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Neocortical Interneuron Subtypes Show an Altered Distribution in a Rat Model of Maldevelopment Associated With Epileptiform Activity

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.

Identiferoai:union.ndltd.org:vcu.edu/oai:scholarscompass.vcu.edu:etd_retro-1030
Date01 January 2007
CreatorsHays, Kimberly Lynne
PublisherVCU Scholars Compass
Source SetsVirginia Commonwealth University
Detected LanguageEnglish
Typetext
Formatapplication/pdf
SourceRetrospective ETD Collection
Rights© The Author

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