Evidence map›Paper›PMID 32651265›Full record

ArticleeNeuro

Traumatic Stress Induces Prolonged Aggression Increase through Synaptic Potentiation in the Medial Amygdala Circuits.

Jacob Nordman, Xiaoyu Ma, Zheng Li

Abstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. Traumatic stress recruits an excitatory orbitofrontal-amygdala pathway to drive maladaptive aggression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. The Anterior BNST Is Required for Novelty-Driven Social Interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  6. Familiarity Gates Socially Transmitted Aggression via the Medial Amygdala.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Distributed circuits regulating defensive state transitions: freezing, flight and fight.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  12. Article
  13. Article
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  15. Article
  16. A New Behavioral Paradigm for Frustrative Nonreward in Juvenile Mice.Biological psychiatry global open science · 2024
    Article
  17. Article
  18. Article
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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

3 authors.

Jacob NordmanSection on Synapse Development and Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892.ORCID 0000-0003-2513-7831
Xiaoyu MaSection on Synapse Development and Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892.ORCID 0000-0001-7673-7533
Zheng LiSection on Synapse Development and Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, lizheng2@mail.nih.gov.ORCID 0000-0002-2978-2531

Funding

Non-apoptotic function of casapses in synapsesZIAMH002881 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI LI, ZHENG · 2009 to 2025
$18.9M
Apoptotic molecules in synapse plasticityZ01MH002881 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI LI, ZHENG · 2007 to 2008
$1.1M
Neural Mechanisms in the Medial Amygdala Underlying AggressionFI2GM119962 · NIGMS · U.S. NATIONAL INSTITUTE OF MENTAL HEALTH · PI NORDMAN, JACOB · 2016 to 2016
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Intramural NIH HHS Z01 MH002881NIGMS NIH HHS FI2 GM119962
6 · The paper itself

Abstract

Traumatic stress can lead to heightened aggression which may be a symptom of psychiatric diseases such as PTSD and intermittent explosive disorder. The medial amygdala (MeA) is an evolutionarily conserved subnucleus of the amygdala that regulates attack behavior and behavioral responses to stressors. The precise contribution of the MeA in traumatic stress-induced aggression, however, requires further elucidation. In this study, we used foot shock to induce traumatic stress in mice and examine the mechanisms of prolonged aggression increase associated with it. Foot shock causes a prolonged increase in aggression that lasts at least one week. In vivo electrophysiological recordings revealed that foot shock induces potentiation of synapses formed between the MeA and the ventromedial hypothalamus (VmH) and bed nucleus of the stria terminalis (BNST). This synaptic potentiation lasts at least one week. Induction of synaptic depotentiation with low-frequency photostimulation (LFPS) immediately after foot shock suppresses the prolonged aggression increase without affecting non-aggressive social behavior, anxiety-like and depression-like behaviors, or fear learning. These results show that potentiation of the MeA-VmH and MeA-BNST circuits is essential for traumatic stress to cause a prolonged increase in aggression. These circuits may be potential targets for the development of therapeutic strategies to treat the aggression symptom associated with psychiatric diseases.

Indexed as

Corticomedial Nuclear ComplexSeptal NucleiAggressionAmygdalaAnimalsFearMiceaggressionmedial amygdalaPTSDsynaptic plasticitytraumatic stress

Identifiers

PMID32651265
PMCPMC7385664

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Registered trials

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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.