Boyd R S, Donnelly L E, MacDermot J
Department of Clinical Pharmacology, Royal Postgraduate Medical School, London, UK.
Eur J Pharmacol. 1994 Apr 15;267(2):161-6. doi: 10.1016/0922-4106(94)90167-8.
Treatment of NCB-20 neuronal hybrid cells in culture with 100 microM ATP, 100 microM carbachol or 1 microM bradykinin is followed by a transient rise in intracellular calcium ion concentration ([Ca2+]i). Exposure of these cells to any one of these three agonists (ATP, carbachol or bradykinin) is also followed by heterologous desensitization of responses mediated by either of the other two classes of agonist. The heterologous desensitization is not inhibited by Ro-31-2880 (a selective protein kinase C inhibitor), neither is it accompanied by a reduction in the receptor-dependent increase in inositol trisphosphate. Cells were pre-treated in the absence or presence of extracellular Ca2+ with 1 microM bradykinin, 100 microM carbachol or carrier alone, and thereafter exposed to 1 microM ionomycin. The results showed that pre-treatment with bradykinin or carbachol reduced the maximum increase in [Ca2+]i triggered by ionomycin. Exposure of cells to 1 microM ionomycin in the absence of extracellular Ca2+ totally eliminated the subsequent increase in [Ca2+]i mediated by bradykinin, ATP or carbachol. The results indicate that the heterologous desensitization that follows exposure to bradykinin, ATP or carbachol in NCB-20 cells is mediated by a reduction in a shared pool of intracellular calcium ions.
用100微摩尔ATP、100微摩尔卡巴胆碱或1微摩尔缓激肽处理培养中的NCB - 20神经杂交细胞后，细胞内钙离子浓度（[Ca2+]i）会出现短暂升高。将这些细胞暴露于这三种激动剂（ATP、卡巴胆碱或缓激肽）中的任何一种后，也会导致由其他两类激动剂介导的反应发生异源脱敏。异源脱敏不受Ro - 31 - 2880（一种选择性蛋白激酶C抑制剂）的抑制，也不伴有受体依赖性肌醇三磷酸增加的减少。细胞在无细胞外Ca2+或有细胞外Ca2+存在的情况下，用1微摩尔缓激肽、100微摩尔卡巴胆碱或仅用载体进行预处理，然后暴露于1微摩尔离子霉素。结果表明，用缓激肽或卡巴胆碱预处理可降低离子霉素引发的[Ca2+]i的最大升高。在无细胞外Ca2+的情况下将细胞暴露于1微摩尔离子霉素，可完全消除随后由缓激肽、ATP或卡巴胆碱介导的[Ca2+]i的升高。结果表明，NCB - 20细胞暴露于缓激肽、ATP或卡巴胆碱后发生的异源脱敏是由细胞内共享钙离子池的减少介导的。
