Effects Of Neonatal Stress On Inflammatory Responses In The Brain Of Adult Balb/Cbyj Mice.
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Date
2015
Department
Biology
Program
Master of Science
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This item is made available by Morgan State University for personal, educational, and research purposes in accordance with Title 17 of the U.S. Copyright Law. Other uses may require permission from the copyright owner.
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Abstract
Early childhood stress and trauma are risk factors for depression and other mental health disorders. Increased inflammatory cytokine levels are observed in the same mental health disorders. The hypothalamic-pituitary-adrenal (HPA) axis is known to regulate the inflammatory immune response. We hypothesized that early life stress may predispose the brain to neuroinflammation later in life. This thesis investigates the effects of neonatal stress on the production of pro-inflammatory cytokines, including interleukins (IL) 1β, 2, and 6 and tumor necrosis factor-a (TNF-α), in mature Balb/CByJ mice. Half of the litter was removed for the maternal separation stress procedure (STR), while the other half remained with the dam as littermate controls (LMC). A separate group of age-matched, colony-reared pups (AMC) served as an additional control. First, male and female STR, LMC and AMC mice were analyzed for baseline IL-1β, 2, and 6 and TNF-α levels in cerebral cortex and for corticosterone levels in sera, using commercially available ELISA kits. Second, mice received either saline or LPS injections two hours before being sacrificed for collection of brain tissues and blood for cytokine analysis. No significant differences in baseline levels of cytokines and corticosterone were found in the brains of uninjected STR, LMC and AMC mice. By contrast, LPS injections significantly increased production of IL-6 in brain tissue of STR and LMC mice, regardless of sex. In sera, significant increases of IL-6 and decreases of TNF-α were measured, following LPS injections in the STR and LMC mice compared to AMC controls. These data suggest that neonatal experience in STR and LMC mice may have developmentally reprogrammed inflammatory responses in the brain, thus, producing altered cytokine release to an inflammatory agent in adulthood.