Bastmeyer M, Beckmann M, Schwab M E, Stuermer C A
Friedrich-Miescher-Laboratorium der Max-Planck-Gesellschaft, Tübingen, Germany.
J Neurosci. 1991 Mar;11(3):626-40. doi: 10.1523/JNEUROSCI.11-03-00626.1991.
Encounters of regenerating goldfish retinal axons with oligodendrocytes and CNS myelin of mammals and fish were monitored in in vitro assays. Upon contact with highly branched rat oligodendrocytes, goldfish axons collapsed or grew around but never crossed these cells. However, in the presence of the antibody IN-1 against the oligodendrocyte-associated growth-inhibitory proteins, axons did grow over highly branched oligodencrocytes. In contrast to the mammalian oligodendrocytes, goldfish optic nerve/tract-derived oligodendrocytelike cells allowed the growth of axons across their surface and even along their processes. The fish growth cones avoided entering the region of rat CNS myelin applied to polylysine/laminin-coated coverslips or failed to elongate on this substrate. They were, however, able to pass over CNS myelin of fish. When exposed to rat CNS myelin as the sole substrate, axonal outgrowth from fish retinal explants was inhibited almost entirely. However, outgrowth on fish CNS myelin was substantial, but many more axons extended on fish or rat brain membranes that were depleted of myelin. Thus, goldfish retinal axons are sensitive to the axon-growth-inhibiting cell-surface molecules of mammalian oligodendrocytes as well as CNS myelin. Fish optic nerve oligodendrocytelike cells and fish CNS myelin lack these inhibitory properties and are growth permissive. These in vitro experiments suggest that the success of axonal regeneration in the fish optic nerve is causally related to the presence of growth-permissive properties and to the absence of growth inhibitors on fish optic nerve/tract oligodendrocytelike cells.
在体外实验中监测了再生金鱼视网膜轴突与哺乳动物和鱼类少突胶质细胞及中枢神经系统髓磷脂的相互作用。金鱼轴突与高度分支的大鼠少突胶质细胞接触时，会发生塌陷或绕过这些细胞生长，但从不穿过它们。然而，在存在针对少突胶质细胞相关生长抑制蛋白的抗体IN-1的情况下，轴突确实会在高度分支的少突胶质细胞上生长。与哺乳动物少突胶质细胞不同，金鱼视神经/视束来源的少突胶质细胞样细胞允许轴突在其表面生长，甚至沿着其突起生长。鱼的生长锥避免进入涂有聚赖氨酸/层粘连蛋白的盖玻片上所施加的大鼠中枢神经系统髓磷脂区域，或者在该底物上无法伸长。然而，它们能够越过鱼类的中枢神经系统髓磷脂。当以大鼠中枢神经系统髓磷脂作为唯一底物时，金鱼视网膜外植体的轴突生长几乎完全受到抑制。然而，在鱼类中枢神经系统髓磷脂上的生长很显著，但更多的轴突在去除了髓磷脂的鱼类或大鼠脑膜上延伸。因此，金鱼视网膜轴突对哺乳动物少突胶质细胞以及中枢神经系统髓磷脂的轴突生长抑制性细胞表面分子敏感。鱼类视神经少突胶质细胞样细胞和鱼类中枢神经系统髓磷脂缺乏这些抑制特性，是允许生长的。这些体外实验表明，鱼类视神经中轴突再生的成功与允许生长特性的存在以及鱼类视神经/视束少突胶质细胞样细胞上缺乏生长抑制剂有因果关系。
