Mapping the Changes of Glutamate Using Glutamate Chemical Exchange Saturation Transfer (GluCEST) Technique in a Traumatic Brain Injury Model: A Longitudinal Pilot Study
Mapping the Changes of Glutamate Using Glutamate Chemical Exchange Saturation Transfer (GluCEST) Technique in a Traumatic Brain Injury Model: A Longitudinal Pilot Study
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使用谷氨酸化学交换饱和转移 (GluCEST) 技术绘制创伤性脑损伤模型中谷氨酸的变化：一项纵向试点研究
DOI：
10.1021/acschemneuro.8b00482
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通讯作者：
Wu R
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作者：
Zhuang Z;Shen Z;Chen Y;Dai Z;Zhang X;Mao Y;Zhang B;Zeng H;Chen P;Wu R
谷氨酸兴奋性在创伤性脑损伤（TBI）的病理生理中起着至关重要的作用，通过引发继发性损伤。谷氨酸化学交换饱和转移（Glutamate chemical exchange saturation transfer, GluCEST） MRI是近年来发展起来的一种具有高灵敏度和高空间分辨率的无创活体谷氨酸成像技术。本研究的目的是利用大鼠创伤性脑损伤模型来绘制脑谷氨酸分布的变化，并探讨葡萄糖测试成像检测继发性损伤的能力。在脑外伤前和脑外伤后1、3、7、14天对成年雄性Sprague-Dawley大鼠进行序贯葡萄糖测试成像扫描。与基线和对照组相比，脑损伤后损伤皮质核心病变的葡萄糖水平在第1天升高并达到峰值，同侧海马在第3天达到峰值。颅脑损伤后第14天，血糖水平逐渐下降至基线水平。损伤大鼠第3天同侧海马glest %与正确象限时间呈负相关。脑外伤大鼠同侧海马胶质原纤维酸性蛋白免疫标记显示明显星形胶质细胞活化。IL-6和TNF-α在损伤后第1天达到峰值，同侧海马IL-6和TNF-α在损伤后第3天达到峰值。随后在第14天逐渐降至假水平。结论是，葡萄糖测试成像有潜力成为一种新的神经影像学方法来预测认知结果，并更好地了解脑外伤后的神经炎症。
Glutamate excitoxicity plays a crucial role in the pathophysiology of traumatic brain injury (TBI) through the initiation of secondary injuries. Glutamate chemical exchange saturation transfer (GluCEST) MRI is a newly developed technique to noninvasively image glutamatein vivowith high sensitivity and spatial resolution. The aim of the present study was to use a rat model of TBI to map changes in brain glutamate distribution and explore the capability of GluCEST imaging for detecting secondary injuries. Sequential GluCEST imaging scans were performed in adult male Sprague–Dawley rats before TBI and at 1, 3, 7, and 14 days after TBI. GluCEST% increased and peaked on day 1 after TBI in the core lesion of injured cortex and peaked on day 3 in the ipsilateral hippocampus, as compared to baseline and controls. GluCEST% gradually declined to baseline by day 14 after TBI. A negative correlation between the GluCEST% of the ipsilateral hippocampus on day 3 and the time in the correct quadrant was observed in injured rats. Immunolabeling for glial fibrillary acidic protein showed significant astrocyte activation in the ipsilateral hippocampus of TBI rats. IL-6 and TNF-α in the core lesion peaked on day 1 postinjury, while those in the ipsilateral hippocampus peaked on day 3. These subsequently gradually declined to sham levels by day 14. It was concluded that GluCEST imaging has potential to be a novel neuroimaging approach for predicting cognitive outcome and to better understand neuroinflammation following TBI.