膜电位和胞质游离钙水平调节胰岛素分泌性BTC3细胞中乙酰胆碱诱导的肌醇磷酸生成。

Membrane potential and cytosolic free calcium levels modulate acetylcholine-induced inositol phosphate production in insulin-secreting BTC3 cells.

作者信息

Gromada J, Dissing S

机构信息

Department of Medical Physiology, The Panum Institute, University of Copenhagen, Denmark.

出版信息

Biochim Biophys Acta. 1996 Jan 10;1310(1):145-8. doi: 10.1016/0167-4889(95)00139-5.

DOI:10.1016/0167-4889(95)00139-5

PMID:9244188

Abstract

Effects of membrane potential and cytosolic free Ca2+ concentrations ([Ca2+]i) on acetycholine (ACh)-induced inositol phosphate production were investigated in insulin secreting betaTC3 cells. ACh (10 microM) caused a rapid inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) production and increase in [Ca2+]i reaching a maximum within 5 s. The rise in Ins(1,4,5)P3 production was reduced by 79 +/- 5% when [Ca2+]i was kept low in cells loaded with the Ca2+ chelator BAPTA. The ACh-evoked Ins(1,4,5)P3 production also depended on the membrane potential as it was reduced by 31 +/- 6% in cells hyperpolarized by diazoxide, an opener of ATP-sensitive K+ channels. The Ca2+ ionophore ionomycin caused a rapid increase in [Ca2+]i and in the cellular Ins(1,4,5)P3 content. We conclude that stimulation-induced changes in membrane potential and [Ca2+]i play an important role in controlling Ins(1,4,5)P3 production in insulin-secreting betaTC3 cells.

摘要

在胰岛素分泌βTC3细胞中，研究了膜电位和胞质游离Ca2+浓度（[Ca2+]i）对乙酰胆碱（ACh）诱导的肌醇磷酸生成的影响。ACh（10微摩尔）引起快速的1,4,5-三磷酸肌醇（Ins(1,4,5)P3）生成，并使[Ca2+]i增加，在5秒内达到最大值。当用Ca2+螯合剂BAPTA使细胞内[Ca2+]i保持较低水平时，Ins(1,4,5)P3生成的增加减少了79±5%。ACh诱发的Ins(1,4,5)P3生成也依赖于膜电位，因为在被二氮嗪（一种ATP敏感性钾通道开放剂）超极化的细胞中，其减少了31±6%。Ca2+离子载体离子霉素使[Ca2+]i和细胞内Ins(1,4,5)P3含量迅速增加。我们得出结论，刺激诱导的膜电位和[Ca2+]i变化在控制胰岛素分泌βTC3细胞中Ins(1,4,5)P3生成方面发挥重要作用。