Figure 4

Enhanced post-ischemic neurogenesis and angiogenesis in PrP−/− mice is a consequence of increased infarct size. (a) Infarct volume determined by TTC staining, (b) neuronal density in the striatum determined by NeuN immunohistochemistry, (c) cell proliferation measured by BrdU immunolabeling, (d) neurogenesis evaluated by co-labeling of the immature neuronal marker Dcx and BrdU, (e) neurogenesis assessed by co-labeling of the mature neuronal marker NeuN and BrdU, and (f) angiogenesis examined by co-labeling of the endothelial marker CD31 and BrdU in WT mice exposed to 45 min MCA occlusion and PrP−/− mice exposed to 30 min MCA occlusion followed by 24 h reperfusion (a) or 28 days reperfusion (b–f). Note that in the presence of very similar brain injury (a and b), post-ischemic cell proliferation (c), neurogenesis (d–e) and angiogenesis (f) do not differ between WT and PrP−/− mice