Evidence map›Paper›PMID 29194563›Full record

ArticleBritish journal of pharmacology2018

Cyclic analogues of α-conotoxin Vc1.1 inhibit colonic nociceptors and provide analgesia in a mouse model of chronic abdominal pain.

Joel Castro, Luke Grundy, Annemie Deiteren, Andrea M Harrington, Tracey O'Donnell, Jessica Maddern, Jessi Moore, Sonia Garcia-Caraballo, Grigori Y Rychkov, Rilei Yu and 4 more

Abstract read
In one paragraph

Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.2field-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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. GABAExperimental physiology · 2026
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  6. Experimental colitis-induced visceral hypersensitivity is attenuated by GABA treatment in mice.American journal of physiology. Gastrointestinal and liver physiology · 2024
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  19. Protease-activated receptor-2 in endosomes signals persistent pain of irritable bowel syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
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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

14 authors at 4 institutions in 1 country.

Joel CastroVisceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, 5042, Australia.
Luke GrundyVisceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, 5042, Australia.
Annemie DeiterenVisceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, 5042, Australia.
Andrea M HarringtonVisceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, 5042, Australia.
Tracey O'DonnellVisceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, 5042, Australia.
Jessica MaddernVisceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, 5042, Australia.
Jessi MooreVisceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, 5042, Australia.
Sonia Garcia-CaraballoVisceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, 5042, Australia.
Grigori Y RychkovCentre for Nutrition and Gastrointestinal Diseases, Discipline of Medicine, University of Adelaide, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, SA, 5000, Australia.
Rilei YuInstitute for Molecular Bioscience, University of Queensland, Brisbane, QLD, 4072, Australia.
Quentin KaasInstitute for Molecular Bioscience, University of Queensland, Brisbane, QLD, 4072, Australia.
David J CraikInstitute for Molecular Bioscience, University of Queensland, Brisbane, QLD, 4072, Australia.
David J AdamsIllawarra Health and Medical Research Institute (IHMRI), University of Wollongong, Wollongong, NSW, 2522, Australia.ORCID 0000-0002-7030-2288
Stuart M BrierleyVisceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, 5042, Australia.ORCID 0000-0002-2527-2905
Flinders University · AUThe University of Queensland · AUSouth Australian Health and Medical Research Institute · AUUniversity of Wollongong · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposePatients with irritable bowel syndrome suffer from chronic visceral pain (CVP) and limited analgesic therapeutic options are currently available. We have shown that α-conotoxin Vc1.1 induced activation of GABA EXPERIMENTAL APPROACH: Using ex vivo colonic afferent preparations from mice, we determined the inhibitory actions of cyclized Vc1.1 (cVc1.1) and two cVc1.1 analogues on mouse colonic nociceptors in healthy and chronic visceral hypersensitivity (CVH) states. Using whole-cell patch clamp recordings, we also assessed the inhibitory actions of these peptides on the neuronal excitability of colonic innervating dorsal root ganglion neurons. In vivo, the analgesic efficacy of these analogues was assessed by determining the visceromotor response to colorectal distension in healthy and CVH mice. KEY

resultscVc1.1 and the cVc1.1 analogues, [C2H,C8F]cVc1.1 and [N9W]cVc1.1, all caused concentration-dependent inhibition of colonic nociceptors from healthy mice. Inhibition by these peptides was greater than those evoked by linear Vc1.1 and was substantially greater in colonic nociceptors from CVH mice. cVc1.1 also reduced excitability of colonic dorsal root ganglion neurons, with greater effect in CVH neurons. CVH mice treated with cVc1.1 intra-colonically displayed reduced pain responses to noxious colorectal distension compared with vehicle-treated CVH mice. CONCLUSIONS AND IMPLICATIONS: Cyclic versions of Vc1.1 evoked significant anti-nociceptive actions in CVH states, suggesting that they could be novel candidates for treatment of CVP. LINKED ARTICLES: This article is part of a themed section on Recent Advances in Targeting Ion Channels to Treat Chronic Pain. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.12/issuetoc.

Indexed as

AnalgesiaDisease Models, AnimalAbdominal PainAnimalsCells, CulturedChronic DiseaseColonConotoxinsMaleMiceMice, Inbred C57BLNociceptorsalpha-conotoxin Vc1.1Conotoxins

Identifiers

PMID29194563
PMCPMC5980271
OpenAlexW2772115888

What OpenQuestion holds

Textmetadata
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.