The role of gap junctions in modulating the dynamics of axonal dysfunction in spinal cord white matter injury remains uncertain; hence, I examined the functional role and changes in expression of gap junctions following CNS injury. I hypothesized that inhibition of gap junctions improves axonal conduction during oxygen and glucose deprivation (OGD) in vitro. Carbenoxolone and octanol, gap junction blockers, did not change CAP amplitude in non-injured tissue, yet they
significantly reduced the extent of its decline during OGD. No difference in mRNA expression of connexins 32, 36 was found. However, during OGD in the presence of gap junction blockers, expression of connexins 30, 43 was downregulated. Immunohistochemistry confirmed the presence of connexins in spinal cord slices: connexins 30, 43 overlapping with GFAP, connexin 32 with MBP and connexin 36 with CC1. Thus, blocking gap junctions enhances axonal
conduction during OGD and promotes dynamic changes in connexin mRNA expression.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/30612 |
| Date | 07 December 2011 |
| Creators | Goncharenko, Karina |
| Contributors | Fehlings, Michael G., Carlen, Peter Louis |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
Page generated in 0.0019 seconds