. Article
  16. P2X receptor channels in chronic pain pathways.British journal of pharmacology · 2018
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Congying WangDepartment of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX 77555-1069, USA. conwang@utmb.edu
Guang-Wen Li
Li-Yen Mae Huang
The University of Texas Medical Branch at Galveston · US

Funding

NEURON-GLIA INTERACTIONS IN TRIGEMINAL GANGLIA AS A BASIS FOR FUTURE THERAPYR01DE017813 · NIDCR · UNIVERSITY OF TEXAS MED BR GALVESTON · PI HUANG, LI-YEN M · 2006 to 2017
$3.9M
TRIGEMINAL NEURONS--SUSTAINED RESPONSE TO OPOIDSR01NS030045 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI HUANG, LI-YEN M · 1993 to 2014
$3.7M
OPIOID RECEPTOR GENE TRANSFER-PAIN AND TOLERANCER01DA013668 · NIDA · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI HUANG, LI-YEN M · 2001 to 2005
$1.7M
NIDA NIH HHS DA13668NIDCR NIH HHS DE17813NINDS NIH HHS NS30045
6 · The paper itself

Abstract

Prostaglandin E2 (PGE2) is a well-known inflammatory mediator that enhances the excitability of DRG neurons. Homomeric P2X3 and heteromeric P2X2/3 receptors are abundantly expressed in dorsal root ganglia (DRG) neurons and participate in the transmission of nociceptive signals. The interaction between PGE2 and P2X3 receptors has not been well delineated. We studied the actions of PGE2 on ATP-activated currents in dissociated DRG neurons under voltage-clamp conditions. PGE2 had no effects on P2X2/3 receptor-mediated responses, but significantly potentiated fast-inactivating ATP currents mediated by homomeric P2X3 receptors. PGE2 exerted its action by activating EP3 receptors. To study the mechanism underlying the action of PGE2, we found that the adenylyl cyclase activator, forskolin and the membrane-permeable cAMP analogue, 8-Br-cAMP increased ATP currents, mimicking the effect of PGE2. In addition, forskolin occluded the enhancement produced by PGE2. The protein kinase A (PKA) inhibitors, H89 and PKA-I blocked the PGE2 effect. In contrast, the PKC inhibitor, bisindolymaleimide (Bis) did not change the potentiating action of PGE2. We further showed that PGE2 enhanced alpha,beta-meATP-induced allodynia and hyperalgesia and the enhancement was blocked by H89. These observations suggest that PGE2 binds to EP3 receptors, resulting in the activation of cAMP/PKA signaling pathway and leading to an enhancement of P2X3 homomeric receptor-mediated ATP responses in DRG neurons.

Indexed as

Purinergic P2 Receptor AgonistsAdenosine TriphosphateAnimalsDinoprostoneGanglia, SpinalNeuronsPatch-Clamp TechniquesRatsRats, Sprague-DawleyReceptors, Purinergic P2X3Adenosine TriphosphateDinoprostonePurinergic P2 Receptor AgonistsReceptors, Purinergic P2X3

Identifiers

PMID17692121
PMCPMC2063498
OpenAlexW2027932842

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.