Publication Date
2023
Document Type
Thesis
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)
Abstract
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
40
Department or Program
Department of Neuroscience, Cell Biology and Physiology
Year Degree Awarded
2023
Copyright
Copyright 2023, all rights reserved. My ETD will be available under the "Fair Use" terms of copyright law.
