Nukada H, Dyck P J, Low P A, Lais A C, Sparks M F
J Neuropathol Exp Neurol. 1986 Mar;45(2):140-50. doi: 10.1097/00005072-198603000-00004.
Feeding galactose to rats induces nerve conduction abnormalities, increased levels of nerve galactitol, endoneurial edema, elevated pressure and hypoxia of endoneurial fluid, and pathological abnormalities of nerve fibers. To investigate the cellular mechanisms of the fiber lesions and their possible relationship to alterations in the nerve microenvironment, rat peroneal nerves were morphometrically evaluated eight months after the commencement of galactose feeding. Whereas the density of neurofilaments (NF/micron2) in the transverse axonal area of myelinated fibers was not significantly different between the nerves of galactose-fed and control rats, axonal areas and the number of NF/axon, when related to myelin spiral length, were significantly less in nerves of galactose-fed rats. Myelin alterations, characteristic of axonal atrophy, were also significantly increased. The present data provide evidence of a proportionate decrease in axonal caliber and the number of NF/axon in myelinated fibers in experimental galactose neuropathy, suggesting that galactose induces fibers in experimental galactose neuropathy, suggesting that galactose induces either decreased NF synthesis, assembly or transport. The possible role of microenvironmental alterations, including endoneurial hypoxia and hyperosmolarity, in the production of this axonal atrophy is discussed.
给大鼠喂食半乳糖会诱发神经传导异常、神经半乳糖醇水平升高、神经内膜水肿、神经内膜液压力升高和缺氧以及神经纤维的病理异常。为了研究纤维病变的细胞机制及其与神经微环境改变的可能关系，在开始喂食半乳糖八个月后，对大鼠腓总神经进行了形态计量学评估。虽然喂食半乳糖的大鼠神经与对照大鼠神经相比，有髓纤维横断轴突区域的神经丝密度（NF/平方微米）没有显著差异，但与髓鞘螺旋长度相关的轴突区域和每个轴突的NF数量，在喂食半乳糖的大鼠神经中显著减少。具有轴突萎缩特征的髓鞘改变也显著增加。目前的数据表明，在实验性半乳糖神经病中，有髓纤维的轴突直径和每个轴突的NF数量成比例减少，这表明半乳糖在实验性半乳糖神经病中诱导纤维病变，提示半乳糖诱导NF合成、组装或运输减少。本文讨论了包括神经内膜缺氧和高渗在内的微环境改变在这种轴突萎缩产生中的可能作用。
