Noda M, Ishizaka N, Yokoyama S, Hoshi N, Kimura Y, Hashii M, Taketo M, Egorova A, Knijnik R, Fukuda K, Morikawa H, Brown D A, Higashida H
Department of Biophysics, Kanazawa University School of Medicine, Japan.
J Lipid Mediat Cell Signal. 1996 Sep;14(1-3):175-85. doi: 10.1016/0929-7855(96)00523-8.
Neuroblastoma x glioma hybrid NG 108-15 and neuroblastoma x fibroblast hybrid NL308 cells possess endogenous bradykinin B2 receptors and m4 muscarinic acetylcholine receptors (mAChRs), which couple to phospholipase C and adenylate cyclase, respectively. Four genetic subtypes of mAChRs differed in their effects when stimulated in NG108-15 and NL308 cells overexpressing mAChRs. Broadly speaking, the principal effects fell into two categories: the odd-numbered receptors (m1 and m3) activated phospholipase C and increased inositol trisphosphate/Ca2+, as bradykinin did, whereas the even-numbered receptors (m2 and m4) inhibited adenylate cyclase via a pertussis toxin (PTx)-sensitive G-protein in NG108-15 cells. But all four types of NL308 cells overexpressing each m1, m2, m3 and m4 receptor activated phospholipase C, while keeping the PTx-sensitivity in m2/m4, but not in m1/m3 receptors. Coupling to ion channel effectors showed a comparable dichotomy in NG108-15 cells, while cross-activation occurred in NL308 cells.
神经母细胞瘤x胶质瘤杂交细胞系NG 108-15和神经母细胞瘤x成纤维细胞杂交细胞系NL308细胞具有内源性缓激肽B2受体和M4型毒蕈碱型乙酰胆碱受体（mAChRs），它们分别与磷脂酶C和腺苷酸环化酶偶联。在过表达mAChRs的NG108-15和NL308细胞中受到刺激时，mAChRs的四种基因亚型产生的效应有所不同。大致来说，主要效应分为两类：奇数编号的受体（m1和m3）激活磷脂酶C并增加肌醇三磷酸/Ca2+，如同缓激肽那样，而偶数编号的受体（m2和m4）在NG108-15细胞中通过对百日咳毒素（PTx）敏感的G蛋白抑制腺苷酸环化酶。但是，过表达m1、m2、m3和m4受体的所有四种类型的NL308细胞均激活磷脂酶C，同时m2/m4受体保持对PTx的敏感性，而m1/m3受体则不然。在NG108-15细胞中，与离子通道效应器的偶联表现出类似的二分法，而在NL308细胞中则发生交叉激活。
