Seizure-Induced Oxidative Stress in Temporal Lobe Epilepsy

Figure 5

Immunohistochemistry (IHC) of the brain sections from kainate mouse and rat models of epilepsy at 2 h, 24 h, and 7 days after SE. (a) c-Fos ((A), (B)) expression was more widespread in the hippocampal formation at 2 h after SE (B). More than 3-4-fold increased expression (quantified data not shown) of c-Fos in CA3 pyramidal cell layer was observed (B). CCR2 ((C), (D)) and astrocytic NFκB expression ((F), orange) at 24 hours after SE. (b) By 7 days after SE, there was increased astrogliosis ((H), GFAP, green) and microgliosis ((J), IB1A is marker for microglia, green) compared to controls ((G), (I)). SE induced neurodegeneration (FJB +ve neurons) was observed in CA3 of hippocampus (L). There were increased FJB +ve cells in CA3 of hippocampus (green label in (L), all scale bars 100 μm). The same area was invaded by reactive astrocytes and microglia (green cells in (H) and (J)). Hematoxylin and Eosin stained hippocampal sections ((M), (N)) with pyknotic nucleus and shrunken cytoplasm are evident due to SE-induced changes at 7 days post-SE.

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