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The persistence of Runx1 expression in the vicinity of the injury site, particularly in those regions that play a vital role in orchestrating neurogenesis, suggests that the microglia may play an integral part in the process. The intriguing fact that the number of Runx1+/Iba1+ cells in the DG increased transiently after injury is in line with the hypothesis that there is an increase in microglial proliferation and recruitment to the site of injury.
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We tracked a small population of apoptotic cells for the duration of the experiment. There was a significant increase in the number of apoptotic cells in both the ipsilateral DG and SVZ at both 1 dpi and 3 dpi, indicating increased apoptosis after CCI. At 1 dpi, 2038+/-365 cells/mm2 of DG and 1644+/-145 cells/mm2 of SVZ were immunopositive for active caspase-3 (Figure 5). At 3 dpi, there were 1663+/-223 and 961+/-104 active caspase-3 positive cells/mm2 in the DG and SVZ, respectively. These numbers were similar to those seen at 3 dpi in the CD68+/BrdU- cells in the DG. In line with these observations, there were 2.7- and 1.4-fold increases in the total number of CD68+/active caspase-3+ cells in the DG at 1 and 3 dpi, respectively (Figure 6). In the SVZ, the total number of CD68+/active caspase-3+ cells was increased at 1 dpi and returned to control levels by 3 dpi. In both the DG and SVZ, in the absence of a concomitant decrease in total CD68+ cells at 1 dpi, we infer that the majority of CD68+ cells were not involved in apoptosis, but were actively involved in the neurogenic process.