Brismar T
Metabolism. 1983 Jul;32(7 Suppl 1):112-7. doi: 10.1016/s0026-0495(83)80023-7.
The spontaneously diabetic rat gets a decreased motor-nerve conduction velocity after the onset of diabetes as compared with age- and weight-matched controls. This finding has indicated that these rats develop a neuropathy; but morphological investigations have failed to show structural abnormalities that could explain the decrease in conduction velocity. Measurements of the nervous function revealed a decreased excitability of isolated fibers from sciatic nerves of rats with diabetes duration ranging from 18 days to 6 months. Voltage-clamp analysis of the membrane of the node of Ranvier showed (1) decreased Na-equilibrium potential, reflecting an axoplasmic Na accumulation; (2) decreased specific Na permeability, related both to an increased inactivation of the permeability of the resting node and also a decreased permeability when inactivation had been removed by hyperpolarization of the membrane; and (3) in some nodes a marked increase in the delayed K permeability, which is an early sign of paranodal demyelination. The decrease in Na permeability was the most important factor for the decreased nodal excitability and the decreased conduction velocity. This mechanism may also be involved in the reversible dysfunction found in human diabetic neuropathy.
与年龄和体重匹配的对照相比，自发性糖尿病大鼠在糖尿病发病后运动神经传导速度降低。这一发现表明这些大鼠发生了神经病变；但形态学研究未能显示出可解释传导速度降低的结构异常。神经功能测量显示，糖尿病病程从18天到6个月的大鼠坐骨神经分离纤维的兴奋性降低。对郎飞结膜的电压钳分析显示：（1）钠平衡电位降低，反映轴浆钠蓄积；（2）比钠通透性降低，这与静息结通透性的失活增加以及通过膜超极化去除失活后通透性降低有关；（3）在一些结中，延迟钾通透性显著增加，这是结旁脱髓鞘的早期迹象。钠通透性降低是结兴奋性降低和传导速度降低的最重要因素。这种机制可能也参与了人类糖尿病神经病变中发现的可逆性功能障碍。
