Evidence map›Paper›PMID 20064853›Full record

ArticleThe Journal of physiology2010

Purinergic neuromuscular transmission is selectively attenuated in ulcerated regions of inflamed guinea pig distal colon.

Derek S Strong, Carson F Cornbrooks, Jane A Roberts, Jill M Hoffman, Keith A Sharkey, Gary M Mawe

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
9.3field-weighted citation impact, top 2% 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, 66 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The enteric nervous system in gastrointestinal disease etiology.Cellular and molecular life sciences : CMLS · 2021
    Review
  6. Article
  7. Enteric neuroplasticity and dysmotility in inflammatory disease: key players and possible therapeutic targets.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
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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

6 authors at 2 institutions in 2 countries.

Derek S StrongD403A Given Building, Department of Anatomy and Neurobiology, University of Vermont, Burlington, VT 05405, USA.
Carson F Cornbrooks
Jane A Roberts
Jill M Hoffman
Keith A Sharkey
Gary M Mawe
University of Vermont · USUniversity of Calgary · CA

Funding

Neuronal Excitability and Motility in ColitisR01DK062267 · NIDDK · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI MAWE, GARY M · 2002 to 2016
$3.3M
NIDDK NIH HHS DK62267NIDDK NIH HHS R01 DK062267
6 · The paper itself

Abstract

This study was undertaken to investigate neuromuscular transmission in regions of the inflamed colon in which motility is disrupted. Propulsive motility was evaluated in segments of control guinea pigs and those treated 6 days previously with trinitrobenzene sulfonic acid. Intracellular recordings were then obtained from circular muscle cells to examine excitatory and inhibitory junction potentials (EJPs and IJPs). In inflamed preparations, propulsion of fecal pellets was temporarily halted or obstructed at sites of mucosal damage, whereas the propulsive motility was linear in control colons. The amplitudes of evoked and spontaneous IJPs were significantly reduced in ulcerated regions of inflamed preparations, but EJPs were comparable to controls. Pharmacological dissection of the IJP revealed that the purinergic component was reduced, while the nitrergic IJP was slightly increased. Furthermore, the reduction in the purinergic IJP in inflamed preparations persisted in the presence of hexamethonium, suggesting that the deficit involved the inhibitory motor neuron and/or smooth muscle. Nerve fibre density was not altered in the circular muscle, and pre-contracted rings of inflamed colon relaxed normally to ATP, suggesting that the deficit involves altered ATP release and/or degradation. The P2Y(1) receptor antagonist MRS2179 slowed propulsive motility indicating that decreased purinergic neuromuscular transmission could contribute to the inflammation-induced motor deficit. We conclude that purinergic inhibitory neuronal input to the circular muscle is selectively reduced in regions of the colon in experimental colitis where the mucosa is damaged, and this is likely to contribute to altered motility in colitis by diminishing downstream relaxation during the peristaltic reflex.

Indexed as

Gastrointestinal MotilityAdaptation, PhysiologicalAnimalsColitisColitis, UlcerativeFemaleGuinea PigsMaleMuscle, Smooth

Identifiers

PMID20064853
PMCPMC2834943
OpenAlexW1483144158

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.