Saito M, Macala L J, Roth G A, Bornstein M B, Yu R K
Exp Neurol. 1986 Jun;92(3):752-6. doi: 10.1016/0014-4886(86)90314-6.
To examine the effect of antiglycolipid antibodies on demyelination, myelinated cultures of embryonic mouse spinal cords were treated by antigalactocerebroside (anti-GC), anti-GM1; and anti-GM4 antisera, and the lipid composition of the cultures were studied. The anti-GC antiserum-treated cultures, which exhibited severe morphologic signs of demyelination, revealed a significant reduction of cerebroside. The anti-GM4 or anti-GM1 antiserum-treated cultures, which exhibited mild degrees of demyelination, also had low contents of cerebroside. These results support our previous data showing that antiglycolipid antibodies cause demyelination in cultured mouse spinal cords, and suggest a possible role of myelin-specific glycolipids in the demyelination process.
为研究抗糖脂抗体对脱髓鞘的影响,用抗半乳糖脑苷脂(抗 - GC)、抗GM1和抗GM4抗血清处理胚胎小鼠脊髓的有髓培养物,并研究培养物的脂质组成。抗GC抗血清处理的培养物表现出严重的脱髓鞘形态学迹象,其脑苷脂显著减少。抗GM4或抗GM1抗血清处理的培养物表现出轻度脱髓鞘,其脑苷脂含量也较低。这些结果支持我们之前的数据,即抗糖脂抗体可导致培养的小鼠脊髓脱髓鞘,并提示髓鞘特异性糖脂在脱髓鞘过程中可能发挥作用。