Wanner M, Lang D M, Bandtlow C E, Schwab M E, Bastmeyer M, Stuermer C A
Faculty of Biology, University of Konstanz, Germany.
J Neurosci. 1995 Nov;15(11):7500-8. doi: 10.1523/JNEUROSCI.15-11-07500.1995.
To determine whether optic nerve myelin of goldfish carries mammalian-like neurite growth inhibitory proteins which can be neutralized by the antibody IN-1, myelin fractions of fish optic nerves were used as substrates for fish retinal ganglion cell axons and rat dorsal root ganglia (DRG). Axonal growth was monitored and compared with that of IN-1 treated preparations. Growth of fish retinal axons and rat DRG neurites was substantial on goldfish optic nerve myelin and no improvement was observed with IN-1. In contrast, rat CNS myelin allowed only poor growth, and number of axons and length of DRG neurites increased significantly with IN-1. In addition, proteins of fish optic nerve myelin and bovine CNS myelin were extracted, reconstituted in liposomes and applied to growth cones. When goldfish myelin proteins in liposomes were seeded onto growth cones, 77% of fish and 89% of rat DRG growth cones continued to elongate, and the proportion of elongating fish growth cones (80%) did not significantly change when liposomes were pretreated with IN-1. But 73% of fish and 93% of rat growth cones collapsed with liposomes containing proteins from bovine CNS myelin. Upon IN-1 treatment, only 24% of fish growth cones collapsed. Thus, axon growth in vitro indicates that goldfish optic nerves, which permit successful axon regeneration in vivo, lack mammalian-like neurite growth inhibitors which are neutralized by IN-1.
为了确定金鱼的视神经髓磷脂是否携带可被抗体IN-1中和的类哺乳动物神经突生长抑制蛋白,将鱼视神经的髓磷脂部分用作鱼视网膜神经节细胞轴突和大鼠背根神经节(DRG)的底物。监测轴突生长并与经IN-1处理的制剂进行比较。鱼视网膜轴突和大鼠DRG神经突在金鱼视神经髓磷脂上有显著生长,且用IN-1处理后未观察到改善。相比之下,大鼠中枢神经系统髓磷脂仅允许较差的生长,而IN-1可使DRG神经突的轴突数量和长度显著增加。此外,提取金鱼视神经髓磷脂和牛中枢神经系统髓磷脂的蛋白质,重组成脂质体并应用于生长锥。当将脂质体中的金鱼髓磷脂蛋白接种到生长锥上时,77%的鱼和89%的大鼠DRG生长锥继续伸长,用IN-1预处理脂质体时,伸长的鱼生长锥比例(80%)没有显著变化。但是,含有牛中枢神经系统髓磷脂蛋白的脂质体可使73%的鱼和93%的大鼠生长锥塌陷。经IN-1处理后,只有24%的鱼生长锥塌陷。因此,体外轴突生长表明,在体内允许轴突成功再生的金鱼视神经缺乏可被IN-1中和的类哺乳动物神经突生长抑制剂。