Cited by 107Stress Responses and CortisolTryptophan and brain disordersNeuroinflammation and Neurodegeneration Mechanisms

Psychological stress in adolescent and adult mice increases neuroinflammation and attenuates the response to LPS challenge

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Barnum, Christopher J, Pace, Thaddeus WW, Hu, Fang, Neigh, Gretchen N, Tansey, Malú G·2012·Journal of Neuroinflammation

Abstract

BACKGROUND: There is ample evidence that psychological stress adversely affects many diseases. Recent evidence has shown that intense stressors can increase inflammation within the brain, a known mediator of many diseases. However, long-term outcomes of chronic psychological stressors that elicit a neuroinflammatory response remain unknown. METHODS: To address this, we have modified previously described models of rat/mouse predatory stress (PS) to increase the intensity of the interaction. We postulated that these modifications would enhance the predator-prey experience and increase neuroinflammation and behavioral dysfunction in prey animals. In addition, another group of mice were subjected to a modified version of chronic unpredictable stress (CUS), an often-used model of chronic stress that utilizes a combination of stressors that include physical, psychological, chemical, and other. The CUS model has been shown to exacerbate a number of inflammatory-related diseases via an unknown mechanism. Using these two models we sought to determine: 1) whether chronic PS or CUS modulated the inflammatory response as a proposed mechanism by which behavioral deficits might be mediated, and 2) whether chronic exposure to a pure psychological stressor (PS) leads to deficits similar to those produced by a CUS model containing psychological and physical stressors. Finally, to determine whether acute PS has neuroinflammatory consequences, adult mice were examined at various time-points after PS for changes in inflammation. RESULTS: Adolescent mice subjected to chronic PS had increased basal expression of inflammation within the midbrain. CUS and chronic PS mice also had an impaired inflammatory response to a subsequent lipopolysaccharide challenge and PS mice displayed increased anxiety- and depressive-like behaviors following chronic stress. Finally, adult mice subjected to acute predatory stress had increased gene expression of inflammatory factors. CONCLUSION: Our results demonstrate that predatory stress, an ethologically relevant stressor, can elicit changes in neuroinflammation and behavior. The predatory stress model may be useful in elucidating mechanisms by which psychological stress modulates diseases with an inflammatory component.

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  1. Frank-Cannon TC Tran T Ruhn KA Martinez TN Hong J Marvin M Hartley M Treviño I O'Brien DE Casey B Goldberg MS Tansey MG Parkin deficiency increases vulnerabiity to inflammation-related nigral degeneration J Neurosci 2008 28 PMC2603252 18945890
  2. Audet M-C Jacobson-Pick S Wann BP Anisman H Social defeat promotes specific cytokine variations within the prefrontal cortex upon subsequent aggressive or endotoxin challenges Brain Behavior and Immunity 2011 25 1197 1205 10.1016/j.bbi.2011.03.010 21435391 · DOI

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Authors
Barnum, C. J., Pace, T. W., Hu, F., Neigh, G. N., & Tansey, M. G.
Affiliations
Emory University (US)
Corresponding author
  • Barnum, Christopher J
  • Pace, Thaddeus WW
  • Hu, Fang
  • Neigh, Gretchen N
  • Tansey, Malú G
Venue
Journal of Neuroinflammation
Published
2012-01-16
Volume
9
Issue
1
Pages
9-9
ISSN
1742-2094 (ISSN-L)
OpenAlex
W2121168584
Cited by
107
References
55
Citations by year
2026: 3 · 2025: 8 · 2024: 6 · 2023: 5 · 2022: 8 · 2021: 6 · 2020: 9 · 2019: 12 · 2018: 10 · 2017: 7 · 2016: 7 · 2015: 7 · 2014: 8 · 2013: 10 · 2012: 1
FWCI
3.45
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroinflammation (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (R21MH085210, 5R21MH85210)
  • National Institute of Neurological Disorders and Stroke (R01NS049433, T32NS007480)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
psychological stress, neuroinflammation, chronic unpredictable mild stress, lipopolysaccharide challenge, anxiety-like behavior, depression-like behavior, adolescent mice, inflammatory gene expression, behavioral dysfunction
MeSH terms
Aging, Analysis of Variance, Animals, Brain, Corticosterone, Disease Models, Animal, Encephalitis, Food Preferences, Gene Expression Regulation, Male, Mice, Inbred C57BL, Polysaccharides, RNA, Messenger, Stress, Psychological, Sucrose, Sweetening Agents, Cytokines, Hindlimb Suspension, Mice, Rats

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