Chronic Temporal Lobe Epilepsy Is Associated with Enhanced Alzheimer-Like Neuropathology in 3×Tg-AD Mice (original) (raw)
Figure 6
Images and densitometry showing cell (A–D) and neuronal (E–M) loss in temporal lobe areas in epileptic relative to control 3×Tg-AD mice.
Panels (A–D) shows BACE1 immunolabeled sections, counterstained with cresyl violet, that reveal cell loss in CA1 and CA3 stratum pyramidale (s.p.) in a 14 month-old epileptic mouse (C, D) relative to an age-matched control (A, B). Arrows in A and C point to relatively large neuritic clusters. Mossy fiber sprouting (mfs) in the inner molecular layer is clear in D. Profound loss (green arrows) of immunoreactivity for neuron-specific nuclear antigen (NeuN IR) can be seen in CA1 and CA3, and to a lesser extent in the piriform cortex and amygdala in 11- (F, H) and 14- (K, L) month old epileptic mice relative to controls (E, G, I, J). Graph (M) summarizes normalized levels of densitometric data of NeuN IR in the hippocampal cell layers, amygdala and piriform cortex. The green line represents the mean density (defined as 100%) from all control animals (n = 12). Symbols (circle, triangle or diamond) in the graph represent normalized means from the 3 age groups of the epileptics (9-month: red; 11-month: green; 14-month: blue). NeuN density in somatosensory cortex is shown as negative assay control. Refer to Fig. 1 for abbreviations. Scale bar in (A) = 1 mm in (A, C, E–H); equivalent to 250 µm for (B, D, I–L).