Brain transcriptome profiles in mouse model simulating features of post-traumatic stress disorder
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BACKGROUND: Social-stress mouse model, based on the resident-intruder paradigm was used to simulate features of human post-traumatic stress disorder (PTSD). The model involved exposure of an intruder (subject) mouse to a resident aggressor mouse followed by exposure to trauma reminders with rest periods. C57BL/6 mice exposed to SJL aggressor mice exhibited behaviors suggested as PTSD-in-mouse phenotypes: intermittent freezing, reduced locomotion, avoidance of the aggressor-associated cue and apparent startled jumping. Brain tissues (amygdala, hippocampus, medial prefrontal cortex, septal region, corpus striatum and ventral striatum) from subject (aggressor exposed: Agg-E) and control C57BL/6 mice were collected at one, 10 and 42 days post aggressor exposure sessions. Transcripts in these brain regions were assayed using Agilent's mouse genome-wide arrays. RESULTS: Pathways and biological processes associated with differentially regulated genes were mainly those thought to be involved in fear-related behavioral responses and neuronal signaling. Expression-based assessments of activation patterns showed increased activations of pathways related to anxiety disorders (hyperactivity and fear responses), impaired cognition, mood disorders, circadian rhythm disruption, and impaired territorial and aggressive behaviors. In amygdala, activations of these pathways were more pronounced at earlier time-points, with some attenuation after longer rest periods. In hippocampus and medial prefrontal cortex, activation patterns were observed at later time points. Signaling pathways associated with PTSD-comorbid conditions, such as diabetes, metabolic disorder, inflammation and cardiac infarction, were also significantly enriched. In contrast, signaling processes related to neurogenesis and synaptic plasticity were inhibited. CONCLUSIONS: Our data suggests activations of behavioral responses associated with anxiety disorders as well as inhibition of neuronal signaling pathways important for neurogenesis, cognition and extinction of fear memory. These pathways along with comorbid-related signaling pathways indicate the pervasive and multisystem effects of aggressor exposure in mice, potentially mirroring the pathologic conditions of PTSD patients.
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Non-genetic models, such as stress-induced aggression and other organisms, were not included in this study.
“We noted that non-genetic models, such as stress-induced aggression [27, 81] and other organisms [30, 31, 82], were not included in this study.”
From An integrated analysis of genes and functional pathways for aggression in human and rodent models (2019) · cites this paper as [81]
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- Authors
- Muhie, S., Gautam, A., Meyerhoff, J., Chakraborty, N., Hammamieh, R., & Jett, M.
- Affiliations
- United States Army (US)
- United States Department of the Army (US)
- Corresponding author
- Jett, Marti
- Venue
- Molecular Brain
- Published
- 2015-02-28
- Volume
- 8
- Issue
- 1
- Pages
- 14-14
- ISSN
- 1756-6606 (ISSN-L)
- PMC
- PMC4359441
- OpenAlex
- W2162203404
- Cited by
- 58
- References
- 65
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 5 · 2023: 5 · 2022: 7 · 2021: 6 · 2020: 4 · 2019: 2 · 2018: 5 · 2017: 9 · 2016: 10 · 2015: 1
- FWCI
- 10.35
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Molecular Brain (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Medical Research and Materiel Command (09284002.)
- 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, resident-intruder paradigm, social stress, mouse model, brain transcriptome, differentially expressed genes, amygdala, hippocampus, medial prefrontal cortex, fear extinction, anxiety disorders, neurogenesis, synaptic plasticity, comorbidities, inflammation, C57BL/6 mice
- MeSH terms
- Animals, Behavior, Animal, Brain, Circadian Rhythm, Corticotropin-Releasing Hormone, Disease Models, Animal, Fear, Gene Expression Regulation, Male, Memory, Mice, Inbred C57BL, Organ Specificity, RNA, Messenger, Stress Disorders, Post-Traumatic, Time Factors, Reproducibility of Results, Signal Transduction, Gene Expression Profiling, Gene Regulatory Networks, Transcriptome
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