Evidence map›Paper›PMID 25734510›Full record

ArticleTranslational psychiatry2015

Knockdown of corticotropin-releasing factor in the central amygdala reverses persistent viscerosomatic hyperalgesia.

A C Johnson, L Tran, B Greenwood-Van Meerveld

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 56 citations in OpenAlex.

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  17. Role of estrogen and stress on the brain-gut axis.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Review
  18. Review
  19. Mechanisms of Stress-induced Visceral Pain.Journal of neurogastroenterology and motility · 2018
    Review
  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 1 institution in 1 country.

A C JohnsonOklahoma Center for Neuroscience, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.
L TranOklahoma Center for Neuroscience, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.ORCID 0000000190746495
B Greenwood-Van Meerveld1] Oklahoma Center for Neuroscience, University of Oklahoma Health Science Center, Oklahoma City, OK, USA [2] Department of Physiology, University of Oklahoma Health Science Center, Oklahoma City, OK, USA [3] VA Medical Center, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.
University of Oklahoma Health Sciences Center · US

Funding

Central Molecular Mechanisms of Stress-Induced Visceral HypersensitivityF31DK089871 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI JOHNSON, ANTHONY C · 2010 to 2012
$77k
Central Mechanisms Modulating Visceral SensitivityI01BX002188 · VA · OKLAHOMA CITY VA MEDICAL CENTER · PI HOUCHEN, COURTNEY WAYNE · 2013 to 2022
–
BLRD VA I01 BX002188NIDDK NIH HHS F31 DK089871NIDDK NIH HHS F31DK089871
6 · The paper itself

Abstract

Gastrointestinal nociception is exacerbated by chronic stress through an unknown mechanism. The amygdala is a key nucleus involved in the autonomic and neuroendocrine responses to stress. The goal of this study was to test the hypothesis that prolonged exposure of the central amygdala (CeA) to stress or the stress hormone cortisol (or corticosterone in rats) induces nociceptive behaviors mediated by corticotropin-releasing factor (CRF) within the CeA. We selectively knocked down CRF in the CeA via antisense oligodeoxynucleotides (ASO) in animals with targeted, stereotaxically placed corticosterone (CORT) micropellets or following repeated water avoidance stress (WAS). CRF expression in the CeA was analyzed concurrently with the assessment of visceral hypersensitivity to colonic distension and mechanical somatic withdrawal threshold. The responses were characterized at 7 or 28 days post implantation of the CORT micropellet or following 7 days of WAS. Exposure of the CeA to elevated CORT or WAS increased CRF expression and heightened visceral and somatic sensitivity. Infusion of CRF ASO into the CeA decreased CRF expression and attenuated visceral and somatic hypersensitivity in both models. Our study provides important evidence for a CRF-mediated mechanism specifically within the CeA that regulates stress-induced visceral and somatic nociception.

Indexed as

Analysis of VarianceAnimalsCentral Amygdaloid NucleusCorticosteroneCorticotropin-Releasing HormoneDisease Models, AnimalHyperalgesiaMaleNociceptive PainRatsRats, Inbred F344CorticosteroneCorticotropin-Releasing Hormone

Identifiers

PMID25734510
PMCPMC4354346
OpenAlexW2022749117

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.