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作者通过动物实验发现,在造成大鼠短暂性前脑缺血后,Zn~(2+)首先聚集在传出神经轴突末端,然后汇集在变性中的神经细胞内如海马、大脑皮质、视丘、纹状体、杏仁核等处。Zn~(2+)的聚集和转移作用是神经细胞死亡的一个原因或为一标志性的物质尚不太清楚。 作者用特殊荧光染色法观察了实验性大鼠前脑缺血后不同时间内神经细胞的变化。发现不同部位的神经细胞在出现退行性变之前,已出现Zn~(2+)在神经细胞内聚集现象。 为了阻止细胞外的Zn~(2+)聚集进入轴突后神经元,作者在对动物造成脑缺血前30分钟,先用Ca—EDTA注射到侧脑室,结果注射后大鼠锥体细胞内Zn~(2+)的聚集显著减少,且细胞变性亦较轻。提示传统脑缺血所引
Through animal experiments, we found that after transient forebrain ischemia in rats, Zn ~ (2+) first accumulates in the extremities of axons, and then accumulates in degenerative nerve cells such as hippocampus, cerebral cortex, Mound, striatum, amygdala and other places. Zn ~ (2+) aggregation and metastasis is one of the causes of nerve cell death or as a landmark substance is not yet clear. The authors observed the change of neural cells in different time after forebrain ischemia in experimental rats by special fluorescent staining. Found in different parts of the nerve cells in the emergence of degenerative changes before, Zn ~ (2 +) has been found in nerve cells in the phenomenon of aggregation. In order to prevent the accumulation of extracellular Zn 2+ into neurons in the axon, the animals were injected with Ca-EDTA into the lateral ventricle 30 minutes before the onset of cerebral ischemia. The rats were then injected with pyramidal cells Zn 2+ accumulation was significantly reduced, and cell degeneration was also lighter. Prompted by the traditional cerebral ischemia