Brain circuit dysfunction in post-traumatic stress disorder: from mouse to man

Fenster, Robert J.; Lebois, Lauren A. M.; Ressler, Kerry J.; Suh, Junghyup

doi:10.1038/s41583-018-0039-7

Cited by 456Posttraumatic Stress Disorder ResearchMemory and Neural MechanismsStress Responses and Cortisol

Brain circuit dysfunction in post-traumatic stress disorder: from mouse to man

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Fenster, Robert J., Lebois, Lauren A. M., Ressler, Kerry J., Suh, Junghyup·2018·Nature Reviews Neuroscience

DOI 10.1038/s41583-018-0039-7PMC PMC6148363

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Abstract

Post-traumatic stress disorder (PTSD) is a prevalent, debilitating and sometimes deadly consequence of exposure to severe psychological trauma. Although effective treatments exist for some individuals, they are limited. New approaches to intervention, treatment and prevention are therefore much needed. In the past few years, the field has rapidly developed a greater understanding of the dysfunctional brain circuits underlying PTSD, a shift in understanding that has been made possible by technological revolutions that have allowed the observation and perturbation of the macrocircuits and microcircuits thought to underlie PTSD-related symptoms. These advances have allowed us to gain a more translational knowledge of PTSD, have provided further insights into the mechanisms of risk and resilience and offer promising avenues for therapeutic discovery.

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Much of our understanding draws from studies on the dissociative subtype of PTSD.
“Much of our understanding draws from studies on the dissociative subtype of PTSD [105,143].”
From Treatment of dissociative identity disorder: leveraging neurobiology to optimize success (2024) · cites this paper as [143]
The Avoidance section discusses the dissociative subtype, and the References list several studies of its brain circuitry. The paper does not say that much of our understanding of PTSD draws from those studies; it also describes advances from broader human neuroimaging and animal-circuit research. No page number is available in our copy. (LLM, conf=0.78)
Experimental — accuracy not yet measured
Induced ELS via the maternal separation model reduces pre- and post-synaptic protein expression of inhibitory neurons in the mPFC.
“Additionally, induced ELS via the maternal separation model reduces pre- and post-synaptic protein expression of inhibitory neurons in the mPFC (124).”
From Childhood Trauma, the HPA Axis and Psychiatric Illnesses: A Targeted Literature Synthesis (2022) · cites this paper as [124]
The Intrusion symptoms section discusses prefrontal inhibitory interneurons and fear behaviour, while the Dissociative amnesia and memory deficits section describes stress-related protein changes in the hippocampus. Neither addresses reduced pre- and post-synaptic protein expression in mPFC inhibitory neurons after maternal separation. Searches for maternal separation and inhibitory synaptic proteins found no passage supporting the claim; page numbers were not available in our copy. (LLM, conf=0.76)
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[200]Robinson OJ Towards a mechanistic understanding of pathological anxiety: the dorsal medial prefrontal-amygdala ‘aversive amplification’circuit in unmedicated generalized and social anxiety disorders. Lancet. Psychiatry 1, 294 (2014). 25722962 PMC4337019
[201]Shin LM in Neurobiology of PTSD (eds Shiromani PJ, Keane TM & LeDoux JE) (Humana Press, 2009).

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Authors: Fenster, R. J., Lebois, L. A. M., Ressler, K. J., & Suh, J.
Affiliations: Harvard University (US)
Corresponding author: Ressler, Kerry J.
Suh, Junghyup
ORCID: Fenster, Robert J.
Lebois, Lauren A. M.
Ressler, Kerry J.
Suh, Junghyup
Venue: Nature Reviews Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2018-07-27
Volume: 19
Issue: 9
Pages: 535-551
ISSN: 1471-003X (ISSN-L)
1471-0048
DOI: 10.1038/s41583-018-0039-7
PMC: PMC6148363
OpenAlex: W2884319195
Cited by: 456
References: 227
Citations by year: 2026: 44 · 2025: 51 · 2024: 81 · 2023: 58 · 2022: 57 · 2021: 69 · 2020: 52 · 2019: 38 · 2018: 4 · 2013: 1
FWCI: 6.87
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Neuroscience (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: Biogen
Center of Excellence for Stress and Mental Health
National Institutes of Health
National Institute on Alcohol Abuse and Alcoholism (R21AA027450)
National Institute of Mental Health (R21MH112956, R01MH094757, F32MH109274, R01MH117292, R01MH108665)
Topics: Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords: post-traumatic stress disorder, neural circuits, trauma, resilience, risk factors, translational research, neural circuit manipulation, PTSD treatment, PTSD prevention
MeSH terms: Animals, Brain, Disease Models, Animal, Humans, Neural Pathways, Neurons, Stress Disorders, Post-Traumatic, Mice

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Brain circuit dysfunction in post-traumatic stress disorder: from mouse to man

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