期刊
JOURNAL OF NEUROTRAUMA
卷 30, 期 9, 页码 727-740出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/neu.2012.2650
关键词
astrocytes; blood-brain barrier; cytokines; inflammation; mild traumatic brain injury
Mild traumatic brain injury (mTBI), particularly mild blast type'' injuries resulting from improvised exploding devices and many sport-caused injuries to the brain, result in long-term impairment of cognition and behavior. Our central hypothesis is that there are inflammatory consequences to mTBI that persist over time and, in part, are responsible for resultant pathogenesis and clinical outcomes. We used an adaptation (1 atmosphere pressure) of a well-characterized moderate-to-severe brain lateral fluid percussion (LFP) brain injury rat model. Our mild LFP injury resulted in acute increases in interleukin-1 alpha/beta and tumor necrosis factor alpha levels, macrophage/microglial and astrocytic activation, evidence of heightened cellular stress, and blood-brain barrier (BBB) dysfunction that were evident as early as 3-6 h postinjury. Both glial activation and BBB dysfunction persisted for 18 days postinjury.
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