Fink D J, Purkiss D, Mata M
Diabetes. 1987 Sep;36(9):996-1000. doi: 10.2337/diab.36.9.996.
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.
采用[3H]N-琥珀酰亚胺丙酸酯([3H]NSP)法研究链脲佐菌素诱导的糖尿病大鼠坐骨神经中的逆行轴突运输。在注射[3H]NSP后1天,背根神经节和脊髓腹角中逆行运输的标记蛋白的积累,与在注射[3H]NSP时患糖尿病1天或14天的大鼠的对照组相比,在统计学上无显著差异。然而,在相同时间点,注射[3H]NSP后7天,背根神经节中标记蛋白的积累减少了35%,而注射[3H]NSP后7天向脊髓腹角的运输减少了70%。用胰岛素部分控制糖尿病可使这些缺陷部分逆转。逆行运输缺陷的早期出现表明,这些缺陷可能在神经病变的发病机制中起作用。