Alterations in Retrograde Axonal Transport in Streptozocin-Induced Diabetic Rats
Alterations in Retrograde Axonal Transport in Streptozocin-Induced Diabetic Rats
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DOI：
10.2337/diab.36.9.996
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发表时间：
1987-09
期刊：
影响因子：
7.7
通讯作者：
D. Fink;D. Purkiss;M. Mata
中科院分区：
文献类型：
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作者：
D. Fink;D. Purkiss;M. Mata
用[~ 3 H] N-琥珀酰亚胺基丙酸酯（[~ 3 H]NSP）法研究了链脲佐菌素诱导的糖尿病大鼠坐骨神经轴突逆行运输。在[3 H] NSP注射后1天，大鼠背根神经节和脊髓前角中逆行转运标记蛋白的积累与注射[3 H] NSP后1天或14天的糖尿病大鼠的对照组无统计学显著差异。然而，在相同的时间点，[3 H]NSP注射后7天标记蛋白在背根神经节中的积累减少了35%，[3 H]NSP注射后7天向脊髓前角的转运减少了70%。用胰岛素部分控制糖尿病导致这些缺陷的部分逆转。早期发生的逆行运输缺陷表明，这种缺陷可能在神经病变的发病机制中发挥作用。
Retrograde axonal transport in the sciatic nerve of rats with streptozocin-induced diabetes was studied by the [3H]N-succinimidyl propionate ([3H]NSP) method. The accumulation of retrogradely transported labeled proteins in the dorsal root ganglia and the ventral horn of spinal cord 1 day after [3H]NSP injection was not statistically significantly different from controls in rats diabetic for 1 or 14 days at the time of [3H]NSP injection. However, accumulation of labeled proteins in the dorsal root ganglia 7 days after [3H]NSP injection was reduced by 35% and transport to the ventral horn of spinal cord 7 days after [3H]NSP injection was reduced by 70% at the same time points. Partial control of the diabetes with insulin resulted in a partial reversal of these deficits. The early occurrence of defects in retrograde transport suggests that such defects may play a role in the pathogenesis of the neuropathy.