期刊
JOURNAL OF NEUROSCIENCE
卷 31, 期 13, 页码 4906-4916出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5265-10.2011
关键词
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资金
- National Institutes of Health [R01 NS048192]
- Seay Endowed Fund for Research on Brain and Spinal Cord Injuries in Children
- National Institute of Mental Health
- National Institute of Child Health and Human Development
- Hartwell Foundation
Significant spontaneous recovery occurs after essentially all forms of serious brain injury, although the mechanisms underlying this recovery are unknown. Given that many forms of brain injury such as traumatic brain injury (TBI) induce hippocampal neurogenesis, we investigated whether these newly generated neurons might play a role in recovery. By modeling TBI in transgenic mice, we determined that injury-induced newly generated neurons persisted over time and elaborated extensive dendritic trees that stably incorporated themselves throughout all neuronal layers of the dentate gyrus. When we selectively ablated dividing stem/progenitors at the time of injury with ganciclovir in a nestin-HSV-TK transgenic model, we eliminated injury-induced neurogenesis and subsequently diminished the progenitor pool. Moreover, using hippocampal-specific behavioral tests, we demonstrated that only injured animals with neurogenesis ablated at the time of injury lost the ability to learn spatial memory tasks. These data demonstrate a functional role for adult neurogenesis after brain injury and offer compelling and testable therapeutic options that might enhance recovery.
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