Wu G, Ledeen R W
Department of Neurology, Albert Einstein College of Medicine, Bronx, New York 10461.
J Neurochem. 1991 Jan;56(1):95-104. doi: 10.1111/j.1471-4159.1991.tb02567.x.
Treatment of three neuroblastoma cell types in culture with neuraminidase resulted in enhanced neurite outgrowth. These included the mouse Neuro-2A and rat B104 and B50 lines. The morphological changes depended on the presence of exogenous Ca2+ and were accompanied by modest but statistically significant increases in 45Ca2+ influx. Neuraminidase-stimulated neuritogenesis was blocked by the B subunit of cholera toxin (cholera B) and anti-GM1 antibody, a finding suggesting the effect was due to an increased amount of GM1 on the cell surface. Cholera B also blocked the increase in 45Ca2+ influx. The mouse N1A-103 line, previously characterized as "neurite minus," did not respond to neuraminidase with either neurite outgrowth or enhanced Ca2+ influx. These results point to an influence of GM1 on neuritogenesis in cells with differentiation potential and suggest a mechanism involving modulation of Ca2+ flux.
用神经氨酸酶处理培养中的三种神经母细胞瘤细胞类型,导致神经突生长增强。这些细胞类型包括小鼠Neuro-2A细胞系以及大鼠B104和B50细胞系。形态学变化取决于外源Ca2+的存在,并且伴随着45Ca2+内流适度但具有统计学意义的增加。神经氨酸酶刺激的神经突生成被霍乱毒素B亚基(霍乱B)和抗GM1抗体阻断,这一发现表明该效应是由于细胞表面GM1量的增加所致。霍乱B也阻断了45Ca2+内流的增加。先前被表征为“无神经突”的小鼠N1A-103细胞系,对神经氨酸酶既没有神经突生长反应也没有Ca2+内流增强反应。这些结果表明GM1对具有分化潜能的细胞中的神经突生成有影响,并提示了一种涉及Ca2+通量调节的机制。