Several other studies showed that both, focal and global anoxia can enhance neurogenesis (Lichtenwalner and Parent, 2006) in a predictable time-dependent manner, but most of the experiments have been done on relatively young mice and rats. The three studies (Yagita et al., 2001; Jin et al., 2004; Darsalia et al., 2005) that used older animals produced varied results warranting further investigation. Our experiments agree qualitatively with those of (Yagita et al., 2001) who showed relatively higher post-ischemic neurogenic response in older animals, but with the use of alternative ischemia model (four vessel occlusion) and another rat strain (Wistar). Our study goes further in demonstrating enhanced neurogenesis on day 35 but not on day 90 after ischemia. This enhancement appears to be primarily due to increased proliferation, possibly by type 2 progenitors since it is reflected in the increase of DCX+ cells (Kempermann et al., 2004). This proliferation persists past day 10 and is responsible for a large overall increase in cell production on day 35 (see Figure 2). In contrast, proportional differentiation and consequent expression of DCX did not differ between control and ischemic animals (Table 2). Reduced proliferation of neural progenitors is a main characteristic of aging animals thus the exaggerated response seen after ischemia appears to be an appropriate compensation (McDonald and Wojtowicz, 2005).