Nakagawa-Yagi Y, Saito Y, Kitoh N, Ogane N, Fujisawa E, Nakamura H
Laboratory of Neurochemistry, Snow Brand Milk Products, Tochigi, Japan.
Biochem Biophys Res Commun. 1993 Mar 15;191(2):727-36. doi: 10.1006/bbrc.1993.1278.
We have used human neuroblastoma NB-OK1 cells to investigate the regulatory mechanism of neurite outgrowth. Sodium fluoride suppressed forskolin-stimulated neurite outgrowth in a dose-dependent manner. Sodium fluoride increased intracellular free calcium concentrations ([Ca2+]i), but had no effect on the cAMP level, arachidonic acid (AA) release or phosphoinositide (PI) hydrolysis in NB-OK1 cells. The calcium response of sodium fluoride was dependent on the extracellular Ca2+. The dose-response curve for stimulation of [Ca2+]i elicited by sodium fluoride was similar to that for suppression of neurite outgrowth. The suppressive effect of sodium fluoride on neurite outgrowth was inhibited by nonspecific Ca2+ entry blocker Mn2+ but not by L-, N- and T-type Ca2+ channel blockers. Hence we describe for the first time a possible role for calcium signaling in the regulation of neurite outgrowth by a G protein activator in the human neuron-derived cell line.
我们使用人类神经母细胞瘤NB-OK1细胞来研究神经突生长的调控机制。氟化钠以剂量依赖的方式抑制福斯高林刺激的神经突生长。氟化钠增加细胞内游离钙浓度（[Ca2+]i），但对NB-OK1细胞中的环磷酸腺苷（cAMP）水平、花生四烯酸（AA）释放或磷酸肌醇（PI）水解没有影响。氟化钠的钙反应依赖于细胞外Ca2+。氟化钠引发的[Ca2+]i刺激的剂量反应曲线与神经突生长抑制的曲线相似。氟化钠对神经突生长的抑制作用被非特异性Ca2+进入阻滞剂Mn2+抑制，但不被L型、N型和T型Ca2+通道阻滞剂抑制。因此，我们首次描述了钙信号在人类神经元衍生细胞系中G蛋白激活剂对神经突生长调控中的可能作用。
