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谷氨酸通过激活NMDA和AMPA受体诱导星形胶质细胞内钙含量增加。

Induction of increased intracellular calcium in astrocytes by glutamate through activating NMDA and AMPA receptors.

作者信息

Zhang Qi, Hu Bo, Sun Shenggang, Tong Etang

机构信息

Department of Pathophysiology, School of Basic Medical Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030.

出版信息

J Huazhong Univ Sci Technolog Med Sci. 2003;23(3):254-7. doi: 10.1007/BF02829506.

DOI:10.1007/BF02829506
PMID:14526426
Abstract

To study the effect of glutamate on the intracellular calcium signal of pure cultured rat astrocytes and the role of NMDA and AMPA receptors in the procedure, the change of calcium signal was investigated by monitoring the fluctuation of intracellular Ca2+ concentration ([Ca2+]i) on the basis of Fura-2 single cell fluorescent ratio (F345/F380). The changes in the effect of glutamate on the intracellular calcium signal were observed after blockage of NMDA and (or) AMPA receptors. It was found that L-glutamate could induce an increased [Ca2+]i in most of the cells in concentration- and time-dependent manner. D-(-)-2-amino-5-phosphonopentanoic acid (D-AP-5, a selective antagonist of the NMDA receptor) and 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX, a selective antagonist of the AMPA receptor) could abolish the effects of NMDA and AMPA respectively. The treatment of D-AP-5 and CNQX simultaneously or respectively could attenuate the effect of L-glutamate at varying degrees. All these indicated that glutamate could modulate intracellular Ca2+ of pure cultured rat astrocytes through different pathways. The activation of NMDA and AMPA receptors took part in the complex mechanisms.

摘要

为研究谷氨酸对原代培养大鼠星形胶质细胞内钙信号的影响以及NMDA和AMPA受体在此过程中的作用,基于Fura-2单细胞荧光比率(F345/F380)监测细胞内Ca2+浓度([Ca2+]i)的波动,研究钙信号的变化。在阻断NMDA和(或)AMPA受体后,观察谷氨酸对细胞内钙信号作用的变化。结果发现,L-谷氨酸能以浓度和时间依赖的方式诱导大多数细胞内[Ca2+]i升高。D-(-)-2-氨基-5-磷酸戊酸(D-AP-5,NMDA受体的选择性拮抗剂)和6-氰基-7-硝基喹喔啉-2,3-二酮(CNQX,AMPA受体的选择性拮抗剂)可分别消除NMDA和AMPA的作用。同时或分别给予D-AP-5和CNQX处理可不同程度减弱L-谷氨酸的作用。所有这些表明,谷氨酸可通过不同途径调节原代培养大鼠星形胶质细胞内的Ca2+。NMDA和AMPA受体的激活参与了这一复杂机制。

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