脑髓鞘异常或因接种神经节苷脂诱导出实验性自身免疫性多发性硬化样疾病的兔子。（注：原英文文本“Abnofmalities”拼写错误，正确应为“Abnormalities”）

Abnofmalities in brain myelin or rabbits with experimental autoimmune multiple sclerosis-like disease induced by immunization to gangliosides.

作者信息

Konat G, Offner H, Lev-Ram V, Cohen O, Schwartz M, Cohen I R, Sela B A

出版信息

Acta Neurol Scand. 1982 Nov;66(5):568-74. doi: 10.1111/j.1600-0404.1982.tb03144.x.

DOI:10.1111/j.1600-0404.1982.tb03144.x

Abstract

An experimental autoimmune multiple sclerosis-like disease (EAMSD) was induced in rabbits by immunizing them with bovine brain gangliosides. Forebrain myelin was isolated and fractionated on a discontinuous sucrose gradient into light myelin (LM, buoyant density less than or equal to 0.625 M), and heavy myelin (HM, buoyant density greater than 0.625 M). No abnormalities in either protein or lipid composition of EAMSD myelin fractions were observed. However, the EAMSD tissue yielded 31% less light and 39% more heavy myelin compared to the control brains. Thus, the HL/LM ratio was two-fold greater in experimental than in control myelin. This pathological pattern is similar to that which has been observed in myelin obtained from the brains of multiple sclerosis patients and from the optic nerves of rabbits with experimentally-induced demyelination.

摘要

通过用牛脑神经节苷脂免疫兔子，诱导出实验性自身免疫性多发性硬化样疾病（EAMSD）。分离前脑髓磷脂，并在不连续蔗糖梯度上分级分离为轻髓磷脂（LM，浮力密度小于或等于0.625 M）和重髓磷脂（HM，浮力密度大于0.625 M）。未观察到EAMSD髓磷脂组分的蛋白质或脂质组成有任何异常。然而，与对照脑相比，EAMSD组织产生的轻髓磷脂少31%，重髓磷脂多39%。因此，实验性髓磷脂中的HL/LM比值比对照髓磷脂大两倍。这种病理模式与在多发性硬化症患者大脑和实验性脱髓鞘兔子视神经中获得的髓磷脂中观察到的模式相似。