Defense Date


Document Type


Degree Name

Master of Science


Anatomy & Neurobiology

First Advisor

Gretchen Neigh McCandless, PhD.


Evidence suggests that toxic stressors introduced early in development have prolonged effects on neuronal function due, in part, to the maturation of the hypothalamic- pituitary- adrenal (HPA) axis during adolescence. Early life stress has been implicated as a driver of mood and anxiety disorders, like depression and post-traumatic stress disorder - the extent to which appears to be sex dependent. While it is known that early life stress results in several consequences in adulthood, the mechanisms by which these changes manifest are unclear. Stress-induced changes in mood and behavior are often associated with alterations in inflammatory reactivity in both the brain and in the periphery. Previous work from our lab, and others, demonstrates that both male and female rats respond to chronic adolescent stress (CAS) but may differ in inflammatory markers within the brain and periphery and in the induction of negative affective-like behaviors. Inflammatory reactivity has been targeted as a means of identifying how these sex differences arise in studies of chronic stress in adults. Circulating concentrations of inflammatory cytokines have not been directly employed as predictors of behavioral outcomes of stress exposure in adolescence but may be a useful tool in uncovering mechanisms that protect or predispose an organism from the effects of chronic stress.

To further assess immunological and behavior deficits following chronic stress in adolescence, the current work used a model of chronic adolescent stress where male and female adolescent mice were exposed to a predator stress for 15 consecutive days. In late adolescence, these mice were treated with an acute inflammatory challenge with lipopolysaccharide (LPS)to elicit an inflammatory response. We predicted that chronic, predatory stress experienced during adolescence would induce negative anxiety-like behaviors and alter circulating proinflammatory levels. Furthermore, we expected females to be more susceptible to the effects of adolescent stress than males. We observed that, chronic, predatory stress during adolescence increased anxiety-like behaviors in males and females, but did not alter social behaviors during late adolescence. Predatory stress also impacted circulating levels of TNFα, but no sex differences in LPS-induced cytokine concentrations were apparent.


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