Abnormal axonal inward rectifier in streptozocin-induced experimental diabetic neuropathy.
Abnormal axonal inward rectifier in streptozocin-induced experimental diabetic neuropathy.
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链佐星诱导的实验性糖尿病神经病变中轴突向内整流异常。
DOI：
10.1093/brain/124.6.1149
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
H. Bostock
中科院分区：
文献类型：
--
作者：
Qing Yang;Ryuji Kaji;Tsunekazu Takagi;N. Kohara;N. Murase;Yuichiro Yamada;Yutaka Seino;H. Bostock
为了探讨糖尿病神经病变的病理生理学，我们采用阈值电紧张（TE）技术研究了 20 只患有链佐星诱导糖尿病的成年 Wistar 大鼠的轴突兴奋性的一系列变化。出现持续高血糖后，将大鼠分为两组：9 只喂食含有醛糖还原酶抑制剂（依帕司他 30 mg/kg/天）的饮食（ARI（+）组），11 只喂食不含抑制剂的饮食（ARI（-）组）。还对八只年龄相似的正常对照大鼠（NC 组）进行了研究。我们使用 TE 监测尾部运动轴突的膜特性 3 个月，以测量阈下极化电流引起的兴奋性变化，同时记录尾部肌肉的复合肌肉动作电位 (CMAP)。注射链佐星1个月后，ARI(-)组的CMAP潜伏期显着增加，3个月后，与NC组相比，超极化100毫秒后的兴奋性显着降低。通过注射氯化铯（一种内向整流抑制剂）再现了 TE 的类似变化。相比之下，ARI(+) 组在 3 个月时没有表现出 TE 或潜伏期的显着变化，尽管他们表现出显着的体重减轻和高血糖。这些发现表明，在实验模型中，内向整流会减少，就像在人类糖尿病中一样，而用 ARI 阻断多元醇途径可以防止这种减少。向内整流的减少会增强由活动依赖性超极化引起的传导阻滞，并且可能是糖尿病神经病变早期阶段振动感觉减弱的基础。
In order to explore the pathophysiology of diabetic neuropathy, we studied serial changes of axonal excitability in 20 adult Wistar rats with streptozocin-induced diabetes using the technique of threshold electrotonus (TE). After persistent hyperglycaemia had developed, rats were divided into two groups: nine were fed a diet containing aldose reductase inhibitor (Epalrestat 30 mg/kg/day) (ARI(+) group) and 11 were fed a diet without the inhibitor (ARI(-) group). Eight normal control rats of similar age (NC group) were also studied. We monitored membrane properties of motor axons in the tail for 3 months using TE to measure the changes in excitability induced by subthreshold polarizing currents while recording compound muscle action potentials (CMAPs) in the tail muscle. The ARI(-) group showed a significant increase in CMAP latency 1 month after streptozocin injection, and by 3 months there was significantly lower excitability after hyperpolarization for 100 ms compared with the NC group. A similar change in TE was reproduced by injection of caesium chloride, an inhibitor of inward rectification. By contrast, the ARI(+) group exhibited no significant change in TE or latency at 3 months, although they showed significant body weight loss and hyperglycaemia. These findings indicate that inward rectification is reduced in an experimental model, as in human diabetes, and that blocking the polyol pathway with an ARI prevents this reduction. Reduced inward rectification potentiates conduction block caused by activity-dependent hyperpolarization and may underlie the decreased vibratory sensation seen in the early stage of diabetic neuropathy.
糖尿病神经病变中皮肤传入的特性。
DOI：
10.1093/brain/112.5.1359
发表时间：
1989
期刊：
Brain : a journal of neurology
影响因子：
--
作者：
Mackel,R
通讯作者：
Mackel,R
长期醛糖还原酶抑制（ponalrestat）对自发性糖尿病生物育种大鼠神经传导和腓肠神经结构的预防作用。
DOI：
10.1172/jci114585
发表时间：
1990
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
Sima,AA;Prashar,A;Zhang,WX;Chakrabarti,S;Greene,DA
通讯作者：
Greene,DA