Degree
Master of Science
Program
Anatomy and Cell Biology
Supervisor
Dr. Arthur Brown
Abstract
Neuroplasticity is a key factor in post-stroke functional recovery. A chief inhibitor of post-stroke neuroplasticity is the expression of chondroitin sulfate proteoglycans (CSPGs). Recent research has shown that the transcription factor SOX9 is responsible for upregulating the expression of CSPGs in the injured central nervous system. Accordingly, CSPG levels are significantly lower in mice with the Sox9 gene conditionally knocked out. The purpose of this study was to determine how Sox9 ablation affects neuroplasticity and recovery after stroke. Behavioural test results revealed that Sox9 KO mice exhibited significantly improved functional recovery after stroke compared to controls. This correlated with increased contralesional corticofugal plasticity in the Sox9 KO animals, as highlighted by tract tracing studies. An increase in one type of glutamatergic input marker (VGLUT1) was observed at the deafferented red nucleus of the Sox9 KO mice, but not at the denervated the cervical spinal cord ventral horn. Further investigation into the effects of Sox9 ablation on post-stroke neuroplasticity would be beneficial to determine the potential of Sox9 as a therapeutic target.
Recommended Citation
Bass, Bethany Robin Lenore, "Investigation of Sox9 ablation on neuroplasticity and recovery after ischemic stroke" (2014). Electronic Thesis and Dissertation Repository. 2338.
https://ir.lib.uwo.ca/etd/2338