Itoh K, Kawamura H, Asou H
Children's Hospital Research Foundation, Cincinnati, OH 45229-2899.
Brain Res. 1992 May 15;580(1-2):233-40. doi: 10.1016/0006-8993(92)90949-a.
We have studied the function of carbohydrates of the L1 molecule, a member of the immunoglobulin superfamily of adhesion molecules, using a novel monoclonal antibody, mAb-L1(2E12), against L1 molecule. This antibody was specific for the 200 kDa component of mouse L1 molecule and its epitope was N-linked for complex-type oligosaccharides. The mAb-L1(2E12) was found to induce a rise in intracellular Ca2+ concentration ([Ca2+]i) in cultured mouse embryonic cortical neurons. The rise in [Ca2+]i was dependent on the concentrations of mAb-L1(2E12). The rise seemed to be due to an influx of extracellular Ca2+ as EGTA treatment abolished it. Both cadmium and nifedipine blocked the effect of mAb-L1(2E12), suggesting the Ca2+ influx was through voltage-operated Ca2+ channels, particularly L-type Ca2+ channels. These results provide an important insight for understanding the mechanisms by which oligosaccharides of the L1 molecule influence various functions of neural cells.
我们使用一种针对L1分子的新型单克隆抗体mAb-L1(2E12)，研究了免疫球蛋白超家族粘附分子L1分子碳水化合物的功能。该抗体对小鼠L1分子的200 kDa成分具有特异性，其表位为复杂型寡糖的N-连接。发现mAb-L1(2E12)可诱导培养的小鼠胚胎皮质神经元细胞内Ca2+浓度([Ca2+]i)升高。[Ca2+]i的升高取决于mAb-L1(2E12)的浓度。这种升高似乎是由于细胞外Ca2+的内流，因为EGTA处理可消除它。镉和硝苯地平都阻断了mAb-L1(2E12)的作用，表明Ca2+内流是通过电压门控Ca2+通道，特别是L型Ca2+通道。这些结果为理解L1分子寡糖影响神经细胞各种功能的机制提供了重要的见解。
