Publication Date
2013
Document Type
Thesis
Committee Members
Adrian Corbett (Committee Co-chair), Robert Fyffe (Advisor), Larry Ream (Committee Co-chair)
Degree Name
Master of Science (MS)
Abstract
Peripheral nerve injuries (PNI) cause alternations in central synapses leading to loss of function. The C-bouton synapses onto a-motoneurons in the ventral horn, and has a role in regulating motor output. Following tibial nerve ligation, the somatic C-bouton coverage is depleted (Alvarez et al., 2011), however, it is unknown what happens following crush type injuries. PNI causes neuroglia activation and proliferation that contribute to synaptic alterations, a response that has not been well-characterized in the ventral horn, where motoneurons are located. Therefore, I hypothesize that glia activation following peripheral nerve injury correlates to the degree of depletion of synaptic coverage of C-boutons. To test, I performed Immunohistochemical analysis of rat spinal cord to characterize C-bouton coverage, and activation of glia following two types of PNI. Our results indicate less C-bouton depletion following tibial nerve crush than ligation injuries. In addition, we found less glia activation following crush than ligation injuries.
Page Count
191
Department or Program
Department of Neuroscience, Cell Biology & Physiology
Year Degree Awarded
2013
Copyright
Copyright 2013, all rights reserved. This open access ETD is published by Wright State University and OhioLINK.
