In vivo N-15 MRS study of glutamate metabolism in the rat brain.
In vivo N-15 MRS study of glutamate metabolism in the rat brain.
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DOI：
10.1016/j.ab.2016.08.025
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发表时间：
2017-07-15
影响因子：
2.9
通讯作者：
Kanamori K
中科院分区：
文献类型：
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作者：
Kanamori K
在体内15 N MRS作出了独特的贡献，动力学研究的个别途径，控制谷氨酸在大鼠大脑中的流量。本文综述了以下几个方面的研究进展：（1）活体15 N MRS的优点和局限性，以及15 N MRS的1H偶联间接检测方法;（2）动力学方法;（3）本实验室和其他实验室在以下方面的主要研究成果：（a）细胞外液中谷氨酸的摄取;（B）谷氨酸代谢为谷氨酰胺;（c）谷氨酰胺转运至细胞外液;（d）神经元谷氨酰胺水解为谷氨酸;和（e）亮氨酸转氨作用对补充谷氨酸氮的贡献。在不同血氨水平下测定的谷氨酰胺合成酶活性表明，当血氨浓度> 0.9 μmol/g时，谷氨酰胺合成酶趋于饱和，引起脑氨升高。高氨性脑病的原因的结果的影响进行了讨论。亮氨酸提供>25%的谷氨酸氮。一个有趣的可能性，补充亮氨酸可能恢复脑损伤后的认知功能进行了讨论。最后，15 N MRS的一些特点，可能有利于未来的应用，这种技术在4或7特斯拉的人脑的研究进行了说明。
In vivo 15N MRS has made a unique contribution to kinetic studies of the individual pathways that control glutamate flux in the rat brain. This review covers the following topics: (1) the advantages and limitations of in vivo 15N MRS and its indirect detection through coupled 1H; (2) kinetic methods; (3) major findings from our and other laboratories in the areas: (a) the uptake of the neurotransmitter glutamate from the extracellular fluid into glia; (b) the metabolism of glutamate to glutamine; (c) glutamine transport to the extracellular fluid; (d) hydrolysis of neuronal glutamine to glutamate; and (e) contribution of transamination from leucine to replenish the glutamate nitrogen. In vivo glutamine synthetase activities measured at several levels of hyperammonemia showed that this enzyme becomes saturated at blood ammonia concentration > 0.9 μmol/g, and causes the elevation of brain ammonia. Implications of the results for the cause of hyperammonemic encephalopathy are discussed. Leucine provides >25% of glutamate nitrogen. An intriguing possibility that supplementing leucine may restore cognitive function after brain injury is discussed. Finally, some characteristics of 15N MRS that may facilitate the future application of this technique to the study of the human brain at 4 or 7 Tesla are described.