Brismar T, Sima A A
Acta Physiol Scand. 1981 Dec;113(4):499-506. doi: 10.1111/j.1748-1716.1981.tb06928.x.
Single myelinated nerve fibres were isolated from the sciatic nerves of the spontaneously diabetic BB-Wistar rat after 17-185 days of overt diabetes. Pronounced demyelination and paranodal changes were found in one rat (diabetes duration 185 days), the others had no structural changes that could be detected light-microscopically. Potential clamp analysis of these fibres showed a decreased Na equilibrium potential (UNa), decreased Na currents caused by large inactivation, and a specific increase in the K-permeability. Measurements with high-K solution outside the node revealed that the decreased UNa was caused by high axoplasmic [Na]. Fibres with increased K-permeability had, in addition, increased nodal leak conductance. Decreased excitability was found in the majority of the fibres and was related to the permeability changes. The present findings indicate that axonal dysfunction (Na-accumulation and inactivation of the Na-permeability) precede the changes (increased K-permeability) related to paranodal demyelination.
在明显糖尿病状态持续17 - 185天后，从自发糖尿病BB - Wistar大鼠的坐骨神经中分离出单根有髓神经纤维。在一只大鼠（糖尿病病程185天）中发现了明显的脱髓鞘和结旁改变，其他大鼠在光学显微镜下未检测到结构变化。对这些纤维进行的电压钳分析显示，钠平衡电位（UNa）降低，由大量失活导致钠电流降低，以及钾通透性特异性增加。在结外使用高钾溶液进行测量表明，UNa降低是由高轴浆[Na]引起的。此外，钾通透性增加的纤维结漏电导也增加。在大多数纤维中发现兴奋性降低，这与通透性变化有关。目前的研究结果表明，轴突功能障碍（钠积累和钠通透性失活）先于与结旁脱髓鞘相关的变化（钾通透性增加）出现。
