Zn<SUP>2+</SUP>:: A novel ionic mediator of neural injury in brain disease (vol 21, pg 395, 2000)

作     者：Weiss, JH Sensi, SL Koh, JY 

作者机构：UniversityofCaliforniaIrvineCA92697-4292USA.jweiss@uci.edu 

出 版 物：《TRENDS IN PHARMACOLOGICAL SCIENCES》 (药物科学趋势)

年 卷 期：2000年第21卷第12期

页      面：496-496页

核心收录：

学科分类：1007[医学-药学(可授医学、理学学位)] 10[医学] 

基　　金：National Institutes of Health, NIH, (AG00836, AG00919, NS30884) National Institute of Neurological Disorders and Stroke, NINDS, (R01NS036548) Ministry of Science and Technology, MOST 

主　　题：脑疾病/代谢 钙通道/代谢 神经变性疾病/病因学 神经变性疾病/代谢 神经元/代谢 突触前末梢/代谢 受体 N-甲基-D-天冬氨酸/代谢 信号传导/生理学 锌/代谢 锌/生理学 动物 人类 

摘      要：Zn2+ is the second most prevalent trace element in the body and is present in particularly large concentrations in the mammalian brain. Although Zn^2+ is a cofactor for many enzymes in all tissues, a unique feature of brain Zn^2+ is its vesicular localization in presynaptic terminals, where its release is dependent on neural activity. Although the physiological significance of synaptic Zn^2+ release is little understood, it probably plays a modulatory role in synaptic transmission. Furthermore, several lines of evidence support the idea that, upon excessive synaptic Zn^2+ release, its accumulation in postsynaptic neurons contributes to the selective neuronal loss that is associated with certain acute conditions, including epilepsy and transient global ischaemia. More speculatively, Zn^2+ dis-homeostasis might also contribute to some degenerative conditions, including Alzheimer s disease. Further elucidation of the pathological actions of Zn^2+ in the brain should result in new therapeutic approaches to these conditions.