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目的:研究谷氨酸、NMDA、吗啡对原代培养的大鼠星形胶质细胞的胞内钙信号的影响及受体作用机制。方法:利用LeicaAF6000活细胞工作站,检测谷氨酸、NMDA、吗啡分别灌流前后Fura-2/AM加载的星形胶质细胞内钙信号的动态变化,进一步观察分别阻断代谢性谷氨酸受体5(mGluR5)、NMDA受体(NMDA receptor,NMDAR)和阿片μ受体对诱导的胞内钙振荡的影响。结果:谷氨酸、NMDA、吗啡均可明显升高胞内游离钙的浓度([Ca2+]i),而将其相应受体拮抗后,星形胶质细胞[Ca2+]i升高的现象可以被显著抑制。结论:离体培养的星形胶质细胞膜上存在mGluR5、NMDAR和阿片μ受体,这些受体的激活可以升高星形胶质细胞的[Ca2+]i,且这些受体依赖的[Ca2+]i的调控机制可能是星形胶质细胞与神经元交互作用的重要途径之一。
Objective: To investigate the effects of glutamate, NMDA and morphine on intracellular calcium signaling in primary cultured rat astrocytes and the mechanism of its receptor. Methods: The dynamic changes of calcium signal in astrocytes loaded with Fura-2 / AM before and after glutamate, NMDA and morphine perfusion were detected by Leica AF6000 living cell workstation. The changes of metabotropic glutamate receptors 5 (mGluR5), NMDA receptor (NMDAR) and opiate μ receptor on intracellular Ca2 + oscillations. Results: Glutamate, NMDA and morphine significantly increased the intracellular free calcium concentration ([Ca2 +] i), and the increase of [Ca2 +] i in astrocytes after antagonizing the corresponding receptors Was significantly suppressed. CONCLUSIONS: There are mGluR5, NMDAR and opioid μ receptors on cultured astrocyte membranes. The activation of these receptors can increase the [Ca2 +] i of astrocytes, and these receptor-dependent [Ca2 + The regulatory mechanism of i may be one of the important ways of the interaction between astrocytes and neurons.