The DOI matches its Crossref record; 62 of the 63 references it cites were found in a registry or an index.
Neurobiological Sequelae of Witnessing Stressful Events in Adult Mice
Open accessAbstract
Background It is well known that exposure to severe stress increases the risk for developing mood disorders. However, most chronic stress models in rodents involve at least some form of physically experiencing traumatic events.Methods This study assessed the effects of a novel social stress paradigm that is insulated from the effects of physical stress. Specifically, adult male C57BL/6J mice were exposed to either emotional (ES) or physical stress (PS) for 10 minutes per day for 10 days. The ES mice were exposed to the social defeat of a PS mouse by a larger, more aggressive CD-1 mouse from the safety of an adjacent compartment.Results Like PS mice, ES mice exhibited a range of depression- and anxiety-like behaviors both 24 hours and 1 month after the stress. Increased levels of serum corticosterone, part of the stress response, accompanied these behavioral deficits. Based on previous work that implicated gene expression changes in the ventral tegmental area (a key brain reward region) in the PS phenotype, we compared genome-wide mRNA expression patterns in this brain region of ES and PS mice using RNA-seq. We found significant overlap between these conditions, which suggests several potential gene targets for mediating the behavioral abnormalities observed.Conclusions These findings demonstrate that witnessing traumatic events is a potent stress in adult male mice capable of inducing long-lasting neurobiological perturbations.
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“Stress is another emotional contagion that occurs with either direct observation or interaction with a previously stressed individual.”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [113]
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“Many studies employ a witness or vicarious social defeat paradigm where an observer that is forced to witness a conspecific undergoing the physical component of social defeat stress develops similar depressive-and anxiety-like behaviors [91,113].”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [113]
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“These findings agree with reports demonstrating that PS exposure increases CORT levels for up to 24 hr (12, 23) and reduces weight gain in adult mice (24–26).”
BackgroundMethodInfluentialSelf-citationEssential role of BDNF in the mesolimbic dopamine pathway in social defeat stress
Berton, O., McClung, C. A., DiLeone, R. J., Krishnan, V., Renthal, W., Russo, S. J., Graham, D., Tsankova, N. M., Bolanos, C. A., Rios, M., et al. (2006) · Science · doi:10.1126/science.1120972 · Cited by 2,129
Self-citationThe mesolimbic dopamine reward circuit in depression
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Self-citationAnimal models of neuropsychiatric disorders
Nestler, E. J., & Hyman, S. E. (2010) · Nature Neuroscience · doi:10.1038/nn.2647 · Cited by 2,023
Self-citationSustained hippocampal chromatin regulation in a mouse model of depression and antidepressant action
Tsankova, N. M., Berton, O., Renthal, W., Kumar, A., Neve, R. L., & Nestler, E. J. (2006) · Nature Neuroscience · doi:10.1038/nn1659 · Cited by 1,780
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The brain reward circuitry in mood disorders
Russo, S. J., & Nestler, E. J. (2013) · Nature Reviews Neuroscience · doi:10.1038/nrn3381 · Cited by 1,870
Self-citationHodes, G. E., Pfau, M. L., Leboeuf, M., Golden, S. A., Christoffel, D. J., Bregman, D., Rebusi, N., Heshmati, M., Aleyasin, H., Warren, B. L., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1415191111 · Cited by 692
Self-citationPathogenesis of depression: Insights from human and rodent studies
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Corticoamygdala Transfer of Socially Derived Information Gates Observational Learning
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Metadata
- Authors
- Warren, B. L., Vialou, V. F., Iñiguez, S. D., Alcantara, L. F., Wright, K. N., Feng, J., Kennedy, P. J., LaPlant, Q., Shen, L., Nestler, E. J., & Bolaños-Guzmán, C. A.
- Affiliations
- Florida State University (US)
- Icahn School of Medicine at Mount Sinai (US)
- ORCID
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2013-01
- Volume
- 73
- Issue
- 1
- Pages
- 7-14
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC3498570
- OpenAlex
- W2052639257
- Cited by
- 222
- References
- 63
- Citations by year
- 2026: 9 · 2025: 14 · 2024: 16 · 2023: 23 · 2022: 24 · 2021: 23 · 2020: 18 · 2019: 16 · 2018: 16 · 2017: 16 · 2016: 11 · 2015: 9 · 2014: 19 · 2013: 6
- FWCI
- 4.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (P50 MH66172, P50MH096890, R01 MH-51399, R01MH051399, P50MH066172)
- National Institute on Drug Abuse (F31DA027300, R21DA022351, R01DA026854)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Keywords
- social defeat, emotional stress, physical stress, chronic stress, depression-like behavior, anxiety-like behavior, corticosterone, ventral tegmental area, gene expression, mood disorders, traumatic events
- MeSH terms
- Animals, Anxiety, Behavior, Animal, Corticosterone, Depression, Disease Models, Animal, Fluoxetine, Male, Mice, Inbred C57BL, Mice, Inbred ICR, Photic Stimulation, Social Behavior, Stress, Physiological, Stress, Psychological, Ventral Tegmental Area, Gene Expression Profiling, Mice
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