Dentate Gyrus Proliferative Responses After Traumatic Brain Injury and Binge Alcohol in Adult Rats
Autor: | Gwendolyn L. Kartje, Jack P Gerling, Shih-Yen Tsai, Timothy E. O'Brien, Kevin Hsu, Ian C. Vaagenes, Son T. Ton, Natalie S. Adamczyk, Joanna Y. Wu |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0303 health sciences
medicine.medical_specialty Binge alcohol Traumatic brain injury business.industry General Neuroscience Public health Dentate gyrus traumatic brain injury proliferation medicine.disease lcsh:RC321-571 hippocampal dentate gyrus 03 medical and health sciences 0302 clinical medicine Anesthesia medicine business lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry hilar ectopic granule cells 030217 neurology & neurosurgery 030304 developmental biology Original Research |
Zdroj: | Neuroscience Insights Neuroscience Insights, Vol 15 (2020) |
ISSN: | 2633-1055 |
Popis: | Background: Traumatic brain injury is a significant public health issue that results in serious disability in survivors. Traumatic brain injury patients are often intoxicated with alcohol when admitted to the hospital; however, it is not clear how acute intoxication affects recovery from a traumatic brain injury. Our group has previously shown that binge alcohol prior to traumatic brain injury resulted in long-term impairment in a fine sensorimotor task that was correlated with a decreased proliferative and neuroblast response from the subventricular zone. However, whether binge alcohol prior to traumatic brain injury affects the proliferative response in the hippocampal dentate gyrus is not yet known. Methods: Male rats underwent binge alcohol (3 g/kg/day) by gastric gavage for 3 days prior to traumatic brain injury. Cell proliferation was labeled by BrdU injections following traumatic brain injury. Stereological quantification and immunofluorescence confocal analysis of BrdU+ cells in the hippocampal dorsal dentate gyrus was performed at 24 hours, 1 week and 6 weeks post traumatic brain injury. Results: We found that either traumatic brain injury alone or binge alcohol alone significantly increased dentate gyrus proliferation at 24 hours and 1 week. However, a combined binge alcohol and traumatic brain injury regimen resulted in decreased dentate gyrus proliferation at 24 hours post-traumatic brain injury. At the 6 week time point, binge alcohol overall reduced the number of BrdU+ cells. Furthermore, more BrdU+ cells were found in the dentate hilar region of alcohol traumatic brain injury compared to vehicle traumatic brain injury groups. The location and double-labeling of these mismigrated BrdU+ cells was consistent with hilar ectopic granule cells. Conclusion: The results from this study showed that pre-traumatic brain injury binge alcohol impacts the injury-induced proliferative response in the dentate gyrus in the short-term and may affect the distribution of newly generated cells in the dentate gyrus in the long-term. |
Databáze: | OpenAIRE |
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