Figure 3. Cell proliferation increases dramatically following injury.

(A–D, M) At 1 day post injury, proliferation began to increase in the VZs and parenchyma of the lesioned telencephalic hemispheres. (E–H, M) Extensive proliferation was evident in both ipsilesional and contralesional hemispheres by 2 days post-lesion, especially in the germinative zones and throughout the parenchyma of the ipsilesional hemispheres after QA- more than vehicle-induced lesions. (I–L, M) The number of proliferative cells was elevated to a lesser extent at 4 (I–L) and 7 (M) days post-injury and remained only slightly increased at 14 days (M). (M) Proliferating cell numbers were quantified at various timepoints following QA- (red) or vehicle-induced (blue) injury in the ipsilesional (solid) and contralesional (hatched) telencephalic hemispheres. Analysis of variance (ANOVA) results indicated significant main effects on proliferation for lesion type (F(2, 76) = 81.943, p < 0.0001) and days post lesion (F(8, 154) = 21.224, p < 0.0001), as well as a significant interaction effect for type of lesion x days post lesion (F(8, 154) = 14.482, p < 0.0001). Post-hoc analyses (Tukey HSD) for proliferation across type of lesion indicated significant differences in proliferation in the injured hemisphere among QA-lesioned, vehicle-lesioned and uninjured brains, and in the uninjured hemisphere between QA-lesioned and vehicle-lesioned or uninjured brains. Results from pairwise comparisons within each day (Student’s t-test with additional Bonferroni corrections) and with uninjured telencephalic hemispheres are indicated on the graph and in Table 1. * p < 0.01, ** p < 0.001, + p < 0.01 compared to uninjured (denoted by the dashed horizontal line). Scale bar = 100 μm.