Sivron T, Schwab M E, Schwartz M
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
J Comp Neurol. 1994 May 8;343(2):237-46. doi: 10.1002/cne.903430205.
This study shows that the fish optic nerve, which is able to regenerate after injury, contains myelin-associated growth inhibitors similar to the growth inhibitors present in mammalian central nervous system (CNS) myelin. The ability of nerves to regenerate was previously correlated with the ability of sections from these nerves to support neuronal attachment and axonal growth in vitro. Thus neuroblastoma cells or embryonic neurons became attached to and grew axons on sections of rat sciatic nerve or fish optic nerve, which are spontaneously regenerating systems, but not on sections of rat optic nerve, a nonregenerating system. Failure of the latter to support axonal growth has been attributed, at least in part, to growth inhibitors. Recently it was shown that adult neurons, which differ in their growth requirement from embryonic neurons, are unable to extend neurites on sections of normal sciatic nerve but are able to extend neurites on sections of sciatic nerve that was injured prior to its excision. We found a similar situation in the fish optic nerve, i.e., that the nerve is normally not permissive to growth of adult retinal axons but becomes growth permissive after injury. The nonpermissiveness of the normal fish optic nerve was found to correlate with the presence of myelin-associated growth-inhibitory molecules. This inhibitory activity of fish myelin was neutralized by IN-1 antibodies, known to neutralize rat myelin growth inhibitors. The results thus demonstrate that fish optic nerve myelin contains inhibitors apparently similar or even identical to those of rat, but possibly present in lower amounts than in the rat. Results are discussed with respect to the possibility that fish optic nerve, like the rat sciatic nerve and unlike the rat optic nerve, undergoes certain changes after injury that support regeneration of adult neurons. Such changes might include elimination or neutralization of growth inhibitors.
本研究表明，鱼的视神经在损伤后能够再生，其中含有与哺乳动物中枢神经系统（CNS）髓鞘中存在的生长抑制因子类似的髓鞘相关生长抑制因子。神经的再生能力先前与这些神经的切片在体外支持神经元附着和轴突生长的能力相关。因此，神经母细胞瘤细胞或胚胎神经元能够附着在大鼠坐骨神经或鱼视神经的切片上并长出轴突，这两种神经是自发再生系统，但不能附着在大鼠视神经切片上，大鼠视神经是一个非再生系统。后者不能支持轴突生长至少部分归因于生长抑制因子。最近有研究表明，成年神经元在生长需求上与胚胎神经元不同，它们不能在正常坐骨神经切片上延伸神经突，但能够在切除前受过损伤的坐骨神经切片上延伸神经突。我们在鱼的视神经中发现了类似的情况，即该神经通常不允许成年视网膜轴突生长，但在损伤后变得允许生长。发现正常鱼视神经的这种不允许生长与髓鞘相关生长抑制分子的存在有关。鱼髓鞘的这种抑制活性被已知能中和大鼠髓鞘生长抑制因子的IN-1抗体所中和。因此，结果表明鱼视神经髓鞘含有明显与大鼠相似甚至相同的抑制因子，但含量可能比大鼠中的少。就鱼视神经与大鼠坐骨神经类似但与大鼠视神经不同，在损伤后会发生某些支持成年神经元再生的变化这一可能性进行了讨论。这些变化可能包括生长抑制因子的消除或中和。
