Evidence map›Paper›PMID 22087024›Full record

ArticleEndocrinology2012

Acute glucocorticoid administration rapidly suppresses basal and stress-induced hypothalamo-pituitary-adrenal axis activity.

Marcus H Andrews, Susan A Wood, Richard J Windle, Stafford L Lightman, Colin D Ingram

Open access · hybridAbstract read
In one paragraph

Article in Endocrinology, 2012. 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
1.7field-weighted citation impact, top 19% 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, 47 citations in OpenAlex.

  1. Trial
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  8. Direct Modulation of CRH Nerve Terminal Function by Noradrenaline and Corticosterone.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. A users guide to HPA axis research.Physiology & behavior · 2017
    Review
  17. Article
  18. Article
  19. Influence of starvation on heart contractility and corticosterone level in rats.Pflugers Archiv : European journal of physiology · 2015
    Article
  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

5 authors at 3 institutions in 1 country.

Marcus H AndrewsHenry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Bristol BS1 3NY, United Kingdom.
Susan A Wood
Richard J Windle
Stafford L Lightman
Colin D Ingram
University of Bristol · GBNewcastle University · GBQueen's Medical Centre · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H015779/1Wellcome Trust 051846Wellcome Trust 055348
6 · The paper itself

Abstract

Hypothalamo-pituitary-adrenal (HPA) axis activity is subject to negative feedback control by glucocorticoids. Although the rapid component of this feedback is widely considered to contribute to regulation of dynamic HPA activity, few in vivo data exist on the temporal and pharmacological characteristics of this phenomenon. Thus, frequent automated blood sampling was undertaken in rats to determine the effects of acute glucocorticoid administration on basal and stress-induced corticosterone secretion. The glucocorticoid agonist methylprednisolone (5-2000 μg) or dexamethasone (5-500 μg) injected iv at the peak of the diurnal rhythm caused dose-dependent suppression of basal corticosterone secretion, which was attenuated by the glucocorticoid receptor antagonist RU38486. With 50 μg methylprednisolone, the onset of this suppression occurred at 40 min and remained significant for 120 min. However, although higher doses led to a greater and more sustained suppression of endogenous corticosterone, the response was delayed by the emergence of an initial stimulatory response that imposed a finite minimum delay. A corticosterone response to injection of CRH (1 μg, iv) during the period of maximal suppression indicated a suprapituitary site for the inhibitory effect glucocorticoid activation. This mechanism was supported by glucocorticoid injection immediately before a psychological stress (30 min, white noise); methylprednisolone caused dose-dependent attenuation of stress-induced corticosterone release and expression of the activity marker c-fos mRNA in the paraventricular nucleus but did not block the pituitary response to CRH. Thus, in rats, glucocorticoid receptor activation rapidly suppresses basal and stress-induced HPA activity that operates, at least in part, through a central mechanism of action.

Indexed as

AnimalsCircadian RhythmCorticosteroneCorticotropin-Releasing HormoneDexamethasoneFeedback, PhysiologicalFemaleGlucocorticoidsHormone AntagonistsHypothalamo-Hypophyseal SystemMethylprednisoloneMifepristonePituitary-Adrenal SystemRatsRats, Sprague-DawleyReceptors, GlucocorticoidCorticosteroneCorticotropin-Releasing HormoneDexamethasoneGlucocorticoidsHormone AntagonistsMethylprednisoloneMifepristoneReceptors, Glucocorticoid

Identifiers

PMID22087024
PMCPMC3279736
OpenAlexW2048505384

What OpenQuestion holds

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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.