Kleitman N, Simon D K, Schachner M, Bunge R P
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110.
Exp Neurol. 1988 Dec;102(3):298-306. doi: 10.1016/0014-4886(88)90223-3.
Explants from embryonic rat retina plated on Schwann cell monolayers were used to examine the mechanisms by which these central neurons interact with Schwann cell surfaces. Embryonic retinal explants extend neurites reliably on Schwann cell surfaces (Kleitman et al., 1988, J. Neurosci. 8: 653). Antibodies to molecules thought to be present on Schwann cell surfaces (laminin and the 217C antigen), on retinal neurite surfaces (Thy-1.1), or on both surfaces (L1) were tested for their ability to influence this neurite growth. Of these, only antibodies to L1 were effective in blocking retinal neurite extension on Schwann cells. Inhibition of neurite growth by anti-L1 was shown to be specific to growth on Schwann cell surfaces because neurite growth on air-dried collagen (a substratum known to support retinal neurite outgrowth) was not affected. This blockage was dose-dependent. At a low titer of anti-L1 Fab fragments defasciculation of neurites was prominent; at high titers 95% of neurite outgrowth was inhibited. This virtual elimination of the ability of Schwann cell surfaces to support embryonic retinal neurite growth in the presence of antibodies to L1 indicates that binding of the L1 molecule is a critical component of the mechanism by which Schwann cells foster the growth of these neurites. The present experiments concur with the growing body of evidence that L1 plays an important role in supporting neurite growth on cell surfaces and raise the possibility that L1 may also mediate the striking ability of adult retinal axons to regenerate in a peripheral nerve environment.
将胚胎大鼠视网膜外植体接种在雪旺细胞单层上，用于研究这些中枢神经元与雪旺细胞表面相互作用的机制。胚胎视网膜外植体可在雪旺细胞表面可靠地延伸神经突（Kleitman等人，1988年，《神经科学杂志》8:653）。对被认为存在于雪旺细胞表面（层粘连蛋白和217C抗原）、视网膜神经突表面（Thy-1.1）或两者表面（L1）的分子的抗体，测试其影响这种神经突生长的能力。其中，只有抗L1抗体能有效阻断视网膜神经突在雪旺细胞上的延伸。抗L1对神经突生长的抑制作用显示出对在雪旺细胞表面生长具有特异性，因为在风干的胶原蛋白（一种已知支持视网膜神经突生长的基质）上的神经突生长不受影响。这种阻断是剂量依赖性的。在低滴度的抗L1 Fab片段时，神经突的解束现象很明显；在高滴度时，95%的神经突生长受到抑制。在存在抗L1抗体的情况下，雪旺细胞表面支持胚胎视网膜神经突生长的能力几乎完全丧失，这表明L1分子的结合是雪旺细胞促进这些神经突生长机制的关键组成部分。本实验与越来越多的证据一致，即L1在支持细胞表面神经突生长方面起重要作用，并提出L1也可能介导成年视网膜轴突在周围神经环境中显著的再生能力的可能性。
