Adrian Corbett (Committee Co-chair), Robert Fyffe (Advisor), Larry Ream (Committee Co-chair)
Master of Science (MS)
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.
Department or Program
Department of Neuroscience, Cell Biology & Physiology
Year Degree Awarded
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