OTSUKA-LONG-EVANS-TOKUSHIMA FATTY糖尿病大鼠周围神经的结构蛋白改变

STRUCTURAL PROTEIN ALTERATIONS IN PERIPHERAL NERVE OF OTSUKA-LONG-EVANS-TOKUSHIMA FATTY DIABETIC RATS

为了解 Otsuka-Long-Evans-Tokushima Fatty( OLETF)糖尿病大鼠周围神经的结构蛋白改变 ,使用 OL ETF大鼠 10只/L ong-Evans-Tokushima-Otsuka( LETO)对照大鼠 6只 ,于糖尿病发病后 6个月取坐骨神经 ,制成冰冻切片和单纤维贴片 ,进行神经结构蛋白的免疫组织化学染色。在光镜下观察到 OLETF大鼠周围神经部分区域有结构异常。轴索结构中 ,Ranvier结区的钠离子通道蛋白密度降低并向结旁区移位 ,近结旁段的钾离子通道蛋白 ( Kv1.1)向 Ranvier结区和节间段弥散 ,神经丝着色浅淡且不均匀。髓鞘结构中 ,结旁段的髓鞘相关糖蛋白着色不均匀并向节间段弥散 ,致密髓鞘层的髓鞘碱性蛋白和 Schwann细胞表面的半乳糖脑苷脂基本正常。上述结果提示 Ranvier结区的轴膜和结旁段的髓鞘是 OL

In order to observe the structural protein alterations in peripheral nerves of Otsuka-Long-Evans-Tokushima Fatty(OLETF)diabetic rats, the sciatic nerves which were obtained from 10 OLETF rats and 6 control Long-Evans-Tokushima-Otsuka(LETO)rats in 6 months after onset of diabetes were sectioned on cryostat and teased into single fibers to prepare for immunohistochemistry. Some segments of the sciatic nerves in OLETF rats had lesions. The density of Na +-channel protein in Ranvier's node decreased and part of it displaced into paranode. Kv1.1-channel protein spread from juxtaparanode into Ranvier's node and internode and neurofilament degenerated. Myelin associated glycoprotein of paranode myelin decreased and migrated into internode. whereas myelin basic protein in compact myelin and glactocerebroside on Schwann's cell surface was kept intact. The results indicate that the lesion of peripheral nerve in OLTEF diabetic rats initiates from axonal membrane of Ranvier's node and myelin of paranode.