链脲佐菌素诱导的糖尿病大鼠中结构蛋白轴突运输减少。
Decreased axonal transport of structural proteins in streptozotocin diabetic rats.
作者信息
Jakobsen J, Sidenius P
出版信息
J Clin Invest. 1980 Aug;66(2):292-7. doi: 10.1172/JCI109856.
Abstract
We have examined the various axonal transport rates in sciatic nerve of streptozotocin diabetic rats 3 h and 10,25, and 50 d after the injection of tritiated proline into the fifth lumbar dorsal root ganglion. Proline-labeled proteins conveyed by the slow transport system were advanced more slowly in diabetic rats. No compensation for this delay took place in terms of protein synthesis, half-life, or transported amount. The decreased deliverance of slowly transported proteins (structural proteins) to the axons may well account for the reduced axon calibre shown in earlier reports. A hypothesis is proposed suggesting that the primary event in the development of neurological abnormalities in diabetes is an impairment of the retrograde axonal transport, secondarily leading to the abnormality of the anterograde transport of structural proteins.
摘要
我们研究了链脲佐菌素诱导的糖尿病大鼠坐骨神经中不同的轴突运输速率，这些大鼠在将氚标记的脯氨酸注入第五腰段背根神经节后3小时以及10、25和50天。由慢速运输系统转运的脯氨酸标记蛋白在糖尿病大鼠中运输得更慢。在蛋白质合成、半衰期或运输量方面，并未对这种延迟进行补偿。向轴突缓慢运输的蛋白质（结构蛋白）的递送减少很可能是早期报告中所示轴突直径减小的原因。本文提出了一个假说，认为糖尿病神经病变发展过程中的主要事件是逆行轴突运输受损，继而导致结构蛋白顺行运输异常。
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