Evidence map›Paper›PMID 21807003›Full record

ReviewNeuropharmacology2012

Stress and anxiety: structural plasticity and epigenetic regulation as a consequence of stress.

Bruce S McEwen, Lisa Eiland, Richard G Hunter, Melinda M Miller

Abstract readReview
In one paragraph

Review in Neuropharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 255 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
255citing papers in PubMed, 4 pooled it
14.7field-weighted citation impact, top 1% 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

255 citing papers in PubMed, 4 syntheses or guidelines pooled it, 579 citations in OpenAlex.

  1. Pooled it
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  5. Trial
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  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. The word Dementia should be retired.Communications medicine · 2026
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  16. Article
  17. Review
  18. Trajectories of late-life depression: insights from molecular imaging.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
  19. Article
  20. Corticosterone accelerates behavioral inflexibility via plasticity-related gene expression in the dorsal striatum.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article

195 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Bruce S McEwenLaboratory of Neuroendocrinology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. mcewen@rockefeller.edu
Lisa Eiland
Richard G Hunter
Melinda M Miller
Rockefeller University · US

Funding

Probing Systems-Level Function of Fronto-TemporalP50MH058911 · NIMH · NEW YORK UNIVERSITY · PI MCEWEN, BRUCE F · 1999 to 2008
$19.4M
STRESS, ADRENAL STEROIDS AND THE BRAINR01MH041256 · NIMH · ROCKEFELLER UNIVERSITY · PI MCEWEN, BRUCE S. · 1986 to 2015
$4.3M
NIMH NIH HHS P50 MH058911NIMH NIH HHS P50 MH58911NIMH NIH HHS R01 MH041256NIMH NIH HHS R01 MH41256
6 · The paper itself

Abstract

The brain is the central organ of stress and adaptation to stress because it perceives and determines what is threatening, as well as the behavioral and physiological responses to the stressor. The adult, as well as developing brain, possess a remarkable ability to show reversible structural and functional plasticity in response to stressful and other experiences, including neuronal replacement, dendritic remodeling, and synapse turnover. This is particularly evident in the hippocampus, where all three types of structural plasticity have been recognized and investigated, using a combination of morphological, molecular, pharmacological, electrophysiological and behavioral approaches. The amygdala and the prefrontal cortex, brain regions involved in anxiety and fear, mood, cognitive function and behavioral control, also show structural plasticity. Acute and chronic stress cause an imbalance of neural circuitry subserving cognition, decision making, anxiety and mood that can increase or decrease expression of those behaviors and behavioral states. In the short term, such as for increased fearful vigilance and anxiety in a threatening environment, these changes may be adaptive; but, if the danger passes and the behavioral state persists along with the changes in neural circuitry, such maladaptation may need intervention with a combination of pharmacological and behavioral therapies, as is the case for chronic or mood anxiety disorders. We shall review cellular and molecular mechanisms, as well as recent work on individual differences in anxiety-like behavior and also developmental influences that bias how the brain responds to stressors. Finally, we suggest that such an approach needs to be extended to other brain areas that are also involved in anxiety and mood. This article is part of a Special Issue entitled 'Anxiety and Depression'.

Indexed as

BrainEpigenesis, GeneticAnxietyHumansNeuronal PlasticityStress, Psychological

Identifiers

PMID21807003
PMCPMC3196296
OpenAlexW1983494600

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.