Evidence map›Paper›PMID 24845185›Full record

ArticlePsychoneuroendocrinology2014

Glucocorticoid receptors in the nucleus of the solitary tract (NTS) decrease endocrine and behavioral stress responses.

Sriparna Ghosal, Jana Bundzikova-Osacka, C Mark Dolgas, Brent Myers, James P Herman

Open access · greenAbstract read
In one paragraph

Article in Psychoneuroendocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 51 citations in OpenAlex.

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  10. Overtraining Syndrome as a Complex Systems Phenomenon.Frontiers in network physiology · 2021
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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

5 authors at 1 institution in 1 country.

Sriparna GhosalDepartment of Psychiatry and Behavioral Neuroscience, University of Cincinnati Metabolic Diseases Institute, Cincinnati, OH 45237, United States. Electronic address: ghosalsa@mail.uc.edu.
Jana Bundzikova-OsackaDepartment of Psychiatry and Behavioral Neuroscience, University of Cincinnati Metabolic Diseases Institute, Cincinnati, OH 45237, United States.
C Mark DolgasDepartment of Psychiatry and Behavioral Neuroscience, University of Cincinnati Metabolic Diseases Institute, Cincinnati, OH 45237, United States.
Brent MyersDepartment of Psychiatry and Behavioral Neuroscience, University of Cincinnati Metabolic Diseases Institute, Cincinnati, OH 45237, United States.
James P HermanDepartment of Psychiatry and Behavioral Neuroscience, University of Cincinnati Metabolic Diseases Institute, Cincinnati, OH 45237, United States.
University of Cincinnati · US

Funding

Brainstem Mechanisms of Stress RegulationR01MH069860 · NIMH · UNIVERSITY OF CINCINNATI · PI HERMAN, JAMES P · 2004 to 2014
$3.5M
NIMH NIH HHS MH069860NIMH NIH HHS R01 MH069860
6 · The paper itself

Abstract

Stress activates the hypothalamo-pituitary-adrenal (HPA) axis, leading to adrenocortical secretion of glucocorticoids. The magnitude and duration of the HPA axis response is mediated in large part by the glucocorticoid receptor (GR). The nucleus of the solitary tract (NTS) abundantly expresses the GR and is a key brain region for processing autonomic and endocrine stress responses. This study tests the hypothesis that GR within the NTS plays an important role in inhibiting stress-induced endocrine and behavioral responses. Cohorts of rats received bilateral micropellet (30 μg) implantations of crystalline corticosterone, mifepristone (a GR antagonist) or cholesterol (control) directed into the region of the NTS, and were subsequently subjected to either acute psychogenic (restraint) stress or chronic variable stress (CVS). We found that NTS GR antagonism increased acute stress-induced corticosterone levels, whereas GR activation within the NTS attenuated this response. Following CVS, basal and 15 min post-restraint plasma corticosterone levels were increased by NTS GR antagonism, which was associated with an increase in Fos immunoreactivity within the PVN. Using the elevated plus maze (EPM) and forced swim test (FST), we assessed the effect of NTS GR inhibition on anxiety- and depression-like behaviors, respectively. GR inhibition within the NTS decreased open arm exploratory behavior in the EPM and increased immobility in the FST relative to controls. Together, the findings reveal a novel role of NTS GR signaling for inhibiting both endocrine and behavioral responses to stress.

Indexed as

Stress, PsychologicalAnimalsBehavior, AnimalCorticosteroneDown-RegulationDrug ImplantsHormonesMaleMaze LearningMifepristoneRatsRats, Sprague-DawleyReceptors, GlucocorticoidSolitary NucleusCorticosteroneDrug ImplantsHormonesMifepristoneReceptors, GlucocorticoidChronic stressChronic variable stressCorticosteroneDepressionHPA axis

Identifiers

PMID24845185
PMCPMC4076411
OpenAlexW2121701067

What OpenQuestion holds

Textmetadata
LicenceTDM
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.