Evidence map›Paper›PMID 21193524›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011

Modulation of visceral hypersensitivity by glial cell line-derived neurotrophic factor family receptor α-3 in colorectal afferents.

T Tanaka, M Shinoda, B Feng, K M Albers, G F Gebhart

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Optical clearing reveals TNBS-induced morphological changes of VGLUT2-positive nerve fibers in mouse colorectum.American journal of physiology. Gastrointestinal and liver physiology · 2021
    Article
  3. Article
  4. Visceral pain from colon and rectum: the mechanotransduction and biomechanics.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review
  5. Article
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  7. Review
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  14. Article
  15. Article
  16. Colitis decreases mechanosensitive K2P channel expression and function in mouse colon sensory neurons.American journal of physiology. Gastrointestinal and liver physiology · 2011
    Article
  17. 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 at 1 institution in 1 country.

T TanakaCenter for Pain Research, Departments of Anesthesiology, University of Pittsburgh, Pennsylvania, USA. Tanaka_Takahiro1@takeda.co.jp
M Shinoda
B Feng
K M Albers
G F Gebhart
University of Pittsburgh · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
NEUROTROPHINS MODULATE SENSORY DEVELOPMENT AND FUNCTIONR01NS033730 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ALBERS, KATHRYN MARIE · 1995 to 2014
$4.1M
MECHANISMS AND MODULATION OF VISCERAL PAINR01NS019912 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GEBHART, GERALD F · 1985 to 2009
$3.7M
NCATS NIH HHS UL1 TR000005NINDS NIH HHS NS-19912NINDS NIH HHS R01 NS033730
6 · The paper itself

Abstract

Irritable bowel syndrome is characterized by colorectal hypersensitivity and contributed to by sensitized mechanosensitive primary afferents and recruitment of mechanoinsensitive (silent) afferents. Neurotrophic factors are well known to orchestrate dynamic changes in the properties of sensory neurons. Although pain modulation by proteins in the glial cell line-derived neurotrophic factor (GDNF) family has been documented in various pathophysiological states, their role in colorectal hypersensitivity remains unexplored. Therefore, we investigated the involvement of the GDNF family receptor α-3 (GFRα3) signaling in visceral hypersensitivity by quantifying visceromotor responses (VMR) to colorectal distension before and after intracolonic treatment with 2,4,6-trinitrobenzene sulfonic acid (TNBS). Baseline responses to colorectal distension did not differ between C57BL/6 and GFRα3 knockout (KO) mice. Relative to intracolonic saline treatment, TNBS significantly enhanced the VMR to colorectal distension in C57BL/6 mice 2, 7, 10, and 14 days posttreatment, whereas TNBS-induced visceral hypersensitivity was significantly suppressed in GFRα3 KO mice. The proportion of GFRα3 immunopositive thoracolumbar and lumbosacral colorectal dorsal root ganglion neurons was significantly elevated 2 days after TNBS treatment. In single fiber recordings, responses to circumferential stretch of colorectal afferent endings in C57BL/6 mice were significantly increased (sensitized) after exposure to an inflammatory soup, whereas responses to stretch did not sensitize in GFRα3 KO mice. These findings suggest that enhanced GFRα3 signaling in visceral afferents may contribute to development of colorectal hypersensitivity.

Indexed as

Mechanotransduction, CellularAnimalsColitisColonDisease Models, AnimalElectromyographyEvoked PotentialsGanglia, SpinalGlial Cell Line-Derived Neurotrophic Factor ReceptorsHyperalgesiaMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNeurons, AfferentPressureArtn protein, mouseGfra3 protein, mouseGlial Cell Line-Derived Neurotrophic Factor ReceptorsNerve Tissue ProteinsTrinitrobenzenesulfonic Acid

Identifiers

PMID21193524
PMCPMC3064124
OpenAlexW2098063416

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.