Experimental neurology
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Experimental neurology · Nov 2006
Comparative StudyAlterations in hippocampal neurogenesis following traumatic brain injury in mice.
Clinical and experimental data show that traumatic brain injury (TBI)-induced cognitive changes are often manifest as deficits in hippocampal-dependent functions of spatial information processing. The underlying mechanisms for these effects have remained elusive, although recent studies have suggested that the changes in neuronal precursor cells in the dentate subgranular zone (SGZ) of the hippocampus might be involved. Here, we assessed the effects of unilateral controlled cortical impact on neurogenic cell populations in the SGZ in 2-month-old male C57BL6 mice by quantifying numbers of dying cells (TUNEL), proliferating cells (Ki-67) and immature neurons (Doublecortin, Dcx) up to 14 days after TBI. ⋯ No differences were noted in oligodendrocytes (BrdU/NG2). Taken together, these data demonstrate that TBI alters both neurogenesis and gliogenesis. Such alterations may play a contributory role in TBI-induced cognitive impairment.
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Experimental neurology · Nov 2006
Comparative StudyLocal and distal responses to injury in the rapid functional recovery from spinal cord contusion in rat pups.
Young rats display an accelerated rate of locomotor recovery after contusive spinal cord injury (SCI) compared to adults subjected to a similar standardized injury. We examined possible differences in the responses to SCI at the injury site and in the distal cord that might contribute to this rapid recovery. P14-15 rats were studied at 1, 3, 5, 7, and 28 days after injury at T8 produced with a weight drop device (10 g x 2.5 cm). ⋯ No evidence of oligodendrocyte loss in spared white matter was detected at 24 h after injury, as compared to the 50% loss reported in adults. Rather, there was a significant increase in the density of oligodendrocytes by 5 days after injury that was associated with a dramatic upregulation of markers for glial progenitor cells after pup SCI. Our results suggest that an altered glial response near the injury epicenter as compared to that in adults is likely to contribute to the more rapid rate of recovery in hindlimb locomotor function in young rats after SCI.