Department of Biomedical Engineering, Wayne State University, Detroit, MI, USA.
NMR Biomed. 2012 Dec;25(12):1331-9. doi: 10.1002/nbm.2805. Epub 2012 May 1.
Blast-induced neurotrauma is a major concern because of the complex expression of neuropsychiatric disorders after exposure. Disruptions in neuronal function, proximal in time to blast exposure, may eventually contribute to the late emergence of clinical deficits. Using magic angle spinning ¹H MRS and a rodent model of blast-induced neurotrauma, we found acute (24-48 h) decreases in succinate, glutathione, glutamate, phosphorylethanolamine and γ-aminobutyric acid, no change in N-acetylaspartate and increased glycerophosphorylcholine, alterations consistent with mitochondrial distress, altered neurochemical transmission and increased membrane turnover. Increased levels of the apoptotic markers Bax and caspase-3 suggested active cell death, consistent with increased FluoroJade B staining in the hippocampus. Elevated levels of glial fibrillary acidic protein suggested ongoing inflammation without diffuse axonal injury measured by no change in β-amyloid precursor protein. In conclusion, blast-induced neurotrauma induces a metabolic cascade associated with neuronal loss in the hippocampus in the acute period following exposure.
爆炸诱导的神经创伤是一个主要关注点，因为暴露后会出现复杂的神经精神障碍表现。与爆炸暴露时间接近的神经元功能紊乱，最终可能导致临床缺陷的迟发性出现。我们使用魔角旋转 ¹H MRS 和爆炸诱导的神经创伤的啮齿动物模型发现，在急性（24-48 小时）期间琥珀酸、谷胱甘肽、谷氨酸、磷乙醇胺和γ-氨基丁酸减少，N-乙酰天冬氨酸没有变化，甘油磷酸胆碱增加，这些变化与线粒体窘迫、神经化学传递改变和膜周转率增加一致。凋亡标志物 Bax 和 caspase-3 的增加表明细胞凋亡活跃，这与在海马体中氟罗丹明 B 染色增加一致。神经胶质纤维酸性蛋白水平升高表明存在持续的炎症，而β-淀粉样前体蛋白没有变化则表明没有弥漫性轴索损伤。总之，爆炸诱导的神经创伤会在暴露后急性期间引发与海马体神经元丢失相关的代谢级联反应。
