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Journal Title:

Journal of Neuroinflammation

Volume:

Volume 9, Number 9

Publisher:

BioMed Central | 2012-01-16, Pages 1-15

Type of Work:

Article | Final Publisher PDF

Abstract: BackgroundThere 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.MethodsTo 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.ResultsAdolescent 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.ConclusionOur 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.

Subject: Biology, Neuroscience - Research Funding: This work was supported by the NIH-NINDS institutional training grant Training in translational research in Neurology T32NS007480, CJB, the Michael J. Fox Foundation for Parkinson's Research CJB, the National Institutes of Health grants 2R01NS049433 MGT, and 5R21MH85210 TWWP.





Autor: Christopher J. Barnum, Thaddeus Pace, Fang Hua, Gretchen Neigh, Malu Tansey,

Fuente: https://open.library.emory.edu/



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