Evidence map›Paper›PMID 16842630›Full record

ArticleMolecular pain2006

The mu opioid agonist morphine modulates potentiation of capsaicin-evoked TRPV1 responses through a cyclic AMP-dependent protein kinase A pathway.

Irina Vetter, Bruce D Wyse, Gregory R Monteith, Sarah J Roberts-Thomson, Peter J Cabot

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 109 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Frontiers in neuroinformatics · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. TRPV1 in Pain and Itch.Advances in experimental medicine and biology · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Methanol Extract ofBiomolecules · 2020
    Article
  16. Review
  17. Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019
    Review
  18. MBD1 Contributes to the Genesis of Acute Pain and Neuropathic Pain by Epigenetic Silencing ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  19. Endogenous and Exogenous Opioids in Pain.Annual review of neuroscience · 2018
    Review
  20. Review
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

5 authors at 1 institution in 1 country.

Irina VetterThe School of Pharmacy, The University of Queensland, Brisbane, 4072, Australia. i.vetter@pharmacy.uq.edu.au
Bruce D Wyse
Gregory R Monteith
Sarah J Roberts-Thomson
Peter J Cabot
University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe vanilloid receptor 1 (TRPV1) is critical in the development of inflammatory hyperalgesia. Several receptors including G-protein coupled prostaglandin receptors have been reported to functionally interact with the TRPV1 through a cAMP-dependent protein kinase A (PKA) pathway to potentiate TRPV1-mediated capsaicin responses. Such regulation may have significance in inflammatory pain. However, few functional receptor interactions that inhibit PKA-mediated potentiation of TRPV1 responses have been described.

resultsIn the present studies we investigated the hypothesis that the mu opioid receptor (MOP) agonist morphine can modulate forskolin-potentiated capsaicin responses through a cAMP-dependent PKA pathway. HEK293 cells were stably transfected with TRPV1 and MOP, and calcium (Ca2+) responses to injection of the TRPV1 agonist capsaicin were monitored in Fluo-3-loaded cells. Pre-treatment with morphine did not inhibit unpotentiated capsaicin-induced Ca2+ responses but significantly altered capsaicin responses potentiated by forskolin. TRPV1-mediated Ca2+ responses potentiated by the direct PKA activator 8-Br-cAMP and the PKC activator Phorbol-12-myristate-13-acetatewere not modulated by morphine. Immunohistochemical studies confirmed that the TRPV1 and MOP are co-expressed on cultured Dorsal Root Ganglion neurones, pointing towards the existence of a functional relationship between the G-protein coupled MOP and nociceptive TRPV1.

conclusionThe results presented here indicate that the opioid receptor agonist morphine acts via inhibition of adenylate cyclase to inhibit PKA-potentiated TRPV1 responses. Targeting of peripheral opioid receptors may therefore have therapeutic potential as an intervention to prevent potentiation of TRPV1 responses through the PKA pathway in inflammation.

Indexed as

CapsaicinCell LineCyclic AMPCyclic AMP-Dependent Protein KinasesHumansMorphinePhosphorylationReceptors, Opioid, muRecombinant ProteinsTetradecanoylphorbol AcetateTransfectionTRPV Cation ChannelsCapsaicinCyclic AMPCyclic AMP-Dependent Protein KinasesMorphineReceptors, Opioid, muRecombinant ProteinsTetradecanoylphorbol AcetateTRPV1 protein, humanTRPV Cation Channels

Identifiers

PMID16842630
PMCPMC1553434
OpenAlexW2171691483

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.