Gene expression patterns in the hippocampus and amygdala of endogenous depression and chronic stress models
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The etiology of depression is still poorly understood, but two major causative hypotheses have been put forth: the monoamine deficiency and the stress hypotheses of depression. We evaluate these hypotheses using animal models of endogenous depression and chronic stress. The endogenously depressed rat and its control strain were developed by bidirectional selective breeding from the Wistar-Kyoto (WKY) rat, an accepted model of major depressive disorder (MDD). The WKY More Immobile (WMI) substrain shows high immobility/despair-like behavior in the forced swim test (FST), while the control substrain, WKY Less Immobile (WLI), shows no depressive behavior in the FST. Chronic stress responses were investigated by using Brown Norway, Fischer 344, Lewis and WKY, genetically and behaviorally distinct strains of rats. Animals were either not stressed (NS) or exposed to chronic restraint stress (CRS). Genome-wide microarray analyses identified differentially expressed genes in hippocampi and amygdalae of the endogenous depression and the chronic stress models. No significant difference was observed in the expression of monoaminergic transmission-related genes in either model. Furthermore, very few genes showed overlapping changes in the WMI vs WLI and CRS vs NS comparisons, strongly suggesting divergence between endogenous depressive behavior- and chronic stress-related molecular mechanisms. Taken together, these results posit that although chronic stress may induce depressive behavior, its molecular underpinnings differ from those of endogenous depression in animals and possibly in humans, suggesting the need for different treatments. The identification of novel endogenous depression-related and chronic stress response genes suggests that unexplored molecular mechanisms could be targeted for the development of novel therapeutic agents.
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Strain-dependent responses to restraint or chronic mild stress have been shown, indicating complex genetics regulate risk and resilience to chronic stress.
“Strain–dependent responses to other physical stressors such as restraint or CMS have been shown, underscoring the role of complex genetics in regulating risk and resilience to chronic stress32–34.”
From Neurobiology of resilience (2012) · cites this paper as [34]
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- Authors
- Andrus, B. M., Blizinsky, K., Vedell, P. T., Dennis, K., Shukla, P. K., Schaffer, D. J., Radulovic, J., Churchill, G. A., & Redei, E. E.
- Affiliations
- Northwestern University (US)
- Jackson Laboratory (US)
- Corresponding author
- Redei, E E
- Venue
- Molecular Psychiatry
- Published
- 2010-11-16
- Volume
- 17
- Issue
- 1
- Pages
- 49-61
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC3117129
- OpenAlex
- W1991766265
- Cited by
- 178
- References
- 92
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 8 · 2023: 5 · 2022: 17 · 2021: 9 · 2020: 13 · 2019: 10 · 2018: 12 · 2017: 15 · 2016: 11 · 2015: 19 · 2014: 15 · 2013: 17 · 2012: 10
- FWCI
- 4.56
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- www.springer.com/tdm (unspecified)
- Locations
- Molecular Psychiatry (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- Davee Foundation
- National Institutes of Health
- National Institute of Mental Health (MH077234, R21MH077234)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- endogenous depression, chronic stress, hippocampus, amygdala, gene expression, forced swim test, immobility, restraint stress, Wistar-Kyoto rats, major depressive disorder, rat strains, therapeutic target
- MeSH terms
- Adrenal Cortex Hormones, Adrenal Glands, Amygdala, Animals, Body Weight, Depressive Disorder, Disease Models, Animal, Gene Expression Regulation, Hippocampus, Male, Organ Size, Radioimmunoassay, Rats, Inbred F344, Rats, Inbred WKY, Stress, Psychological, Swimming, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Freezing Reaction, Cataleptic, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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