锌对培养的视网膜神经元谷氨酸神经毒性的保护作用。
Protective action of zinc against glutamate neurotoxicity in cultured retinal neurons.
作者信息
Kikuchi M, Kashii S, Honda Y, Ujihara H, Sasa M, Tamura Y, Akaike A
机构信息
Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
出版信息
Invest Ophthalmol Vis Sci. 1995 Sep;36(10):2048-53.
PURPOSE
To examine the effects of Zn2+ on glutamate-induced neurotoxicity in cultured retinal neurons.
METHODS
Primary cultures obtained from fetal rat retinas (16 to 19 days gestation) were used. The neurotoxic effects of excitatory amino acids were quantitatively assessed using the trypan blue exclusion method.
RESULTS
A brief exposure of retinal cultures to glutamate or N-methyl-D-aspartate (NMDA) induced delayed cell death. Zn2+ at concentrations of 3 to 30 microM ameliorated glutamate- and NMDA-induced neurotoxicity in a dose-dependent manner. By contrast, neurotoxicity induced by a 1-hour exposure to kainate was not affected by Zn2+.
CONCLUSIONS
These findings demonstrate that Zn2+ protects retinal neurons from NMDA receptor-mediated glutamate neurotoxicity.
目的
研究锌离子（Zn2+）对培养的视网膜神经元中谷氨酸诱导的神经毒性的影响。
方法
使用从胎鼠视网膜（妊娠16至19天）获得的原代培养物。采用台盼蓝排斥法对兴奋性氨基酸的神经毒性进行定量评估。
结果
视网膜培养物短暂暴露于谷氨酸或N-甲基-D-天冬氨酸（NMDA）会诱导延迟性细胞死亡。浓度为3至30微摩尔的Zn2+以剂量依赖的方式改善了谷氨酸和NMDA诱导的神经毒性。相比之下，暴露于海人藻酸1小时所诱导的神经毒性不受Zn2+的影响。
结论
这些发现表明，Zn2+可保护视网膜神经元免受NMDA受体介导的谷氨酸神经毒性的影响。
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