Koizumi S, Inoue K
Division of Pharmacology, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya, Tokyo 158, Japan.
Biochem Biophys Res Commun. 1998 Jun 18;247(2):293-8.
The caffeine-evoked effects on the intracellular Ca2+ concentration ([Ca2+]i) and on the release of dopamine by PC12 cells were investigated. Stimulation by caffeine resulted in a transient Ca2+ release which was followed by a sustained phase of Ca2+ entry through a non-voltage dependent pathway. Treatment with cyclopiazonic acid (CPA) or thapsigargin, inhibitors of the Ca2+ATPase pump of the endoplasmic reticulum, resulted in only a sustained rise in [Ca2+]i in the presence of extracellular Ca2+. Pretreatment of cells with CPA or thapsigargin abolished the subsequent Ca2+ responses to caffeine. Caffeine also evoked the release of dopamine from the cells only in the presence of extracellular Ca2+, which was mimicked by CPA. These results suggest that store-dependent Ca2+ entry evoked by caffeine has an indispensable role in the secretory response in an excitable cell line, PC12 cells.
研究了咖啡因对PC12细胞内钙离子浓度（[Ca2+]i）及多巴胺释放的影响。咖啡因刺激导致钙离子短暂释放，随后通过非电压依赖性途径持续进入钙离子。用内质网Ca2+ATP酶泵抑制剂环匹阿尼酸（CPA）或毒胡萝卜素处理，仅在细胞外存在钙离子时导致[Ca2+]i持续升高。用CPA或毒胡萝卜素预处理细胞可消除随后咖啡因引起的钙离子反应。咖啡因也仅在细胞外存在钙离子时引起细胞释放多巴胺，CPA可模拟此作用。这些结果表明，咖啡因引起的储存依赖性钙离子内流在可兴奋细胞系PC12细胞的分泌反应中起不可或缺的作用。
