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体外剥夺葡萄糖对大鼠颈上神经节超微结构和功能的影响。

The effect of deprivation of glucose on the ultrastructure and function of the superior cervical ganglion of the rat in vitro.

作者信息

Nicolescu P, Dolivo M, Rouiller C, Foroglou-Kerameus C

出版信息

J Cell Biol. 1966 May;29(2):267-85. doi: 10.1083/jcb.29.2.267.

Abstract

The superior cervical sympathetic ganglion of the rat kept in vitro in a bicarbonate-buffered Krebs' solution retains its capacity for synaptic transmission and axonal conduction during more than 36 hr. After glucose withdrawal, synaptic transmission is lost in 2(1/2) hr and this loss is irreversible; on the other hand, axonal conduction can still be measured on the postganglionic nerve for more than 24 hr after glucose deprivation. Electrophysiological measurements as well as electron microscope studies revealed specific changes at the level of the presynaptic terminal processes, while the ganglion cells and the satellite cells remained relatively unaltered. The presynaptic lesion due to lack of glucose can be prevented by keeping the preparation in vitro at 6 degrees C. This strongly suggests that this lesion results from a major disturbance of the metabolism of the presynaptic fibers.

摘要

在碳酸氢盐缓冲的克雷布斯溶液中体外保存的大鼠颈上神经节,在超过36小时的时间内保持其突触传递和轴突传导能力。葡萄糖撤除后,2.5小时内突触传递丧失且这种丧失是不可逆的;另一方面,在葡萄糖剥夺后,节后神经上的轴突传导仍可测量超过24小时。电生理测量以及电子显微镜研究揭示了突触前终末过程水平的特定变化,而神经节细胞和卫星细胞保持相对未改变。通过将制剂在体外6摄氏度保存,可防止因缺乏葡萄糖导致的突触前损伤。这强烈表明这种损伤是由突触前纤维代谢的重大紊乱引起的。

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