Date of Award

January 2016

Degree Type


Degree Name

Master of Science (MS)


Psychological Sciences

First Advisor

Amy L Brewster

Committee Member 1

Christie Sahley

Committee Member 2

Susan Sangha

Committee Member 3

Kimberly Kinzig


Status epilepticus (SE) triggers pathological changes to hippocampal dendrites that may promote epileptogenesis. The microtubule associated protein 2 (Map2) helps stabilize microtubules of the dendritic cytoskeleton. Recently, we reported a substantial decline in Map2 that coincided with robust microglia accumulation in the CA1 hippocampal region after an episode of SE. A spatial correlation between Map2 loss and reactive microglia was also reported in human cortex from refractory epilepsy. New evidence supports that microglia are guided by proteins of the classical complement pathway (C1q and C3) to prune dendritic structures. Furthermore, components of complement have been shown to be upregulated in human and experimental epilepsy. Thus, to identify a potential role of the classical complement pathway in SE-induced Map2 and microglial changes, we characterized the spatiotemporal profile of these events. We used immunohistochemistry to determine the distribution of Map2 and the microglia marker IBA1 in the hippocampus after pilocarpine-induced SE from 4 hours to 35 days. We found a decline in Map2 immunoreactivity in the CA1 area that reached minimal levels at 14 days post-SE and partially increased thereafter. In contrast, maximal microglia accumulation occurred in the CA1 area at 14 days post-SE. We then mapped the spatiotemporal profile of C1q using immunohistochemistry at 3-35 days after SE, where substantial Map2 and microglial alterations were observed. We used western blot to determine the levels of C3 and its cleavage products. C1q and C3 were both increased in the hippocampus at 14 days after SE, when Map2 and microglia changes were most profound. Our data indicate that SE-induced Map2 and microglial changes parallel each other’s spatiotemporal profiles. These findings also suggest a potential role for the classical complement pathway in SE-induced Map2-microglial interactions.