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目的 研究谷氨酸 (glutamate,Glu)触发大鼠大脑皮质神经元Ca2 + 内流特性 ,蛋白酪氨酸激酶 (PTK)抑制剂genistein及蛋白酪氨酸磷酸酶 (PTP)抑制剂vanadate对其影响 ,揭示PTK与Glu触发大鼠大脑皮质神经元Ca2 + 内流的内在联系。方法 采用Fura 2 /AM荧光测定胞浆Ca2 + 变化技术 ,在原代培养的大鼠大脑皮质神经元上观察药物对Glu触发Ca2 + 内流的影响。结果 Glu触发的Ca2 + 内流不受电压依赖性钙通道 (VDCC)阻断剂尼莫地平影响 ,亦不受非VDCC阻断剂SK&F96 36 5影响 ,但可被PTK抑制剂genis tein抑制 ,被PTP抑制剂vanadate增强。genistein(1～ 30μmol·L-1)呈浓度依赖性抑制Glu触发的Ca2 + 内流。vana date则浓度依赖性增强Glu触发的Ca2 + 内流。结论 对尼莫地平敏感的VDCC及对SK&F96 36 5敏感的非VDCC没有参与Glu触发的Ca2 + 内流。PTK激活参与了Glu触发的Ca2 + 内流
Objective To investigate the effects of glutamate (Glu) on Ca2 + influx, genistein inhibitor of protein tyrosine kinase (PTK) and vanadate inhibitor of protein tyrosine phosphatase (PTP) in rat cerebral cortex neurons , Revealing the intrinsic relationship between PTK and Glu trigger Ca2 + influx in rat cerebral cortical neurons. Methods The changes of Ca2 + in cytoplasm were detected by Fura 2 / AM fluorescence. The effect of Glu on Ca2 + influx was observed in primary cultured rat cortical neurons. Results Glu-triggered Ca 2+ influx was not affected by voltage-dependent calcium channel (VDCC) blocker Nimodipine nor was it affected by the non-VDCC blocker SK & F96 36 5 but inhibited by the PTK inhibitor genistein PTP inhibitor vanadate enhanced. Genistein (1 ~ 30μmol·L-1) inhibited Glu-triggered Ca2 + influx in a concentration-dependent manner. vana date increased Glu-triggered Ca2 + influx in a concentration-dependent manner. Conclusion VDCC sensitive to nimodipine and non-VDCC sensitive to SK & F96 365 were not involved in Glu-triggered Ca2 + influx. PTK activation is involved in Glu-triggered Ca2 + influx