神经科学
中枢神经系统
谷氨酸的
平衡
肌萎缩侧索硬化
神经调节
缺锌(植物性疾病)
神经退行性变
神经系统
锌
生物
突触可塑性
锌毒性
谷氨酸受体
疾病
医学
化学
内分泌学
病理
受体
有机化学
生物化学
作者
Byron K.Y. Bitanihirwe,Miles G. Cunningham
出处
期刊:Synapse
[Wiley]
日期:2009-07-20
卷期号:63 (11): 1029-1049
被引量:236
摘要
Abstract Zinc is a life‐sustaining trace element, serving structural, catalytic, and regulatory roles in cellular biology. It is required for normal mammalian brain development and physiology, such that deficiency or excess of zinc has been shown to contribute to alterations in behavior, abnormal central nervous system development, and neurological disease. In this light, it is not surprising that zinc ions have now been shown to play a role in the neuromodulation of synaptic transmission as well as in cortical plasticity. Zinc is stored in specific synaptic vesicles by a class of glutamatergic or “gluzinergic” neurons and is released in an activity‐dependent manner. Because gluzinergic neurons are found almost exclusively in the cerebral cortex and limbic structures, zinc may be critical for normal cognitive and emotional functioning. Conversely, direct evidence shows that zinc might be a relatively potent neurotoxin. Neuronal injury secondary to in vivo zinc mobilization and release occurs in several neurological disorders such as Alzheimer's disease and amyotrophic lateral sclerosis, in addition to epilepsy and ischemia. Thus, zinc homeostasis is integral to normal central nervous system functioning, and in fact its role may be underappreciated. This article provides an overview of zinc neurobiology and reviews the experimental evidence that implicates zinc signals in the pathophysiology of neuropsychiatric diseases. A greater understanding of zinc's role in the central nervous system may therefore allow for the development of therapeutic approaches where aberrant metal homeostasis is implicated in disease pathogenesis. Synapse 63:1029–1049, 2009. © 2009 Wiley‐Liss, Inc.
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