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利用原代培养的大鼠胎鼠皮层神经元 ,采用乳酸脱氢酶 (LDH)测定和32 P参入方法 ,研究谷氨酸 (Glu)对皮层神经元损伤 ,钙 /钙调蛋白依赖性蛋白激酶 (Ca MK )活性的影响及其机理 .Glu(50- 1 0 0 0μmol· L-1)作用 1 0 min,导致皮层神经元Ca MK 活性立即明显下降 ,神经元形态及 LDH释放早期无明显改变 ,2 4 h时 LDH释放显著增加 ,神经元损伤 .N-甲基 - D-天冬氨酸 (NMDA)受体拮抗剂地佐环平 (MK- 80 1 )明显降低 LDH释放 ,保护Ca MK 活性 ,而非 NMDA受体拮抗剂 6,7-二硝基喹口恶啉二酮 (DNQX)无保护作用 .去除胞外 Ca2 +可明显保护 Ca MK 活性 .Ca MK 抑制剂 KN- 62可明显拮抗 Ca MK 活性下降 ,部分保护神经元损伤 .结果提示 ,Glu兴奋毒引起皮层神经元迟发性损伤和 Ca MK 活性早期明显下降 ,主要由 NMDA受体介导和胞外 Ca2 +内流增加有关 .
Using primary cultured rat fetal rat cortical neurons, we examined the effects of glutamate (Glu) on cortical neurons, calcium / calmodulin-dependent protein kinase (Ca MK) activity and its mechanism.Glu (50-1 000μmol · L-1) for 10 min resulted in an immediate and significant decrease in Ca MK activity of cortical neurons and no significant change in neuronal morphology and early release of LDH , Release of LDH increased significantly at 24 h, and neuronal damage was inhibited.Diluzapine (MK- 80 1), an N-methyl-D-aspartate (NMDA) receptor antagonist, significantly reduced LDH release and protected Ca MK But not NMDA receptor antagonist 6,7-dinitroquiketone (DNQX), and the activity of Ca MK could be obviously protected by removing extracellular Ca 2+. Antagonizing the decrease of Ca-MK activity and partially protecting the neuronal injury.The results suggest that Glu excitotoxic induced delayed injury of cortical neurons and early decrease of Ca-MK activity mainly due to the increase of NMDA receptor-mediated and extracellular Ca2 + influx .