Rosenbluth J, Hasegawa M, Schiff R
Department of Physiology, New York University School of Medicine, New York 10016.
Neurosci Lett. 1989 Feb 13;97(1-2):35-40. doi: 10.1016/0304-3940(89)90135-3.
Previous studies of the myelin-deficient rat spinal cord have suggested that astrocytes may play a role in preventing the formation of myelin in this mutant, or causing its breakdown. Comparison of mutant and normal littermate spinal cords shows a marked hypertrophy of astrocytes in the mutant in both gray matter and fiber tract regions. Nevertheless, when normal fetal spinal cord fragments are transplanted into mutant host spinal cord, clusters of normal-looking myelin sheaths develop with no sign of attack by host astrocytes.
先前对髓磷脂缺乏大鼠脊髓的研究表明，星形胶质细胞可能在该突变体中阻止髓磷脂形成或导致其分解方面发挥作用。对突变体和正常同窝出生大鼠脊髓的比较显示，突变体的灰质和纤维束区域的星形胶质细胞均有明显肥大。然而，当将正常胎儿脊髓片段移植到突变体宿主脊髓中时，会形成外观正常的髓鞘簇，且没有宿主星形胶质细胞攻击的迹象。
