Short and Long-Term Analysis and Comparison of Neurodegeneration and Inflammatory Cell Response in the Ipsilateral and Contralateral Hemisphere of the Neonatal Mouse Brain after Hypoxia/Ischemia

Figure 4

Nissl staining showing H/I effects on the hippocampus and corpus callosum of the contralateral (CL) (right side of the panel), and ipsilateral hemisphere (IL) (left side of the panel), from 7 to 100 days (d) after hypoxia. At 7 d (a–h), overall hippocampal atrophy (b), layer disruption in ipsilateral CA3 (e), and increased cellularity in the ipsilateral corpus callosum (f) are seen. At 14 d (i–p) neuronal degeneration is widespread in hippocampus (i, j, m, and n). At 30 d (q–x) and 100 d (y–af), hippocampal atrophy (compare r to s, z to aa) and massive neuronal loss is seen in CA1 while CA3 is almost disorganized (r, u, and v for 30 d, z, ac, and ad for 100 d), along with the disorganized DG (compare q to t, y to ab). Increased cellularity in the corpus callosum is also visible (v and ad). Scale bars (low magnifications: b, c, j, k, r, s, z, aa) = 100 μm; scale bar in all other micrographs = 25 μm. CA1: cornu ammonis 1; CA3: cornu ammonis 3; CC: corpus callosum; DG: Dentate gyrus.