Publication Date


Document Type


Committee Members

Michael B. Hennessy, Ph.D. (Advisor); Michal J. Kraszpulski, Ph.D. (Committee Member); Patricia A. Schiml, Ph.D. (Committee Member)

Degree Name

Master of Science (MS)


Early-life stress appears to sensitize neuroinflammatory signaling to increase later vulnerability for stress-related mental disorders. How stress initiates this process is unknown, but sympathetic nervous system activation during the early stress may be key. Isolated guinea pig pups display inflammatory-mediated depressive-like behavior and fever that sensitize on repeated isolation. We assessed whether sympathetic nervous system activity contributed to the sensitization process in guinea pig pups. In Experiment 1, the adrenergic agonist ephedrine, either alone or with cortisol, did not increase depressive-like behavior or fever during an initial isolation the following day. In Experiment 2, both depressive-like behavior and fever sensitized with repeated isolation, but beta-adrenergic receptor blockade with propranolol did not affect either of these responses or their sensitization. Results suggest sympathetic nervous system activation is neither necessary nor sufficient to induce the increased neuroinflammatory signaling underlying sensitization of depressive-like behavioral or febrile responses in developing guinea pigs.

Page Count


Department or Program

Department of Neuroscience, Cell Biology and Physiology

Year Degree Awarded


Included in

Anatomy Commons