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目的和方法:本文观察中毒剂量谷氨酸对大鼠大脑皮质神经细胞内Ca2+ 含量变化的影响,并对其机制进行探讨。将1 m mol/L谷氨酸加入大脑皮质神经细胞培养液中通过激光共聚焦扫描显微镜(laser confocalscanning microscope,LCSM) 观察细胞内Ca2+ 含量的变化。结果:①1 m mol/L谷氨酸作用后在观察的86 个细胞中,71 % 的细胞内游离Ca2+ 浓度发生钙振荡,发生钙振荡的波型均为尖峰型:②在抑制细胞内钙库释放后加入1 m mol/L 谷氨酸,细胞内Ca2+ 浓度上升,但没有产生钙振荡;而抑制细胞外Ca2 + 内流后加入1 mmol/L 谷氨酸,细胞内Ca2 + 发生钙振荡,但振荡幅度逐渐下降直至振荡消失。结论:中毒剂量谷氨酸引起神经细胞钙振荡形成的可能机制是:细胞内钙库的释放和摄取是Ca2 + 发生振荡的必要条件,而振荡的维持则依赖于细胞外Ca2+ 的内流
PURPOSE AND METHODS: The purpose of this study was to investigate the effect of glutamic acid at toxic dose on the content of Ca2 + in cerebral cortical neurons of rats and its mechanism. The concentration of 1 mol / L glutamate was added into the culture medium of cerebral cortex neurons to observe the change of intracellular Ca2 + content by laser confoccanning microscope (LCSM). RESULTS: After 1 mol / L glutamate treatment, 71% intracellular free Ca2 + concentration in the 86 cells observed had calcium oscillation, and the type of Ca2 + oscillations was spike type. (2) In the inhibition of intracellular calcium pool Release of glutamate after adding 1 m mol / L, the intracellular Ca2 concentration increased, but did not produce calcium oscillations; and inhibit the influx of extracellular Ca2 + 1 mmol / L glutamate, Ca2 + intracellular calcium oscillation occurs, However, the oscillation amplitude gradually decreases until the oscillation disappears. CONCLUSION: The possible mechanism of calcium oscillation induced by glutamate at toxic dose is that the intracellular Ca2 + release and uptake are the necessary conditions for Ca2 + oscillations, while the maintenance of oscillation depends on the influx of extracellular Ca2 +