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Tianfu Li, Gaoying Ren, Theresa Lusardi, Andrew Wilz, Jing Q. Lan, Takuji Iwasato, Shigeyoshi Itohara, Roger P. Simon, Detlev Boison
Published in Volume 118, Issue 2
J Clin Invest. 2008; 118(2):571–582 doi:10.1172/JCI33737
Abstract | Full text | PDF
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Figure 1
Characterization of spontaneously epileptic mice 3 weeks after intraamygdaloid injection of KA.

(AD) Representative cresyl violet–stained coronal brain section showing the hippocampal formation contralateral (A and C) or ipsilateral (B and D) to the KA injection. Note the CA3 selective cell loss in the ipsilateral hippocampus (B and D). (E and F) Adjacent coronal brain section from the same animal stained with the nuclear stain DAPI showing an increase in the number of cell nuclei in the injured CA3. (G and H) The same section stained with NFM indicating the presence of dense neuronal networks within the injured CA3. (IN) ADK immunoreactivity within the hippocampal formation visualized with diaminobenzidine contralateral (I, K, and M) or ipsilateral (J, L, and N) to the KA injection. Note the focal overexpression of ADK in the ipsilateral CA3. IL are from the same animal and adjacent to those shown in AH. M and N are derived from the same animal at a more caudal location, representing the level of cell transplantations (see Figure 10). Arrows in J and N point to upregulated ADK in ipsilateral CA3. (OR) Confocal analysis of ADK (red) and GFAP (green) immunoreactivity in the contralateral (O and P) and ipsilateral (Q and R) CA3. Note prominent astrogliosis (GFAP) and overexpression and redistribution of ADK in the ipsilateral CA3 (Q and R). Bottom: Representative EEG recordings obtained from electrodes inserted into the ipsilateral CA3 or CA1 or placed onto the cortex. Scale bars: 300 μm (A, B, I, J, M, and N), 75 μm (C and D), 37.5 μm (E, F, G, H, K, and L), 12 μm (O and Q), and 5 μm (P and R). EEG scale bar: 2 s.