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Cognitive deficits, behavioral changes and gene expression profiling in a mouse model of repeated mild traumatic brain injury

University of British Columbia

Repeated mild traumatic brain injury (rmTBI) has been thought to result in cumulative damage to cells of the brain, but the molecular mechanisms are not known. We investigated the effect of rmTBI on cognition, behavior and hippocampal gene expression using microarray analysis. Mice applied with rmTBI for 25 successive days and tested at 1 week and 4 weeks after the injury respectively, showed transient neurological deficit, impaired weekly body weight growth rate (BWGR), changed behaviors in elevated plus maze and deficit in spatial memory in the Morris water maze compared with sham injury mice. Microarray analysis suggested several rmTBI-induced expression differences in intracellular signaling, apoptosis and cell cycle, angiogenesis, cellular architecture, inflammation, oxidative stress, metabolism and transcriptional regulation, and neuronal plasticity-related genes. This study highlights some of the potential mechanisms that may play an important role in the development of rmTBI-induced functional deficits. Further studies at different time points and in additional subregions of the brain are of interest in the search for molecular mechanisms behind rmTBI-induced neuronal pathogenesis after the injury.

Text

2011-03-24

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/32853

Neuroscience

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-nc-nd/4.0/