Drazba J, Lemmon V
Department of Neurobiology, Anatomy, and Cell Science, University of Pittsburgh School of Medicine, Pennsylvania 15261.
Dev Biol. 1990 Mar;138(1):82-93. doi: 10.1016/0012-1606(90)90178-l.
The roles of neural cell adhesion molecule (NCAM), L1, N-cadherin, and integrin in neurite outgrowth on various substrates were studied. Antibodies against these cell surface molecules were added to explants of chick retina and the neurites from retinal ganglion cells were examined for effects of the antibodies on neurite length and fasciculation. On laminin, an anti-integrin antibody completely inhibited neurite outgrowth. The same antibody did not inhibit neurite outgrowth on polylysine or Müller cells. Antibodies to NCAM, L1, and N-cadherin did not significantly inhibit neurite outgrowth on laminin but produced significant inhibition on Müller cells. The inhibition of neurite outgrowth on glia by anti-L1 antibodies supports the hypothesis that L1 is capable of acting in a heterophilic binding mechanism. On laminin, both anti-N-cadherin and anti-L1 caused defasciculation of neurites from retinal ganglion cells, while anti-NCAM did not. None of these antibodies produced defasciculation on Müller cells. The results indicate that these three cell adhesion molecules may be very important in interactions with glia as axons grow from the retina to the tectum and may be less important in axon-axon interactions along this pathway. No evidence was found supporting the role of integrins in axon growth on Müller cells.
研究了神经细胞黏附分子（NCAM）、L1、N-钙黏着蛋白和整合素在不同底物上神经突生长中的作用。将针对这些细胞表面分子的抗体添加到鸡视网膜外植体中，并检测视网膜神经节细胞的神经突，以观察抗体对神经突长度和束状化的影响。在层粘连蛋白上，抗整合素抗体完全抑制了神经突的生长。相同的抗体在聚赖氨酸或穆勒细胞上并未抑制神经突的生长。针对NCAM、L1和N-钙黏着蛋白的抗体在层粘连蛋白上并未显著抑制神经突的生长，但在穆勒细胞上产生了显著抑制作用。抗L1抗体对神经胶质细胞上神经突生长的抑制支持了L1能够通过异嗜性结合机制发挥作用的假说。在层粘连蛋白上，抗N-钙黏着蛋白和抗L1均导致视网膜神经节细胞神经突的去束状化，而抗NCAM则没有。这些抗体在穆勒细胞上均未产生去束状化作用。结果表明，在轴突从视网膜向顶盖生长的过程中，这三种细胞黏附分子在与神经胶质细胞的相互作用中可能非常重要，而在这条通路中轴突-轴突相互作用中可能不太重要。未发现支持整合素在穆勒细胞上轴突生长中发挥作用的证据。
