AMPA受体
神经毒性
红藻氨酸受体
NMDA受体
谷氨酸的
谷氨酸受体
化学
毒性
长时程增强
锌毒性
细胞外
致电离效应
药理学
生物物理学
受体
神经科学
细胞生物学
生物
生物化学
有机化学
作者
John H. Weiss,Dean M. Hartley,Jae‐Young Koh,Dennis W. Choi
出处
期刊:Neuron
[Elsevier]
日期:1993-01-01
卷期号:10 (1): 43-49
被引量:255
标识
DOI:10.1016/0896-6273(93)90240-r
摘要
Extracellular Zn2+ attenuates NMDA receptor-mediated neurotoxicity and increases AMPA receptor-mediated toxicity. Known electrophysiological effects of Zn2+ predict only the former. We considered the possibility that the latter rather reflects AMPA potentiation of Zn2+ toxicity, perhaps mediated by neuronal depolarization and Zn2+ entry through voltage-gated Ca2+ channels. High K+ or kainate also potentiated Zn2+ toxicity, and AMPA plus Zn2+ toxicity was attenuated by raising extracellular Ca2+, or by Ca2+ channel blockers. AMPA plus Zn2+ exposure induced an increase in fluorescence from neurons loaded with the Zn(2+)-sensitive dye TS-Q and increased subsequent 45Ca2+ accumulation. The ability of AMPA receptor activation to potentiate Zn2+ toxicity may be relevant to neuronal death associated with intense activation of glutamatergic pathways.
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