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Full-Text Articles in Medicine and Health Sciences
Inhibition Of Injury-Induced Cell Proliferation In The Dentate Gyrus Impairs Cognitive Recovery Following Traumatic Brain Injury, Teresa Daniels
Inhibition Of Injury-Induced Cell Proliferation In The Dentate Gyrus Impairs Cognitive Recovery Following Traumatic Brain Injury, Teresa Daniels
Theses and Dissertations
Traumatic brain injury (TBI) induces a robust cellular proliferative response among neural stem/progenitor cells (NS/NPCs) in the dentate gyrus of the hippocampus. This proliferative effect is thought to contribute to the innate cognitive recovery observed following TBI. Inhibition of hippocampal neurogenesis impairs cognitive function. Furthermore, enhancement of injury-induced hippocampal neurogenesis via intraventricular administration of basic fibroblast growth factor (bFGF) improves cognitive function in animals following TBI. In this experiment, we investigated the direct association between injury-induced hippocampal neurogenesis and cognitive recovery utilizing an antimitotic agent, arabinofuranosyl cytidine (Ara-C). In this study, adult rats received a moderate lateral fluid percussion injury …
The Role Of Calcineurin In Dendritic Remodeling And Epileptogenesis In A Rat Model Of Traumatic Brain Injury, John Campbell
The Role Of Calcineurin In Dendritic Remodeling And Epileptogenesis In A Rat Model Of Traumatic Brain Injury, John Campbell
Theses and Dissertations
Traumatic brain injury (TBI), a leading cause of death and disability in the United States, causes potentially preventable damage in part through the dysregulation of neural calcium levels. This dysregulation likely affects the activity of the calcium-sensitive phosphatase, calcineurin, with serious implications for neural function. To test this possibility, the present study characterized the role of calcineurin in a rat model of brain trauma, the lateral fluid percussion injury model. Golgi-Cox histochemistry revealed an acute post-TBI loss and delayed overgrowth of dendritic spines on principal cortical cells. The spine loss appeared to require calcineurin activity, since administering a calcineurin inhibitor, …