Evidence map›Paper›PMID 15774518›Full record

ArticleThe Journal of physiology2005

Synaptic facilitation and enhanced neuronal excitability in the submucosal plexus during experimental colitis in guinea-pig.

Alan E Lomax, Gary M Mawe, Keith A Sharkey

Open access · greenAbstract readComparative Study
In one paragraph

Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. The enteric nervous system.Physiological reviews · 2023
    Review
  6. Review
  7. The enteric nervous system in gastrointestinal disease etiology.Cellular and molecular life sciences : CMLS · 2021
    Review
  8. To learn, to remember, to forget-How smart is the gut?Acta physiologica (Oxford, England) · 2020
    Review
  9. Enteric neuroplasticity and dysmotility in inflammatory disease: key players and possible therapeutic targets.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Paradoxical regulation of ChAT and nNOS expression in animal models of Crohn's colitis and ulcerative colitis.American journal of physiology. Gastrointestinal and liver physiology · 2013
    Article
  18. Article
  19. Article
  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

3 authors at 2 institutions in 2 countries.

Alan E LomaxDepartment of Physiology and Biophysics, University of Calgary, 3330 Hospital Dr. NW, Calgary, Alberta T2N 4N1, Canada.
Gary M Mawe
Keith A Sharkey
University of Calgary · CAUniversity of Vermont · US

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

Intestinal secretion is regulated by submucosal neurones of the enteric nervous system. Inflammation of the intestines leads to aberrant secretory activity; therefore we hypothesized that the synaptic and electrical behaviours of submucosal neurones are altered during colitis. To test this hypothesis, we used intracellular microelectrode recording to compare the excitability and synaptic properties of submucosal neurones from normal and trinitrobenzene sulphonic acid (TNBS)-inflamed guinea-pig colons. Inflammation differentially affected the electrophysiological characteristics of the two functional classes of submucosal neurones. AH neurones from inflamed colons were more excitable, had shorter action potential durations and reduced afterhyperpolarizations. Stimulus-evoked fast and slow excitatory postsynaptic potentials (EPSPs) in S neurones were larger during colitis, and the incidence of spontaneous fast EPSPs was increased. In control preparations, fast EPSPs were almost completely blocked by the nicotinic receptor antagonist hexamethonium, whereas fast EPSPs in inflamed S neurones were only partially inhibited by hexamethonium. In inflamed tissues, components of the fast EPSP in S neurones were sensitive to blockade of P2(X) and 5-HT(3) receptors while these antagonists had little effect in control preparations. Control and inflamed S neurones were equally sensitive to brief application of acetylcholine, ATP and 5-HT, suggesting that synaptic facilitation was due to a presynaptic mechanism. Immunoreactivity for 5-HT in the submucosal plexus was unchanged by inflammation; this indicates that altered synaptic transmission was not due to anatomical remodelling of submucosal nerve terminals. This is the first demonstration of alterations in synaptic pharmacology in the enteric nervous system during inflammation.

Indexed as

Excitatory Postsynaptic PotentialsNeuronsSynaptic TransmissionAdaptation, PhysiologicalAnimalsColitisColonDisease Models, AnimalGuinea PigsIntestinal MucosaMaleSubmucous PlexusTrinitrobenzenesulfonic AcidTrinitrobenzenesulfonic Acid

Identifiers

PMID15774518
PMCPMC1464458
OpenAlexW2108513730

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.