Lambert D G, Nahorski S R
Department of Pharmacology and Therapeutics, University of Leicester, UK.
J Physiol Paris. 1992;86(1-3):77-82. doi: 10.1016/s0928-4257(05)80010-5.
M3 muscarinic receptors expressed on SH-SY5Y human neuroblastoma cells are linked to phosphoinositide turnover and rises in [Ca2+]i. The rise in [Ca2+]i is biphasic with the peak phase being due to release from an intracellular Ins(1,4,5)P3-sensitive site and the plateau phase being due to Ca2+ entry across the plasma membrane. Ca2+ entry does not appear to involve voltage sensitive Ca2+ channels, a pertussis toxin sensitive G-protein-operated Ca2+ channel or Ins(1,4,5)P3/Ins(1,3,4,5)P4-operated Ca2+ channel. We suggest that carbachol-stimulated Ca2+ entry in SH-SY5Y human neuroblastoma cells occurs via receptor operated Ca2+ channels and through capacitive refilling.
在SH-SY5Y人神经母细胞瘤细胞上表达的M3毒蕈碱受体与磷酸肌醇代谢和细胞内钙离子浓度([Ca2+]i)升高有关。[Ca2+]i的升高呈双相性,峰值期是由于从细胞内对肌醇-1,4,5-三磷酸(Ins(1,4,5)P3)敏感的位点释放,而平台期是由于钙离子通过质膜进入。钙离子进入似乎不涉及电压敏感性钙离子通道、百日咳毒素敏感的G蛋白偶联钙离子通道或Ins(1,4,5)P3/肌醇-1,3,4,5-四磷酸(Ins(1,3,4,5)P4)偶联的钙离子通道。我们认为,卡巴胆碱刺激的SH-SY5Y人神经母细胞瘤细胞中的钙离子进入是通过受体操纵的钙离子通道并通过容量性钙内流发生的。