Evidence map›Paper›PMID 25698616›Full record

ArticleBrain research2015

The amygdala central nucleus is required for acute stress-induced bladder hyperalgesia in a rat visceral pain model.

Jennifer J DeBerry, Meredith T Robbins, Timothy J Ness

Open access · greenAbstract read
In one paragraph

Article in Brain research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Jennifer J DeBerryDepartment of Anesthesiology, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Psychology, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: jenjdeb@uab.edu.
Meredith T RobbinsDepartment of Anesthesiology, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Psychology, University of Alabama at Birmingham, Birmingham, AL, USA.
Timothy J NessDepartment of Anesthesiology, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Psychology, University of Alabama at Birmingham, Birmingham, AL, USA.
University of Alabama at Birmingham · US

Funding

QUANTITATIVE STUDY OF URINARY BLADDER SENSORY PROCESSINGR01DK051413 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DEBERRY, JENNIFER J, NESS, TIMOTHY J · 1997 to 2025
$5.4M
NIDDK NIH HHS R01 DK051413PHS HHS NIDDKDK051413
6 · The paper itself

Abstract

Chronic stress has been implicated in the pathogenesis of chronic visceral pain conditions, such as interstitial cystitis (IC), and bouts of acute stress exacerbate clinical urological pain. Studies using animal models have shown that exposure to chronic footshock stress augments reflex responses to urinary bladder distension (UBD) in animal models, however acute effects in animal models are largely unknown, as are the central nervous system mechanisms of stress-related increases in nociception. The amygdala is a salient structure for integration of sensory and cognitive/emotional factors. The present study determined the role of the central nucleus of the amygdala (CeA) in stress-related bladder hypersensitivity. We examined the effects of CeA manipulations (lesions and chemical stimulation) on visceromotor responses (abdominal muscle contractions) to UBD in adult, female Sprague-Dawley rats. We report that acute footshock stress produces bladder hyperalgesia that can be prevented by bilateral CeA lesions, despite no effect of lesions on baseline somatic sensation, as indicated by flinch/jump thresholds to electrical shock. Further, acute glucocorticoid stimulation of the CeA recapitulated stress-induced hyperalgesia. Of note is that CeA lesions, but not chemical stimulation, significantly affected HPA axis activation, as indicated by measurements of circulating corticosterone. Our findings conclusively show that the CeA is necessary for the generation of bladder hyperalgesia in response to acute stress. The CeA may play multiple stress-related roles in nociceptive modulation, i.e., via direct facilitation of the HPA axis during acute stress, or via modulation of other systems that augment acute stress responsiveness.

Indexed as

AnimalsCentral Amygdaloid NucleusDisease Models, AnimalElectroshockFemaleHyperalgesiaNociceptionRatsRats, Sprague-DawleyStress, PsychologicalUrinary BladderVisceral PainAmygdalaAnxietyGlucocorticoidHyperalgesiaStressVisceral

Identifiers

PMID25698616
PMCPMC4388818
OpenAlexW1989718094

What OpenQuestion holds

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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.