Evidence map›Paper›PMID 25436222›Full record

ArticleNeurobiology of stress2015

The Effects of Stress Exposure on Prefrontal Cortex: Translating Basic Research into Successful Treatments for Post-Traumatic Stress Disorder.

Amy F T Arnsten, Murray A Raskind, Fletcher B Taylor, Daniel F Connor

Open access · hybridAbstract read
In one paragraph

Article in Neurobiology of stress, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed
6.9field-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

154 citing papers in PubMed, 357 citations in OpenAlex.

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  6. Neurofeedback for functional neurological disorders: future directions for research and clinical practice.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
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  9. Reinventing amlodipine.The Journal of pharmacology and experimental therapeutics · 2026
    Review
  10. Article
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  12. Locus coeruleus-amygdala circuit disrupts prefrontal control to impair fear extinction.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  13. Brexpiprazole for the Treatment of Agitation Associated with Dementia due to Alzheimer's Disease: Clinical Perspectives.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
    Review
  14. Article
  15. Methylone promotes neurite outgrowth and has long-lasting effects on fear extinction learning.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
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94 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 4 institutions in 1 country.

Amy F T ArnstenDept. Neurobiology, Yale University School of Medicine, New Haven, CT 06510.
Murray A RaskindMadigan Army Medical Center and VA Northwest Network Mental Illness, VA Puget Sound Health Care System, 1660 S. Columbian Way, Seattle, WA 98108.
Fletcher B TaylorRainier Associates, Tacoma, WA 98467.
Daniel F ConnorDept. Psychiatry, University of Connecticut Medical School, Farmington, CT 06030.
Tacoma Housing Authority · USUniversity of Connecticut · USVA Northwest Network · USYale University · US

Funding

Highly evolved brain circuits in primates: molecular vulnerabilities for diseaseDP1AG047744 · NIA · YALE UNIVERSITY · PI ARNSTEN, AMY F.T. · 2013 to 2017
$4.1M
NIA NIH HHS DP1 AG047744
6 · The paper itself

Abstract

Research on the neurobiology of the stress response in animals has led to successful new treatments for Post-Traumatic Stress Disorder (PTSD) in humans. Basic research has found that high levels of catecholamine release during stress rapidly impair the top-down cognitive functions of the prefrontal cortex (PFC), while strengthening the emotional and habitual responses of the amygdala and basal ganglia. Chronic stress exposure leads to dendritic atrophy in PFC, dendritic extension in the amygdala, and strengthening of the noradrenergic (NE) system. High levels of NE release during stress engage low affinity alpha-1 adrenoceptors, (and likely beta-1 adrenoceptors), which rapidly reduce the firing of PFC neurons, but strengthen amygdala function. In contrast, moderate levels of NE release during nonstress conditions engage higher affinity alpha-2A receptors, which strengthen PFC, weaken amygdala, and regulate NE cell firing. Thus, either alpha-1 receptor blockade or alpha-2A receptor stimulation can protect PFC function during stress. Patients with PTSD have signs of PFC dysfunction. Clinical studies have found that blocking alpha-1 receptors with prazosin, or stimulating alpha-2A receptors with guanfacine or clonidine can be useful in reducing the symptoms of PTSD. Placebo-controlled trials have shown that prazosin is helpful in veterans, active duty soldiers and civilians with PTSD, including improvement of PFC symptoms such as impaired concentration and impulse control. Open label studies suggest that guanfacine may be especially helpful in treating children and adolescents who have experienced trauma. Thus, understanding the neurobiology of the stress response has begun to help patients with stress disorders.

Indexed as

clonidinedopamineguanfacinenorepinephrinepediatricprazosin

Identifiers

PMID25436222
PMCPMC4244027
OpenAlexW1987605932

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.