Hippocampal gene expression changes underlying stress sensitization and recovery
Open accessAbstract
Chronic and acute stressors have been linked to changes in hippocampal function and anxiety-like behaviors. Both produce changes in gene expression, but the extent to which these changes endure beyond the end of stress remains poorly understood. As an essential first step to characterize abnormal patterns of gene expression after stress, this study demonstrates how chronic restraint stress (CRS) modulates gene expression in response to a novel stressor in the hippocampus of wild-type mice and the extent to which these changes last beyond the end of CRS. Male C57/bl6 mice were subjected to (1) a forced swim test (FST), (2) corticosterone (Cort) or vehicle injections, (3) CRS for 21 days and then a FST, or (4) allowed to recover 21 days after CRS and subjected to FST. Hippocampal mRNA was extracted and used to generate cDNA libraries for microarray hybridization. Naive acute stressors (FST and vehicle injection) altered similar sets of genes, but Cort treatment produced a profile that was distinct from both FST and vehicle. Exposure to a novel stress after CRS activated substantially more and different genes than naive exposure. Most genes increased by CRS were decreased after recovery but many remained altered and did not return to baseline. Pathway analysis identified significant clusters of differentially expressed genes across conditions, most notably the nuclear factor kappa-light-chain-enhancer of B cells (NF-κB) pathway. Quantitative reverse transcription-PCR (qRT-PCR) validated changes from the microarrays in known stress-induced genes and confirmed alterations in the NF-κB pathway genes, Nfkbia, RelA and Nfkb1. FST increased anxiety-like behavior in both the naive and recovery from CRS conditions, but not in mice 24h subsequent to their CRS exposure. These findings suggest that the effects of naive stress are distinct from Cort elevation, and that a history of stress exposure can permanently alter gene expression patterns in the hippocampus and the behavioral response to a novel stressor. These findings establish a baseline profile of normal recovery and adaptation to stress. Importantly, they will serve as a conceptual basis to facilitate the future study of the cellular and regional basis of gene expression changes that lead to impaired recovery from stress, such as those that occur in mood and anxiety disorders.
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Adverse experiences and environments cause problems over the life course in which there is no such thing as reversibility but rather a change in trajectory.
“Adverse experiences and environments cause problems over the life course in which there is no such thing as “reversibility” (i.e., “rolling the clock back”) but rather a change in trajectory”
From Neurobiological and Systemic Effects of Chronic Stress (2017) · cites this paper as [10]
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- Authors
- Gray, J. D., Rubin, T. G., Hunter, R. G., & McEwen, B. S.
- Affiliations
- Rockefeller University (US)
- University of Massachusetts Boston (US)
- Corresponding author
- McEwen, B S
- Venue
- Molecular Psychiatry
- Published
- 2013-12-17
- Volume
- 19
- Issue
- 11
- Pages
- 1171-1178
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC4061278
- OpenAlex
- W2164012002
- Cited by
- 242
- References
- 46
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 9 · 2023: 23 · 2022: 18 · 2021: 19 · 2020: 21 · 2019: 22 · 2018: 27 · 2017: 24 · 2016: 33 · 2015: 12 · 2014: 18
- FWCI
- 9.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (MH-41256, R37MH041256, R01MH041256)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- hippocampal gene expression, chronic restraint stress, stress recovery, anxiety-like behavior, forced swim test, corticosterone, NF-κB signaling, NFKBIA, RelA, NFKB1, stress adaptation, stress sensitization, mood and anxiety disorders
- MeSH terms
- NF-KappaB Inhibitor alpha, Acute Disease, Animals, Anxiety, Chronic Disease, Corticosterone, Disease Models, Animal, Hippocampus, Male, Mice, Inbred C57BL, Neuropsychological Tests, Psychotropic Drugs, Restraint, Physical, RNA, Messenger, Stress, Psychological, Swimming, Gene Expression, I-kappa B Proteins, Transcription Factor RelA, NF-kappa B p50 Subunit
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