作者: Yuto Ueda , Aya Kitamoto , L. James Willmore , Toshio Kojima
DOI: 10.1007/S11064-013-1037-9
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摘要: Traumatic brain injury occasionally causes posttraumatic epilepsy. To elucidate the molecular events responsible for epilepsy, we established a rodent model that involved injection of microliter quantities FeCl3 solution into amygdalar nuclear complex. We previously compared hippocampal gene expression profiles in traumatic epilepsy and normal rats at 5 days after (acute phase) to determine role inflammation. In this study, focused on later stages epileptogenesis. 5, 15 (sub-chronic phase), 30 (chronic identify temporal changes networks A total 81 genes were significantly (at least twofold) up- or downregulated over course disease progression. found related lipid metabolism, namely, Apoa1, Gh, Mc4r, Oprk1, Pdk4, temporarily upregulated sub-chronic phase. Changes metabolism regulation might be seizure propagation during This description throughout epileptogenesis provides clues potential markers phases new therapeutic targets.