Enhanced neurogenesis in the rodent hippocampus following traumatic brain injury

Recent studies have shown that neurogenesis in the dentate gyrus of the rod ent hippocampus continues throughout life. Several physiological and pathol ogical conditions have been reported to alter the rate of progenitor cell d ivision resulting in the increased production of mature granule neurons. Ex citotoxic and mechanical lesions of the granule cell layer also stimulate t he proliferation of precursor cells suggesting that the death of pre-existi ng granule neurons may act as a trigger for enhanced neurogenesis. Hippocam pal pyramidal neurons, and to a lesser extent granule neurons, have been re ported to die as a result of traumatic brain injury in rodents. To determin e if the proliferation of precursor cells is enhanced as a result of brain injury in rodents, newly divided cells were labeled with the thymidine anal og, bromodeoxyuridine (BrdU), Traumatic brain injury increased the producti on of BrdU-labeled cells in the dentate gyrus with a maximal rate observed at 3 days post-injury. These cells, a proportion of which co-localize with the immature neuronal marker TOAD-64, implanted themselves into the granule cell layer where they accumulated over time. When examined 1 month post-in jury, the majority of BrdU-labeled cells co-labeled with the mature neurona l marker calbindin. These findings show that traumatic brain injury increas es neurogenesis in the granule cell layer and suggests that these new cells may contribute to the function of the hippocampus, (C) 2001 Wiley-Liss, In c.