Petersen O H, Gallacher D V, Wakui M, Yule D I, Petersen C C, Toescu E C
MRC Secretory Control Research Group, University of Liverpool, UK.
Cell Calcium. 1991 Feb-Mar;12(2-3):135-44. doi: 10.1016/0143-4160(91)90015-7.
Receptor-activated cytoplasmic Ca2+ oscillations have been investigated using both single cell microfluorometry and voltage-clamp recording of Ca(2+)-dependent Cl- current in single internally perfused acinar cells. In these cells there is direct experimental evidence showing that the ACh-evoked [Ca2+]i fluctuations are due to an inositol trisphosphate-induced small steady Ca2+ release which in turn evokes repetitive Ca2+ spikes via a caffeine-sensitive Ca(2+)-induced Ca2+ release process. There is indirect evidence suggesting that receptor-activation in addition to generating the Ca2+ releasing messenger, inositol trisphosphate, also produces another regulator involved in the control of Ca2+ signal spreading. Intracellular inositol trisphosphate or Ca2+ infusion produce short duration repetitive spikes confined to the cytoplasmic area close to the plasma membrane, but these signals can be made to progress throughout the cell by addition of caffeine or by receptor activation.
已使用单细胞显微荧光测定法和对单个内部灌注腺泡细胞中钙依赖性氯电流的电压钳记录,对受体激活的细胞质钙离子振荡进行了研究。在这些细胞中,有直接的实验证据表明,乙酰胆碱诱发的细胞内钙离子浓度波动是由于三磷酸肌醇诱导的小幅度稳定钙离子释放,而这反过来又通过对咖啡因敏感的钙诱导钙释放过程引发重复性钙离子尖峰。有间接证据表明,受体激活除了产生钙离子释放信使三磷酸肌醇外,还产生另一种参与控制钙离子信号传播的调节剂。细胞内注入三磷酸肌醇或钙离子会产生局限于靠近质膜的细胞质区域的短时间重复性尖峰,但通过添加咖啡因或受体激活可使这些信号在整个细胞中传播。