ABSTRACT
The persistence of neural stem cells into adulthood has been an area of intense investigation in recent years. There is limited knowledge about how an acquired brain injury might affect the ability of neural precursor cells to proliferate and repopulate injured areas. In the present study we utilize a controlled cortical impact model of traumatic brain injury in adult mice and subsequent BrdU labeling to demonstrate that there is significant proliferation of neural precursors in response to traumatic brain injury in areas both proximal and distal to the injury site. The fate of the proximal proliferation is almost exclusively astrocytic at 60-days post injury and demonstrates that newly generated cells make up much of the astrogliotic scar. Moreover, in areas more distal from the injury site, neurogenesis occurs within the granular layer of the dentate gyrus at a level more than five-fold greater than in controls. These data demonstrate that neural proliferation plays key roles in the remodeling that occurs after traumatic brain injury and suggests a mechanism as to how functional recovery after traumatic brain injuries continues to occur long after the injury itself.
