Gangliosides and ceramides change in a mouse model of blast induced traumatic brain injury.
Gangliosides and ceramides change in a mouse model of blast induced traumatic brain injury.
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DOI：
10.1021/cn300216h
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发表时间：
2013-04
影响因子：
5
通讯作者：
A. Woods;B. Colsch;S. Jackson;Jeremy D Post;Kathrine Baldwin;Aurélie Roux;B. Hoffer;B. Cox;M. Hoffer;V. Rubovitch;C. Pick;J. Schultz;C. Balaban
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文献类型：
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作者：
A. Woods;B. Colsch;S. Jackson;Jeremy D Post;Kathrine Baldwin;Aurélie Roux;B. Hoffer;B. Cox;M. Hoffer;V. Rubovitch;C. Pick;J. Schultz;C. Balaban
爆炸爆炸会产生大气压力变化，从而产生非穿透性爆炸引起的“轻度”创伤性脑损伤（bTBI）。轻度 bTBI 的结构基础一直存在极大争议。本研究应用基质辅助激光解吸/电离 (MALDI) 质谱成像来追踪暴露于极低水平爆炸爆炸（2.5-5.5 psi 峰值超压）的小鼠脑组织中神经节苷脂的分布。我们观察到单次爆炸暴露后海马、丘脑和下丘脑中的神经节苷脂 GM2 显着增加。此外，这些变化还伴随着神经酰胺的消耗。使用标准光学显微镜技术无法推断出神经或脑结构损伤迹象。第一个变异源是由爆炸和组织采样之间的延迟（爆炸波的峰值强度）产生的。这些发现表明，细胞内膜和质膜区室中细微的分子变化可能是对轻度 bTBI 的生物反应的生物标志物。这也是第一份关于非遗传性病因导致成熟小鼠大脑中 GM2 增加的报告。
Explosive detonations generate atmospheric pressure changes that produce nonpenetrating blast induced "mild" traumatic brain injury (bTBI). The structural basis for mild bTBI has been extremely controversial. The present study applies matrix-assisted laser desorption/ionization (MALDI) mass spectrometry imaging to track the distribution of gangliosides in mouse brain tissue that were exposed to very low level of explosive detonations (2.5-5.5 psi peak overpressure). We observed major increases of the ganglioside GM2 in the hippocampus, thalamus, and hypothalamus after a single blast exposure. Moreover, these changes were accompanied by depletion of ceramides. No neurological or brain structural signs of injury could be inferred using standard light microscopic techniques. The first source of variability is generated by the Latency between blast and tissue sampling (peak intensity of the blast wave). These findings suggest that subtle molecular changes in intracellular membranes and plasmalemma compartments may be biomarkers for biological responses to mild bTBI. This is also the first report of a GM2 increase in the brains of mature mice from a nongenetic etiology.