Fig. 3.

Histological analysis of Wt andSod1 +/− mice after ischemia. A, Representative low-magnification photograph of cresyl violet staining at 24 hr after 1 hr of MCA occlusion. The caudate putamen level at 3 mm from the anterior tip (top) and the hippocampal level at 6 mm from the anterior tip (bottom) are represented. Infarction is represented in the left hemisphere as a pale, stained area. The ischemic hemisphere is much more enlarged inSod1 +/− than in Wt mice. Note that hippocampal CA1 pyramidal neurons are also involved in the infarction inSod1 +/− mice. Scale bar, 2 mm. B, Distribution of infarction and hemisphere enlargement in the brain.B₁, Sequential changes of percentage of infarct area expressed as infarct area/ischemic hemisphere area × 100%.B₂, Sequential changes of percentage of hemisphere enlargement expressed as (ischemic hemisphere area − nonischemic hemisphere area)/nonischemic hemisphere area × 100%.X-axis shows the distance of the sections from the anterior tip of the brain. Data show mean ± SEM (n = 5–8). C, Temporal profile of infarct volume and hemisphere enlargement in the whole brain of Wt andSod1 +/−^cep mice. The percentages of total infarct volume (C₁) and percentages of total hemisphere enlargement (C₂) were calculated by the accumulation in consecutive brain sections and expressed in the same manner as in Figure 3B. Data show mean ± SEM (n = 4–8). Asterisks indicate a significant increase, compared with Wt mice (*p < 0.05, **p < 0.01), and NS indicates no significance between Wt and Sod1 +/−^cep(Fisher’s PLSD test).