【摘要】 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 Ｋ８０１（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。更多还原

【Abstract】 This study was intended to further explain the mechanism of glutamate (Glu) mediated neurotoxicity. The concentrations of TCa and Ca 2+ i were measured in 32 cortical neuron cultures, which were divided into four groups: normal control group ( n =8); 0.5 mmol/L Glu group (Glu group n =8); 0.5 mmol/L Glu+100 mmol/L Nimodipine group (antagonist Ⅰ, n =8); 0.5mmol/L Glu+12μmol/L MK 801 group (antagonist Ⅱ, n =8). The results showed that TCa and Ca 2+ i concentrations in Glu group were significantly higher than those in normal control group ( P <0.05); TCa and Ca 2+ i in both antagonist Ⅰ and Ⅱ groups were evidently lower than those in Glu group ( P <0.05); No difference was found between antagonist Ⅰ and Ⅱ groups. The results suggest that Glu neurotoxicity is due to the intracellular calcium overload, which may be from the pathway of voltage dependent calcium channels (VDCCs) and NMDA receptor operated channels (NROCs).更多还原