Evidence map›Paper›PMID 32424020›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020

Potentiation of Divergent Medial Amygdala Pathways Drives Experience-Dependent Aggression Escalation.

Jacob C Nordman, Xiaoyu Ma, Qinhua Gu, Michael Potegal, He Li, Alexxai V Kravitz, Zheng Li

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Traumatic stress recruits an excitatory orbitofrontal-amygdala pathway to drive maladaptive aggression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. The Anterior BNST Is Required for Novelty-Driven Social Interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  7. Sex differences in the neural circuitry of aggression.bioRxiv : the preprint server for biology · 2025
    Article
  8. Familiarity Gates Socially Transmitted Aggression via the Medial Amygdala.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  9. Estrogen Control of Social Behaviors.Annual review of neuroscience · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Developmental Shifts in Amygdala Function.Current topics in behavioral neurosciences · 2025
    Review
  15. Article
  16. Review
  17. Article
  18. Oxytocin treatment rescues irritability-like behavior in Cc2d1a conditional knockout mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  19. Substance P in the medial amygdala regulates aggressive behaviors in male mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Jacob C NordmanSection on Synapse Development and Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.ORCID 0000-0003-2513-7831
Xiaoyu MaSection on Synapse Development and Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.ORCID 0000-0001-7673-7533
Qinhua GuSection on Synapse Development and Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.ORCID 0000-0003-0384-7306
Michael PotegalProgram in Occupational Therapy, Center for Neurobehavioral Development, University of Minnesota, Minneapolis, Minnesota 55455.
He LiDepartment of Psychiatry, Uniformed Services University, Bethesda, Maryland 20892.ORCID 0000-0002-7388-8464
Alexxai V KravitzEating and Addiction Section, Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.ORCID 0000-0001-5983-0218
Zheng LiSection on Synapse Development and Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 lizheng2@mail.nih.gov.ORCID 0000-0002-2978-2531
National Institutes of Health · USUniformed Services University of the Health Sciences · USUniversity of Minnesota · US

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
–
Intramural NIH HHS Z01 MH002881NIGMS NIH HHS FI2 GM119962
6 · The paper itself

Abstract

Heightened aggression can be serious concerns for the individual and society at large and are symptoms of many psychiatric illnesses, such as post-traumatic stress disorder. The circuit and synaptic mechanisms underlying experience-induced aggression increase, however, are poorly understood. Here we find that prior attack experience leading to an increase in aggressive behavior, known as aggression priming, activates neurons within the posterior ventral segment of the medial amygdala (MeApv). Optogenetic stimulation of MeApv using a synaptic depression protocol suppresses aggression priming, whereas high-frequency stimulation enhances aggression, mimicking attack experience. Interrogation of the underlying neural circuitry revealed that the MeApv mediates aggression priming via synaptic connections with the ventromedial hypothalamus (VmH) and bed nucleus of the stria terminalis (BNST). These pathways undergo NMDAR-dependent synaptic potentiation after attack. Furthermore, we find that the MeApv-VmH synapses selectively control attack duration, whereas the MeApv-BNST synapses modulate attack frequency, both with no effect on social behavior. Synaptic potentiation of the MeApv-VmH and MeApv-BNST pathways contributes to increased aggression induced by traumatic stress, and weakening synaptic transmission at these synapses blocks the effect of traumatic stress on aggression. These results reveal a circuit and synaptic basis for aggression modulation by experience that can be potentially leveraged toward clinical interventions.

Indexed as

AggressionAnimalsCorticomedial Nuclear ComplexMaleMice, Inbred C57BLNeural PathwaysNeuronal PlasticityPsychological DistressSynaptic Transmissionaggressionattack experiencemedial amygdalasynaptic plasticitytraumatic stress

Identifiers

PMID32424020
PMCPMC7326350
OpenAlexW3024716470

What OpenQuestion holds

Textmetadata
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.