Evidence map›Paper›PMID 19959818›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010

The mechanisms underlying the generation of the colonic migrating motor complex in both wild-type and nNOS knockout mice.

Eamonn J Dickson, Dante J Heredia, Conor J McCann, Grant W Hennig, Terence K Smith

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
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

47 citing papers in PubMed.

  1. Article
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  3. Morphological, molecular, and functional characterization of mouse glutamatergic myenteric neurons.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  4. CaPhysiological reviews · 2024
    Review
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  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Control of colonic motility using electrical stimulation to modulate enteric neural activity.American journal of physiology. Gastrointestinal and liver physiology · 2021
    Article
  14. Article
  15. Akt phosphorylation of neuronal nitric oxide synthase regulates gastrointestinal motility in mouse ileum.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

5 authors.

Eamonn J DicksonDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV, USA. tksmith@medicine.nevada.edu
Dante J Heredia
Conor J McCann
Grant W Hennig
Terence K Smith

Funding

Relex Pathways Controlling Intestinal MotilityR01DK045713 · NIDDK · UNIVERSITY OF NEVADA RENO · PI SMITH, TERENCE KEITH · 1999 to 2012
$3.1M
NIDDK NIH HHS R01 DK045713NIDDK NIH HHS R01 DK45713
6 · The paper itself

Abstract

Colonic migrating motor complexes (CMMCs) propel fecal contents and are altered in diseased states, including slow-transit constipation. However, the mechanisms underlying the CMMCs are controversial because it has been proposed that disinhibition (turning off of inhibitory neurotransmission) or excitatory nerve activity generate the CMMC. Therefore, our aims were to reexamine the mechanisms underlying the CMMC in the colon of wild-type and neuronal nitric oxide synthase (nNOS)(-/-) mice. CMMCs were recorded from the isolated murine large bowel using intracellular recordings of electrical activity from circular muscle (CM) combined with tension recording. Spontaneous CMMCs occurred in both wild-type (frequency: 0.3 cycles/min) and nNOS(-/-) mice (frequency: 0.4 cycles/min). CMMCs consisted of a hyperpolarization, followed by fast oscillations (slow waves) with action potentials superimposed on a slow depolarization (wild-type: 14.0 +/- 0.6 mV; nNOS(-/-): 11.2 +/- 1.5 mV). Both atropine (1 microM) and MEN 10,376 [neurokinin 2 (NK2) antagonist; 0.5 microM] added successively reduced the slow depolarization and the number of action potentials but did not abolish the fast oscillations. The further addition of RP 67580 (NK1 antagonist; 0.5 microM) blocked the fast oscillations and the CMMC. Importantly, none of the antagonists affected the resting membrane potential, suggesting that ongoing tonic inhibition of the CM was maintained. Fecal pellet propulsion, which was blocked by the NK2 or the NK1 antagonist, was slower down the longer, more constricted nNOS(-/-) mouse colon (wild-type: 47.9 +/- 2.4 mm; nNOS(-/-): 57.8 +/- 1.4 mm). These observations suggest that excitatory neurotransmission enhances pacemaker activity during the CMMC. Therefore, the CMMC is likely generated by a synergistic interaction between neural and interstitial cells of Cajal networks.

Indexed as

Action PotentialsAnalgesicsAnimalsAtropineColonEnzyme InhibitorsIntestinal MucosaIsoindolesMaleMembrane PotentialsMiceMice, Inbred C57BLMice, Mutant StrainsMuscarinic AntagonistsMuscle, SmoothMyoelectric Complex, Migrating7,7-diphenyl-2-(1-imino-2-(2-methoxyphenyl)ethyl)perhydroisoindol-4-oneAnalgesicsAtropineEnzyme InhibitorsIsoindolesMuscarinic AntagonistsNitric OxideNitric Oxide Synthase Type INitroarginineNos1 protein, mouse

Identifiers

PMID19959818
PMCPMC2822500

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Registered trials

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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.