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目的:探讨谷氨酸通过(NMDA)受体对外向钾电流的影响以及引起神经元损伤的作用机制。方法:以分离出的孕18d SD大鼠胎鼠的皮层神经元作为实验对象,分为对照组和谷氨酸处理组,利用全细胞膜片钳的方法记录外向钾电流的变化,通过细胞形态学和TUNEL的方法分别观察谷氨酸处理后神经元的损伤情况。结果:谷氨酸能明显引起外向钾电流的增大,而NMDA受体抑制剂MK-801明显抑制由谷氨酸引起的外向钾电流的增大。形态学以及TUNEL实验研究表明,谷氨酸明显引起神经元的损伤(P<0.01),而MK-801、钾通道抑制剂TEA以及高浓度的外钾溶液能明显减缓由谷氨酸引起的细胞损伤(P<0.01)。结论:外向钾电流参与了谷氨酸引起的神经元的损伤,但其机制仍需进一步的探讨。
AIM: To investigate the effect of glutamate-mediated (NMDA) receptor on outward potassium current and the mechanism of neuronal damage. Methods: The cortical neurons isolated from pregnant rats of 18 d SD rats were divided into control group and glutamate-treated group. The changes of outward potassium current were recorded by whole-cell patch-clamp method. And TUNEL method were observed after glutamate treatment of neuronal damage. Results: Glutamate obviously induced the increase of outward potassium current, whereas NMDA receptor inhibitor MK-801 significantly inhibited the increase of outward potassium current induced by glutamate. Morphology and TUNEL experiments showed that glutamate obviously induced neuronal damage (P <0.01), while MK-801, potassium channel inhibitor TEA and high concentration of extra-potassium solution significantly slowed glutamate-induced cell death Injury (P <0.01). Conclusion: Outward potassium current is involved in glutamate-induced neuronal damage, but the mechanism remains to be further explored.