Publication Date
2025
Document Type
Dissertation
Committee Members
R. Andrew McKinley, Ph.D. (Committee Co-Chair); David Ladle, Ph.D. (Committee Co-Chair); Michael Matott, Ph.D. (Committee Member); Michael Markey, Ph.D. (Committee Member); Robert Lober, M.D., Ph.D. (Committee Member)
Degree Name
Doctor of Philosophy (PhD)
Abstract
Hypoxia disrupts brain function due to the high demand for oxygen, leading to significant cognitive impairments. While vagus nerve stimulation (VNS) has been shown to enhance cognition, its ability to counteract hypoxia-induced deficits remains unclear. In this study, male Sprague–Dawley rats were assigned to sham, hypoxia, or VNS + hypoxia groups, with VNS delivered during hypoxia (8% oxygen) using biphasic pulses (100 μs, 30 Hz, 0.8 mA). Cognitive performance was evaluated using multiple behavioral paradigms, and hippocampal tissue was analyzed for neurotrophin expression through quantitative PCR and immunohistochemistry. Among the behavioral measures, hypoxia specifically impaired performance on the passive avoidance test, and VNS ameliorated this deficit. At the molecular level, hypoxia reduced NGF and BDNF mRNA expression in the hippocampus, whereas VNS restored NGF mRNA and protein expression to sham levels and partially increased BDNF mRNA without altering protein expression. These findings suggest that VNS can mitigate hypoxia-induced cognitive impairment by modulating hippocampal neurotrophin expression, highlighting its potential as a therapeutic strategy.
Page Count
99
Department or Program
Biomedical Sciences
Year Degree Awarded
2025
Copyright
Copyright 2025, all rights reserved. My ETD will be available under the "Fair Use" terms of copyright law.
