兴奋性氨基酸类神经毒剂与粉防己碱（ｔｅｔｒａｎｄｒｉｎｅ，Ｔｅｔ）共同作用于原代培养胎鼠大脑皮层神经元２４小时，发现１０７，１０６ｍｏｌ·Ｌ１Ｔｅｔ明显降低５０μｍｏｌ·Ｌ１谷氨酸（ｇｌｕｔａｍａｔｅ，Ｇｌｕ），３００μｍｏｌ·Ｌ１βＮｍｅｔｈｙｌａｍｉｎｏＬａｌａｎｉｎｅ（ＢＭＡＡ，ＮＭＤＡ受体激动剂）和２０μｍｏｌ·Ｌ１βＮｏｘａｌｙｌａｍｉｎｏＬａｌａｎｉｎｅ（ＢＯＡＡ，ｎｏｎＮＭＤＡ受体激动剂）导致的培养液乳酸脱氢酶（ｌａｃｔａｔｅｄｅｈｙｄｒｏｇｅｎａｓｅ，ＬＤＨ）活性的增高；细胞形态损害减轻，细胞数量增加。对２０μｍｏｌ·Ｌ１ＮＭＤＡ介导的神经元损伤改变无影响。提示Ｔｅｔ对某些Ｇｌｕ类神经毒剂引起的胎鼠大脑皮层神经元损伤有一定保护作用，其机制可能是抑制细胞膜上的Ｎａ＋通道开放，阻止膜去极化而影响电压依赖性Ｃａ２＋通道启动。对ＮＭＤＡ受体可能亦有一定作用。 Excitatory amino acid neurotoxicants and tetrandrine (Tet) acted on the primary cultured rat cortical neurons for 24 hours and found that 10 −7,10 −6 mol·L1Tet significantly reduced 50 μmol·L1 valleys. Glutamate (Glu), 300μmol·L1βNmethylaminoLalanine (BMAA, NMDA receptor agonist) and 20μmol·L1βNoxalylaminoLalanine (BOAA, nonNMDA) Receptor agonists) increase the activity of lactate dehydrogenase (LDH) in the culture medium; the damage of cell morphology is reduced and the number of cells increases. There was no effect on the changes of neuronal damage mediated by 20 μmol·L-1 NMDA. It is suggested that Tet protects fetal cerebral cortical neurons from damage caused by certain Glu neurotoxic agents. The mechanism may be to inhibit the opening of Na+ channels on the cell membrane and prevent membrane depolarization and affect the initiation of voltage-dependent Ca2+ channels. May also have a role in NMDA receptors.