Moran A, Turner R J
Department of Physiology, Faculty of Health Sciences, Ben-Gurion University, Beer-Sheva, Israel.
Mol Cell Biochem. 1996 May 10;158(1):53-6. doi: 10.1007/BF00225882.
We demonstrate that the application of the muscarinic agonist carbachol to the human salivary epithelial cell line HSG elicits the now well-known phenomenon of 'quantal' Ca2+ release; namely, that the application of a submaximal concentration of agonist results in the release of only a portion of the agonist-sensitive intracellular Ca2+ pool. One explanation that has been proposed to account for this effect is that there are multiple intracellular Ca2+ stores, each with a different agonist sensitivity, which release Ca2+ in an 'all-or-none' fashion. We test this hypothesis in intact HSG cells with an experimental protocol designed to preferentially load less-agonist-sensitive stores with 40Ca2+ and more-agonist-sensitive stores with 45Ca2+. However, contrary to the expectations of the above explanation, these cells do not preferentially release 45Ca2+ in response to low concentrations of agonist. Thus our data suggest that quantal Ca2+ release must arise from some other property of the stores or their Ca2+ release channels.
我们证明,将毒蕈碱激动剂卡巴胆碱应用于人类唾液腺上皮细胞系HSG会引发目前广为人知的“量子化”Ca2+释放现象;也就是说,应用次最大浓度的激动剂只会导致部分对激动剂敏感的细胞内Ca2+池释放Ca2+。为解释这种效应而提出的一种解释是,存在多个细胞内Ca2+储存库,每个储存库对激动剂的敏感性不同,它们以“全或无”的方式释放Ca2+。我们在完整的HSG细胞中用一种实验方案来检验这一假设,该方案旨在优先用40Ca2+加载对激动剂敏感性较低的储存库,用45Ca2+加载对激动剂敏感性较高的储存库。然而,与上述解释的预期相反,这些细胞在低浓度激动剂作用下不会优先释放45Ca2+。因此,我们的数据表明,量子化Ca2+释放必定源于储存库或其Ca2+释放通道的其他某种特性。