Evidence map›Paper›PMID 27317579›Full record

ArticleMolecular pain2016

Estrogen-dependent visceral hypersensitivity following stress in rats: An fMRI study.

Catherine S Hubbard, Jane M Karpowicz, Andrew J Furman, Joyce Teixeira da Silva, David A Seminowicz, Richard J Traub

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  8. Gut feelings: the microbiota-gut-brain axis on steroids.American journal of physiology. Gastrointestinal and liver physiology · 2022
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  20. Estrogen modulation of visceral pain.Journal of Zhejiang University. Science. B
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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

6 authors at 2 institutions in 2 countries.

Catherine S HubbardDepartment of Neural and Pain Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA Center for Pain and the Brain, Department of Anesthesiology, Perioperative and Pain Medicine, Boston Children's Hospital, Boston, MA, USA Department of Anaesthesia, Harvard Medical School, Boston, MA, USA.
Jane M KarpowiczDepartment of Neural and Pain Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA.
Andrew J FurmanDepartment of Neural and Pain Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA.
Joyce Teixeira da SilvaDepartment of Neural and Pain Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA Department of Anaesthesia, Harvard Medical School, Boston, MA, USA Department of Anatomy, Institute of Biomedical Science-III, University of Sao Paulo, Sao Paulo, Brazil.
David A SeminowiczDepartment of Neural and Pain Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA Center to Advance Chronic Pain Research, University of Maryland, Baltimore, MD, USA dseminowicz@umaryland.edu.
Richard J TraubDepartment of Neural and Pain Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA Center to Advance Chronic Pain Research, University of Maryland, Baltimore, MD, USA.
University of Maryland, Baltimore · USCenter for Pain and the Brain · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We used functional MRI and a longitudinal design to investigate the brain mechanisms in a previously reported estrogen-dependent visceral hypersensitivity model. We hypothesized that noxious visceral stimulation would be associated with activation of the insula, anterior cingulate cortex, and amygdala, and that estrogen-dependent, stress-induced visceral hypersensitivity would both enhance activation of these regions and recruit activation of other brain areas mediating affect and reward processing. Ovariectomized rats were treated with estrogen (17 β-estradiol, E2) or vehicle (n = 5 per group) and scanned in a 7T MRI at three different time points: pre-stress (baseline), 2 days post-stress, and 18 days post-stress. Stress was induced via a forced-swim paradigm. In a separate group of ovariectomized rats, E2 treatment induced visceral hypersensitivity at the 2 days post-stress time point, and this hypersensitivity returned to baseline at the 18 days post-stress time point. Vehicle-treated rats show no hypersensitivity following stress. During the MRI scans, rats were exposed to noxious colorectal distention. Across groups and time points, noxious visceral stimulation led to activations in the insula, anterior cingulate, and left amygdala, parabrachial nuclei, and cerebellum. A group-by-time interaction was seen in the right amygdala, ventral striatum-pallidum, cerebellum, hippocampus, mediodorsal thalamus, and pontine nuclei. Closer inspection of the data revealed that vehicle-treated rats showed consistent activations and deactivations across time, whereas estrogen-treated animals showed minimal deactivation with noxious visceral stimulation. This unexpected finding suggests that E2 may dramatically alter visceral nociceptive processing in the brain following an acute stressor. This study is the first to examine estrogen-stress dependent interactions in response to noxious visceral stimulation using functional MRI. Future studies that include other control groups and larger sample sizes are needed to fully understand the interactions between sex hormones, stress, and noxious stimulation on brain activity.

Indexed as

Magnetic Resonance ImagingAnimalsColonDisease Models, AnimalEstrogensFemaleHyperalgesiaMotor ActivityRats, Sprague-DawleyRectumStress, PsychologicalVisceraEstrogensACCamygdalacolorectal distensionForced-swimfunctional MRIhippocampusinsulairritable bowel syndrome

Identifiers

PMID27317579
PMCPMC4956385
OpenAlexW2443156510

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.