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目的研究谷氨酸对神经细胞的毒性作用及其作用机制。方法取体外培养的胎鼠大脑皮层神经，分组加入不同浓度的谷氨酸、Ｎ－甲基－Ｄ－天冬氨酸（ＮＭＤＡ）或海藻酸（ＫＡ），ＤＬ－２－ａｍｉｎｏ－５－ｐｈｏｓｐｈｏｎｏｖａｌｅｒｉｃａｃｉｄ（ＡＰＶ）、４－Ｈｙｄｒｏｘｙｑｕｉｎｏｌｉｎｅ－２－ｃａｒｂｏｘｙｌｉｃａｃｉｄｈｙｄｒａｔｅ（ＨＱＣＡ），作用３０ｍｉｎ，２４ｈ后测定培养液内乳酸脱氢酶（ＬＤＨ）含量，并用苔盼蓝鉴定神经细胞活性。结果与空白对照组比较，加入谷氨酸组细胞培养内ＬＨＤ以及神经细胞蓝染率均显著增加（Ｐ＜０．０１），且其程度与加入的药物剂量成正相关。谷氨酸ＬＤ５０为５１．１０±４．２９μｍｏｌ／Ｌ，与ＮＭＤＡ（６６．１７±６．２０μｍｏｌ／Ｌ）相似，但显著低于ＫＡ（１７２．８０±１６．４０μｍｏｌ／Ｌ）。ＡＰＶ或ＨＱＣＡ能显著抑制谷氨酸所致的ＬＤＨ增加。结论谷氨酸的确具有神经毒性作用，这种作用可能主要是通过ＮＭＤＡ受体介导的
Objective To study the toxic effect of glutamate on nerve cells and its mechanism. Methods Cultured fetal rat cerebral cortical neurons were cultured in vitro with different concentrations of glutamic acid, N-methyl-D-aspartic acid (NMDA) or alginate (KA), DL-2-amino-5-phosphonovaleric acid (APV) and 4-Hydroxyquinoline-2-carboxylic acid (HQCA) for 30min and 24h respectively. The content of lactate dehydrogenase (LDH) in the culture medium was determined and the activity of neurons was identified by trypan blue. Results Compared with the blank control group, the LHD and the blue staining rate of neurons in the cell culture with glutamate increased significantly (P <0.01), and the degree was positively correlated with the dosage of the drug. The LD50 of glutamate was 51.10 ± 4.29μmol / L, which was similar to that of NMDA (66.17 ± 6.20μmol / L) but lower than that of KA (172.80 ± 16.40μmol / L). APV or HQCA significantly inhibited glutamate induced LDH increase. Conclusion Glutamate does have neurotoxicity, which may be mainly mediated by NMDA receptors