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 2

Nissl staining showing hypoxia/ischemia (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 3 to 72 hours (hrs) after hypoxia. At 3 hrs (a–h), layer disruption is seen in ipsilateral CA3 (e) and increased cellularity in the ipsilateral corpus callosum (f). At 24 hrs (i–p) neuronal degeneration is widespread in hippocampus (i, j, m, and n). At 48 hrs (q–x) and 72 hrs (y–af), hippocampal atrophy (compare r to s, z to aa) and massive neuronal loss is seen in CA1 and CA3 (r, u, and v for 48 hrs, z, ac and ad for 72 hrs) although the DG is also disorganized (compare q to t, y to ab). Increased cellularity in the corpus callosum is also seen (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.