Assaf S Y, Chung S H
Nature. 1984;308(5961):734-6. doi: 10.1038/308734a0.
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 disease, Pick's disease and epileptic seizures. 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 formation, and it is the postsynaptic neurones of these fibres which are most susceptible to the toxic effects of kainic acid, a potent convulsant, or to chronic exposure to organometallic compounds. Here we demonstrate for the first time that Zn2+ is released into the extracellular space during excitation of hippocampal slices.
二价过渡金属离子在神经功能中的作用尚不清楚。过量时，这些离子与诸如威尔逊氏病、匹克氏病和癫痫发作等神经疾病有关。我们认为，神经末梢中含有的锌离子在神经元活动期间被挤出到细胞外空间。在强烈的神经元激活过程中可能会释放出过量的锌，并导致所观察到的发作和毒性损伤。锌离子在海马结构的苔藓纤维中高浓度存在，而这些纤维的突触后神经元最易受到强力惊厥剂 kainic 酸的毒性作用或长期接触有机金属化合物的影响。在此，我们首次证明在海马切片兴奋期间 Zn2+ 释放到细胞外空间。
