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. 1999 Oct 12;96(21):12096–12101. doi: 10.1073/pnas.96.21.12096

Figure 2.

Figure 2

Comparison of kainate-induced neuronal damage in the hippocampus of PPT-A(+/+) (WT) and PPT-A(−/−) (KO) mice. The segments shown in both groups are the part of CA1 closest to CA2 and the lower curving portion of CA3 located CA3b. (A-F) Hematoxylin/eosin staining in saline-injected controls (A and D), kainate-treated PPT-A(+/+) (B and E), and kainate-treated PPT-A(−/−) mice (C and F). A large number of injured neurons with shrunken, acidophilic cytoplasm and pyknotic nuclei are seen in CA1 (B) and CA3 (E) pyramidal cell layers of PPT-A(+/+) mice 3 days after injection of kainate (35 mg/kg). In comparable sections of kainate-treated PPT-A(−/−) mice, the acute damage was minimal and confined to CA3b (arrows in F) and was absent from CA1 (C). (G–I) Photomicrographs of cresyl violet-stained hippocampus 7 days after injection of kainate, showing neuronal loss. The sections through dorsal hippocampus of PPT-A(+/+) mice showed a thinned and sparsely staining CA1 pyramidal cell layer (arrows in H) and a breach of staining in CA3 pyramidal cell layer (arrowheads in H) compared with saline-injected mice (G). In contrast, neuronal loss was undetectable in PPT-A(−/−) mice treated with the same dose of kainate (I). (Scale bars: 125 μm, A–F; 80 μm, G and H.)