Cytosolic Ca2+ and Ca2+-activated Cl- current dynamics:: Insights from two functionally distinct mouse exocrine cells

被引:63
作者
Giovannucci, DR
Bruce, JIE
Straub, SV
Arreola, J
Sneyd, J
Shuttleworth, TJ
Yule, DI
机构
[1] Univ Rochester, Sch Med & Dent, Dept Physiol & Pharmacol, Rochester, NY 14642 USA
[2] Massey Univ, Auckland, New Zealand
来源
JOURNAL OF PHYSIOLOGY-LONDON | 2002年 / 540卷 / 02期
关键词
D O I
10.1113/jphysiol.2001.013453
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The dynamics of Ca2+ release and Ca2+-activated Cl- currents in two related, but functionally distinct exocrine cells, were studied to gain insight into how the molecular specialization of Ca2+ signalling machinery are utilized to produce different physiological endpoints: in this case, fluid or exocytotic secretion. Digital imaging and patch-clamp methods were used to monitor the temporal and spatial properties of changes in cytosolic Ca2+ concentration ([Ca2+](c)) and Cl- currents following the controlled photolytic release of caged-InsP(3) or caged-Ca2+. In parotid and pancreatic acinar cells, changes in [Ca2+](c) and activation of a Ca2+-activated Cl- current occurred with close temporal coincidence. In parotid, a rapid global Ca2+ signal was invariably induced, even with low-level photolytic release of threshold amounts of InsP(3). In pancreas, threshold stimulation generated an apically delimited [Ca2+](c) signal, while a stronger stimulus induced a global [Ca2+](c) signal which exhibited characteristics of a propagating wave. InsP(3) was more effective in parotid, where [Ca2+](c) signals initiated with shorter latency and exhibited a faster time-to-peak than in pancreas. The increased potency of InsP(3) in parotid probably results from a four-fold higher number of InsP(3) receptors as measured by radiolabelled InsP(3) binding and western blot analysis. The Ca2+ sensitivity of the Cl- channels in parotid and pancreas was determined from the [Ca2+]-current relationship measured during a dynamic 'Ca2+ ramp' produced by the continuous, low-level photolysis of caged-Ca2+. In addition to a greater number of InsP(3) receptors, the Cl- current density of parotid acinar cells was more than four-fold greater than that of pancreatic cells. Whereas activation of the current was tightly coupled to increases in Ca2+ in both cell types, local Ca2+ clearance was found to contribute substantially to the deactivation of the current in parotid. These data reveal specializations of common modules of Ca2+-release machinery and subsequent effector activation that are specifically suited to the distinct functional roles of these two related cell types.
引用
收藏
页码:469 / 484
页数:16
相关论文
共 63 条
[1]   Activation of calcium-dependent chloride channels in rat parotid acinar cells [J].
Arreola, J ;
Melvin, JE ;
Begenisich, T .
JOURNAL OF GENERAL PHYSIOLOGY, 1996, 108 (01) :35-47
[2]   Differences in regulation of Ca2+-activated Cl- channels in colonic and parotid secretory cells [J].
Arreola, J ;
Melvin, JE ;
Begenisich, T .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 1998, 274 (01) :C161-C166
[3]   Regulation of chloride channels in secretory epithelia [J].
Begenisich, T ;
Melvin, JE .
JOURNAL OF MEMBRANE BIOLOGY, 1998, 163 (02) :77-85
[4]   Calcium signalling - an overview [J].
Bootman, MD ;
Collins, TJ ;
Peppiatt, CM ;
Prothero, LS ;
MacKenzie, L ;
De Smet, P ;
Travers, M ;
Tovey, SC ;
Seo, JT ;
Berridge, MJ ;
Ciccolini, F ;
Lipp, P .
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY, 2001, 12 (01) :3-10
[5]   A SIMPLE, SENSITIVE, AND SPECIFIC RADIORECEPTOR ASSAY FOR INOSITOL 1,4,5-TRISPHOSPHATE IN BIOLOGICAL TISSUES [J].
BREDT, DS ;
MOUREY, RJ ;
SNYDER, SH .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1989, 159 (03) :976-982
[6]   Calcium waves in a model with a random spatially discrete distribution of Ca2+ release sites [J].
Bugrim, AE ;
Zhabotinsky, AM ;
Epstein, IR .
BIOPHYSICAL JOURNAL, 1997, 73 (06) :2897-2906
[7]   CALCIUM SIGNALING [J].
CLAPHAM, DE .
CELL, 1995, 80 (02) :259-268
[8]   Generic signals and specific outcomes:: Signaling through Ca2+, calcineurin, and NF-AT [J].
Crabtree, GR .
CELL, 1999, 96 (05) :611-614
[9]   Mitochondria and calcium: from cell signalling to cell death [J].
Duchen, MR .
JOURNAL OF PHYSIOLOGY-LONDON, 2000, 529 (01) :57-68
[10]   Targeted disruption of the NHE1 gene prevents muscarinic agonist-induced up-regulation of Na+/H+ exchange in mouse parotid acinar cells [J].
Evans, RL ;
Bell, SM ;
Schultheis, PJ ;
Shull, GE ;
Melvin, JE .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (41) :29025-29030