Evidence map›Paper›PMID 27590998›Full record

ArticleGut2017

Stress activates pronociceptive endogenous opioid signalling in DRG neurons during chronic colitis.

Raquel Guerrero-Alba, Eduardo E Valdez-Morales, Nestor N Jimenez-Vargas, Cintya Lopez-Lopez, Josue Jaramillo-Polanco, Takanobu Okamoto, Yasmin Nasser, Nigel W Bunnett, Alan E Lomax, Stephen J Vanner

Open access · greenAbstract read
In one paragraph

Article in Gut, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Endosomal signaling of delta opioid receptors is an endogenous mechanism and therapeutic target for relief from inflammatory pain.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. Review
  11. Neuropeptides in gut-brain axis and their influence on host immunity and stress.Computational and structural biotechnology journal · 2020
    Review
  12. Colitis-Induced Microbial Perturbation Promotes Postinflammatory Visceral Hypersensitivity.Cellular and molecular gastroenterology and hepatology · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

10 authors at 5 institutions in 3 countries.

Raquel Guerrero-AlbaGI Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Eduardo E Valdez-MoralesGI Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Nestor N Jimenez-VargasGI Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Cintya Lopez-LopezGI Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Josue Jaramillo-PolancoGI Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Takanobu OkamotoGI Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Yasmin NasserGI Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Nigel W BunnettMonash Institute of Pharmaceutical Sciences and Australian Research Council Centre of Excellence in Convergent Bio-Nano Science and Technology, Monash University, Parkville, Australia.
Alan E LomaxGI Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Stephen J VannerGI Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Kingston General Hospital · CAQueen's University · CAAutonomous University of Aguascalientes · MXAustralian Research Council · AUUniversity of Calgary · CA

Funding

Endosomal Platforms for Signaling PainR01NS102722 · NINDS · NEW YORK UNIVERSITY · PI NIGEL W BUNNETT, Brian L Schmidt · 2017 to 2026
$3.4M
NINDS NIH HHS R01 NS102722
6 · The paper itself

Abstract

AIMS AND

backgroundPsychological stress accompanies chronic inflammatory diseases such as IBD, and stress hormones can exacerbate pain signalling. In contrast, the endogenous opioid system has an important analgesic action during chronic inflammation. This study examined the interaction of these pathways.

methodsMouse nociceptive dorsal root ganglia (DRG) neurons were incubated with supernatants from segments of inflamed colon collected from patients with chronic UC and mice with dextran sodium sulfate (cDSS)-induced chronic colitis. Stress effects were studied by adding stress hormones (epinephrine and corticosterone) to dissociated neurons or by exposing cDSS mice to water avoidance stress. Changes in excitability of colonic DRG nociceptors were measured using patch clamp and Ca

resultsSupernatants from patients with chronic UC and from colons of mice with chronic colitis caused a naloxone-sensitive inhibition of neuronal excitability and capsaicin-evoked Ca

conclusionsStress hormones block the inhibitory actions of endogenous opioids and can change the effect of opioid signalling in DRG neurons to excitation. Targeting these pathways may prevent heavy opioid use in IBD.

Indexed as

AdultAgedAnimalsbeta-EndorphinBiopsyChronic DiseaseColitisColonCytokinesGanglia, SpinalHumansMiceMice, Inbred C57BLMiddle AgedNaloxoneNociceptorsbeta-EndorphinCytokinesNaloxoneABDOMINAL PAININFLAMMATORY BOWEL DISEASENEUROGASTROENTEROLOGYPSYCHOLOGICAL STRESS

Identifiers

PMID27590998
PMCPMC10064864
OpenAlexW2511994914

What OpenQuestion holds

Textmetadata
LicenceTDM
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.