Cortical malformations as a result of altered development are a common cause of human epilepsy. The cellular mechanisms that render neurons of malformed cortex epileptogenic remain unclear. Using a rat model of the malformation of microgyria, a previous study showed an alteration in the number of immunocytochemically-identified parvalbumin cells, a GABAergic inhibitory interneurons subtype (Rosen et al., 1998). A second study showed no change in the total number of GABAergic neurons (Schwarz et al., 2000). Consequently, we hypothesize that interneuron subtypes are differentially affected by maldevelopment. The present study investigated (1) whether interneuron subtype identity is retained in malformed cortex, based on chemical content, and (2) whether the proportion of three chemical subtypes is altered in malformed cortex. Here we demonstrate that three non-overlapping subtype markers remain non-overlapping in malformed cortex, but show altered distributions. These findings suggest that an increase in one subpopulation of interneurons may compensate for a corresponding decrease in a second subset.
| Identifer | oai:union.ndltd.org:vcu.edu/oai:scholarscompass.vcu.edu:etd_retro-1030 |
| Date | 01 January 2007 |
| Creators | Hays, Kimberly Lynne |
| Publisher | VCU Scholars Compass |
| Source Sets | Virginia Commonwealth University |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | Retrospective ETD Collection |
| Rights | © The Author |
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