Nakagawa-Yagi Y, Saito Y, Takada Y, Nakamura H
Yukijirushi Institute of Life Sciences, Tochigi, Japan.
Biochem Biophys Res Commun. 1992 Jan 15;182(1):45-54. doi: 10.1016/s0006-291x(05)80110-x.
We have used human neuroblastoma NB-OK1 cells to investigate the regulation of neurite outgrowth. Carbachol suppressed forskolin-stimulated neurite outgrowth in NB-OK1 cells although forskolin-stimulated cAMP levels were enhanced. The dose-response curve for this suppression was very similar to that for stimulation of inositol monophosphate (IP1) formation and for stimulation of the initial rise of [Ca2+]i elicited by carbachol. Carbachol-mediated changes in neurite outgrowth, IP1 formation and [Ca2+]i displayed high sensitivity for pirenzepine but low sensitivity for AF-DX116. Inhibition of intracellular calcium release with TMB-8 prevented the suppressive effect of carbachol on forskolin-stimulated neurite outgrowth. Hence we describe for the first time a relationship between neurite outgrowth and inositol triphosphate-triggered calcium release mediated by carbachol in the human neuron-derived cell line.
我们使用人神经母细胞瘤NB - OK1细胞来研究神经突生长的调控。尽管福斯高林刺激的环磷酸腺苷（cAMP）水平有所提高，但卡巴胆碱抑制了福斯高林刺激的NB - OK1细胞神经突生长。这种抑制的剂量反应曲线与刺激肌醇单磷酸（IP1）形成以及刺激由卡巴胆碱引发的细胞内钙离子浓度（[Ca2+]i）初始升高的剂量反应曲线非常相似。卡巴胆碱介导的神经突生长、IP1形成和[Ca2+]i的变化对哌仑西平显示出高敏感性，但对AF - DX116显示出低敏感性。用TMB - 8抑制细胞内钙释放可防止卡巴胆碱对福斯高林刺激的神经突生长的抑制作用。因此，我们首次描述了在人神经元衍生细胞系中，神经突生长与卡巴胆碱介导的三磷酸肌醇触发的钙释放之间的关系。
