Diaz M, Bornstein M B, Raine C S
Brain Res. 1978 Oct 13;154(2):231-9. doi: 10.1016/0006-8993(78)90697-2.
The presence of decomplemented anti-CNS antiserum profoundly affects myelinogenesis in cultured mouse embryo spinal cord. Light and electron microscope study has shown that oligodendroglia differentiate and produce an abundance of cell processes which surround the oligodendrocytes in a chaotic, disorganized array. Where the cell processes chance to meet, they form a kind of aberrant swollen myelin. Rarely, the oligodendroglial processes ensheath axons. For the most part, the available axons remain unmyelinated. On removal of the decomplemented antiserum, oligodendroglia differentiate and form normal myelin around the available axons. Myelination of peripheral nervous system (dorsal root ganglion) axons in the same preparations is unaffected by the presence of the antiserum. Thus, under these circumstances, the message from the neuron to the oligodendrocyte to make myelin is apparently intact, yet there is interference with the ability of the oligodendroglial cell process to find, attach to and encircle CNS axons with a normal myelin sheath.
去补体抗中枢神经系统抗血清的存在深刻影响培养的小鼠胚胎脊髓中的髓鞘形成。光镜和电镜研究表明，少突胶质细胞分化并产生大量细胞突起，这些突起以混乱、无序的排列围绕着少突胶质细胞。在细胞突起偶然相遇的地方，它们形成一种异常肿胀的髓磷脂。很少有少突胶质细胞突起包裹轴突。在大多数情况下，可用的轴突仍未髓鞘化。去除去补体抗血清后，少突胶质细胞分化并在可用轴突周围形成正常的髓磷脂。同一制剂中周围神经系统（背根神经节）轴突的髓鞘形成不受抗血清存在的影响。因此，在这些情况下，从神经元到少突胶质细胞产生髓磷脂的信号显然是完整的，但少突胶质细胞突起寻找、附着并以正常髓鞘包裹中枢神经系统轴突的能力受到了干扰。
