Date of Award

5-1-2013

Degree Name

Doctor of Philosophy

Department

Psychology

First Advisor

Hoane, Mike

Abstract

The vagus nerve is the principal pathway by which autonomic sensory information is carried from the periphery to the CNS where it influences the activity of a numerous structures including the locus coeruleus. Electrical stimulation of the vagus nerve has been demonstrated to enhance performance in a variety of memory tasks in both rats and humans and is used clinically for the control of epilepsy in humans. Electrical stimulation of the vagus nerve has also been shown to improve functional recovery following experimental brain injury in rats. The central hypothesis in these experiments is that vagus nerve stimulation exerts its beneficial effects by mediating the release of norepinephrine in the CNS. The results from Experiment I indicate that VNS results in increased extracellular NE concentration in the hippocampus at both the 0.5 and 1.0 mA stimulus intensities, and in the cortex at the 1.0 mA intensity. Increased concentrations of extracellular NE induced by VNS, regardless of structure, were transient, dissipating before the subsequent baseline recording period. Further, VNS-induced alterations in extracellular NE concentrations were observed bilaterally. Insult to the CNS by means of FPI resulted in long lasting depression of extracellular NE concentrations in the cortex of the injured controls and 1.0 mA VNS group that was partially attenuated 1.0 mA VNS. In the 0.5 mA VNS group NE concentrations remained above pre-injury levels for the majority of the post-FPI measurement period. In the hippocampus, mean NE concentrations in the period immediately following FPI were decreased in comparison to pre-FPI concentrations. Concentrations of hippocampal NE remained depressed in the injured control group throughout the 48 hr sample period. Hippocampal NE concentrations in both the 0.5 mA VNS and 1.0 mA VNS group recovered to above pre-injury levels by 14-20 hrs post-FPI and were significantly higher than that of the injured controls in the 20-26 and 26-32 hr post-FPI sampling periods. Further, hippocampal NE concentrations remained significantly higher in 0.5 mA VNS group in comparison to injured controls in the 32-38 and 38-44 hr sampling periods.

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