Evidence map›Paper›PMID 22302180›Full record

ArticleCellular and molecular neurobiology2012

Neural Regulation of the Stress Response: The Many Faces of Feedback.

Brent Myers, Jessica M McKlveen, James P Herman

Abstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 4% 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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
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  7. Review
  8. Article
  9. Oxytocin, Vasopressin and Stress: A Hormetic Perspective.Current issues in molecular biology · 2025
    Review
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  11. Article
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  20. Review

34 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

3 authors at 1 institution in 1 country.

Brent MyersDepartment of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Metabolic Diseases Institute, 2170 E. Galbraith Rd, Cincinnati, OH, 45237-0506, USA, brent.myers@uc.edu.
Jessica M McKlveen
James P Herman
University of Cincinnati · US

Funding

FUNCTIONAL ANATOMY OF LIMBIC NEUROENDOCRINE CIRCUITSR01MH049698 · NIMH · UNIVERSITY OF KENTUCKY · PI HERMAN, JAMES P · 1998 to 2018
$6.2M
PREDOCTORAL TRAINING PROGRAM IN THE NEUROSCIENCEST32NS007453 · NINDS · UNIVERSITY OF CINCINNATI · PI HERMAN, JAMES P · 1997 to 2025
$4.0M
Brainstem Mechanisms of Stress RegulationR01MH069860 · NIMH · UNIVERSITY OF CINCINNATI · PI HERMAN, JAMES P · 2004 to 2014
$3.5M
Training Program in Neuroendocrinology of HomeostasisT32DK059803 · NIDDK · UNIVERSITY OF CINCINNATI · PI WOODS, STEPHEN C · 2001 to 2017
$2.8M
Anatomical Plasticity and HPA Axis DysfunctionR01MH069725 · NIMH · UNIVERSITY OF CINCINNATI · PI HERMAN, JAMES P · 2005 to 2009
$1.9M
Stress Regulation of Non-Coding RNAs in Prefrontal CortexR21MH090574 · NIMH · UNIVERSITY OF CINCINNATI · PI HERMAN, JAMES P · 2011 to 2012
$443k
NIDDK NIH HHS T32 DK059803NIMH NIH HHS R01 MH049698NIMH NIH HHS R01 MH069725NIMH NIH HHS R01 MH069860NIMH NIH HHS R21 MH090574NINDS NIH HHS T32 NS007453
6 · The paper itself

Abstract

The mammalian stress response is an integrated physiological and psychological reaction to real or perceived adversity. Glucocorticoids (GCs) are an important component of this response, acting to redistribute energy resources to both optimize survival in the face of challenge and restore homeostasis after the immediate threat has subsided. Release of GCs is mediated by the hypothalamo-pituitary-adrenocortical (HPA) axis, driven by a neural signal originating in the paraventricular nucleus (PVN). Stress levels of GCs bind to glucocorticoid receptors (GRs) in multiple body compartments, including brain, and consequently have wide-reaching actions. For this reason, GCs serve a vital function in feedback inhibition of their own secretion. Fast, non-genomic feedback inhibition of the HPA axis is mediated at least in part by GC signaling in the PVN, acting by a cannabinoid-dependent mechanism to rapidly reduce both neural activity and GC release. Delayed feedback termination of the HPA axis response is mediated by forebrain GRs, presumably by genomic mechanisms. GCs also act in the brainstem to attenuate neuropeptidergic excitatory input to the PVN via acceleration of mRNA degradation, providing a mechanism to attenuate future responses to stressors. Thus, rather than having a single defined feedback switch, GCs work through multiple neurocircuits and signaling mechanisms to coordinate HPA axis activity to suit the overall needs of multiple body systems.

Identifiers

PMID22302180
PMCPMC3956711
OpenAlexW2004982081

What OpenQuestion holds

Textmetadata
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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.