Zhang H, Miller R H, Rutishauser U
Department of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4901.
J Neurosci. 1992 Aug;12(8):3107-14. doi: 10.1523/JNEUROSCI.12-08-03107.1992.
Formation of axonal pathways involves a variety of molecules that influence cell-cell interactions. The polysialic acid (PSA) moiety of the neural cell adhesion molecule (NCAM) is present on neuronal surfaces during process outgrowth. Our studies reveal that the removal of PSA causes a decrease in the rate of elongation of retinal cell processes on a substrate of neuronal membranes derived from chick tectum. This effect was partially reversed by antibodies against the L1 adhesion molecule, but not by antibodies against NCAM, N-cadherin, or beta 1-integrins. This predominant effect of PSA on L1 was also observed in short-term, cell-cell adhesion assays, suggesting that PSA promotes optimal outgrowth on neuronal substrates by limiting the consequences of L1-mediated adhesion.
轴突通路的形成涉及多种影响细胞间相互作用的分子。在神经突起生长过程中，神经细胞黏附分子（NCAM）的多唾液酸（PSA）部分存在于神经元表面。我们的研究表明，去除PSA会导致视网膜细胞突起在源自鸡顶盖的神经元膜底物上的伸长速率降低。针对L1黏附分子的抗体可部分逆转这种效应，但针对NCAM、N-钙黏着蛋白或β1整合素的抗体则不能。在短期细胞间黏附试验中也观察到了PSA对L1的这种主要作用，这表明PSA通过限制L1介导的黏附后果来促进在神经元底物上的最佳生长。
