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为进一步探讨谷氨酸（ Ｇｌｕ）的神经毒性机理，采用体外培养大鼠大脑皮质神经细胞１２～１４天，再分别加入 Ｇｌｕ（ Ｇｌｕ 组）， Ｇｌｕ＋ 尼莫地平（拮抗剂Ⅰ组）， Ｇｌｕ＋ Ｍ Ｋ８０１（拮抗剂Ⅱ组），检测各组神经细胞胞浆总钙（ Ｔ Ｃａ）及游离钙（ Ｃａ２＋ ｉ）．结果显示： Ｇｌｕ 组 Ｔ Ｃａ 和 Ｃａ２＋ ｉ明显高于正常对照组（ Ｐ＜ ０．０５），拮抗剂Ⅰ、Ⅱ组 Ｔ Ｃａ、和 Ｃａ２＋ ｉ均高于正常对照组（ Ｐ＜ ０．０５）而低于 Ｇｌｕ 组（ Ｐ＜ ０．０５）。提示：谷氨酸通过 Ｃａ２＋ 电压通道和受体依赖通道的激活，导致细胞内 Ｃａ２＋ ｉ沉积而产生神经毒性。
In order to further explore the mechanism of neurotoxicity of glutamic acid (Glu), cultured rat cerebral cortical neurons were cultured in vitro for 12-14 days, then Glu (Glu group), Glu + Nimodipine (antagonist group I), Glu + M K 801 (antagonist group Ⅱ), the test group of neuronal cytoplasmic total calcium (T Ca) and free calcium (Ca2 + i). The results showed that T Ca and Ca2 + i in Glu group were significantly higher than those in normal control group (P <0.05), T Ca and Ca2 + i in antagonist group Ⅰ and Ⅱ were higher than those in control group (P <0.05) Lower than Glu group (P <0.05). Tip: Glutamate is activated by Ca2 + voltage channels and receptor-dependent channels, leading to intracellular Ca2 + i deposition and neurotoxicity.