RELEASE OF ENDOGENOUS ZN-2+ FROM BRAIN-TISSUE DURING ACTIVITY
RELEASE OF ENDOGENOUS ZN-2+ FROM BRAIN-TISSUE DURING ACTIVITY
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DOI：
10.1038/308734a0
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发表时间：
1984-01-01
期刊：
影响因子：
64.8
通讯作者：
CHUNG, SH
中科院分区：
文献类型：
--
作者：
ASSAF, SY;CHUNG, SH
二价过渡金属离子在神经功能中的作用尚不清楚。过量时，这些离子与神经系统疾病有关，如威尔逊氏病、匹克氏病和癫痫发作。我们认为，锌离子，其中包含在神经末梢，挤压到细胞外空间在神经元活动。过量的锌可能在强烈的神经元激活期间释放，并有助于观察到的发作和毒性损伤。锌离子高浓度地存在于海马体的苔藓状纤维中，而正是这些纤维中的突触后神经元最容易受到强效惊厥剂凯尼克酸的毒性作用，或长期暴露于有机金属化合物中。在这里，我们首次证明了Zn2+在海马切片兴奋期间释放到细胞外空间。
The role of divalent transition metal ions in neural function is poorly understood. In excess, these ions are associated with neurological disorders such as Wilson's disease1, Pick's disease2and epileptic seizures3,4. We suggest that zinc ions, which are contained in nerve terminals, are extruded into the extracellular space during neuronal activity. Excessive levels of zinc may be released during intense neuronal activation, and contribute to the paroxysm and toxic damage observed. Zinc ions are contained in high concentrations in mossy fibres of the hippocampal formation5, and it is the postsynaptic neurones of these fibres which are most susceptible to the toxic effects of kainic acid6, a potent convulsant, or to chronic exposure to organometallic compounds7. Here we demonstrate for the first time that Zn2+is released into the extracellular space during excitation of hippocampal slices.