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离子通道与锌:神经毒性和神经退行性变的机制

Ion channels and zinc: mechanisms of neurotoxicity and neurodegeneration.

作者信息

Morris Deborah R, Levenson Cathy W

机构信息

Department of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32306 4300, USA.

出版信息

J Toxicol. 2012;2012:785647. doi: 10.1155/2012/785647. Epub 2012 May 7.

Abstract

Ionotropic glutamate receptors, such as NMDA, AMPA and kainate receptors, are ligand-gated ion channels that mediate much of the excitatory neurotransmission in the brain. Not only do these receptors bind glutamate, but they are also regulated by and facilitate the postsynaptic uptake of the trace metal zinc. This paper discusses the role of the excitotoxic influx and accumulation of zinc, the mechanisms responsible for its cytotoxicity, and a number of disorders of the central nervous system that have been linked to these neuronal ion channels and zinc toxicity including ischemic brain injury, traumatic brain injury, and epilepsy.

摘要

离子型谷氨酸受体,如N-甲基-D-天冬氨酸(NMDA)、α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)和海人藻酸受体,是配体门控离子通道,介导大脑中的大部分兴奋性神经传递。这些受体不仅结合谷氨酸,还受微量金属锌的调节并促进其突触后摄取。本文讨论了锌的兴奋毒性内流和积累的作用、其细胞毒性的机制,以及一些与这些神经元离子通道和锌毒性相关的中枢神经系统疾病,包括缺血性脑损伤、创伤性脑损伤和癫痫。

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