Weiss J H, Sensi S L, Koh J Y
University of California, Irvine, CA 92697-4292, USA.
Trends Pharmacol Sci. 2000 Oct;21(10):395-401. doi: 10.1016/s0165-6147(00)01541-8.
Zn(2+) 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.
锌离子（Zn(2+)）是人体中第二丰富的微量元素，在哺乳动物大脑中的浓度尤其高。尽管锌离子是所有组织中许多酶的辅助因子，但脑内锌离子的一个独特特征是其在突触前终末的囊泡定位，其释放依赖于神经活动。虽然突触锌离子释放的生理意义尚不清楚，但它可能在突触传递中起调节作用。此外，有几条证据支持这样的观点，即突触锌离子过度释放时，其在突触后神经元中的积累会导致与某些急性病症（包括癫痫和短暂性全脑缺血）相关的选择性神经元丢失。更具推测性的是，锌离子稳态失衡也可能导致一些退行性病症，包括阿尔茨海默病。进一步阐明锌离子在大脑中的病理作用应能带来针对这些病症的新治疗方法。
