Publication Date
2007
Document Type
Thesis
Committee Members
Timothy Cope (Advisor)
Degree Name
Master of Science (MS)
Abstract
Peripheral nerve injury is known to induce several changes in the physiology and morphology of the injured afferent. These changes include hyperexcitability, decreased dorsal root potentials (DRP), loss of synaptic vesicles as well as loss of the vesicular glutamate transporter, VGLUT1. While many of the changes caused by peripheral injury revert with regeneration, others appear to be permanent. The loss of the stretch reflex for example is a puzzling outcome of recovery after peripheral nerve transection and regeneration, especially given that the electrical counterpart of the stretch reflex (the H-reflex) recovers after regeneration. We hypothesized that stretch induced transmission is suppressed at the primary afferent - motor neuron synapse and sought to determine whether this was due to a decrease in excitatory transmission or an increase in presynaptic inhibition. To this end, we measured the level of expression of VGLUT1 and 2 as well as the GABA synthesizing enzyme GAD65 in the central terminals of physiologically characterized primary afferents from healthy Wistar rats for comparison with regenerated animals. An inverse relationship appears to exist between VGLUT1 and GAD65 expression. Expression of the two proteins also differ in laminae V, VII and IX, with the highest VGLUT1 immunoreactivity in lamina V and the highest number of GAD65-intense presynaptic boutons in lamina IX. The possible effects of regeneration on this pattern are discussed.
Page Count
78
Department or Program
Department of Neuroscience, Cell Biology & Physiology
Year Degree Awarded
2007
Copyright
Copyright 2007, all rights reserved. This open access ETD is published by Wright State University and OhioLINK.
