Sima A A, Hay K
Neuropathol Appl Neurobiol. 1981 Sep-Oct;7(5):341-50. doi: 10.1111/j.1365-2990.1981.tb00237.x.
Electrophysiological features were studied longitudinally in the spontaneously diabetic insulin-dependent, BB-Wistar rat. These were correlated in time with the state of the patency of the protective barriers in peripheral nerves. Motor nerve conduction velocity was significantly slowed only 3 weeks after the onset of the diabetes. When ultrastructural changes began, the maximal conduction velocity was further diminished. The amplitudes of evoked muscle potentials and distal latencies were significantly altered in diabetic rats. No change in the permeability of the blood-nerve barrier could be demonstrated before, during or after the onset of the nerve conduction defect. The possible pathogenetic mechanisms are discussed and a possible mechanism is suggested, namely a reduced availability of energy to axons in diabetes.
对自发性糖尿病胰岛素依赖型BB-Wistar大鼠的电生理特征进行了纵向研究。这些特征与外周神经保护屏障的通畅状态在时间上相关。糖尿病发病仅3周后，运动神经传导速度就显著减慢。当超微结构改变开始时，最大传导速度进一步降低。糖尿病大鼠诱发肌肉电位的幅度和远端潜伏期显著改变。在神经传导缺陷发生之前、期间或之后，均未发现血神经屏障通透性有变化。文中讨论了可能的发病机制，并提出了一种可能的机制，即糖尿病时轴突能量供应减少。
