ROLE OF EXTRACELLULAR CA2-INDUCED REPETITIVE CA2+ RELEASE IN SUBMANDIBULAR-GLAND ACINAR-CELLS OF THE RAT( IN ACETYLCHOLINE)

Citation
W. Zhang et al., ROLE OF EXTRACELLULAR CA2-INDUCED REPETITIVE CA2+ RELEASE IN SUBMANDIBULAR-GLAND ACINAR-CELLS OF THE RAT( IN ACETYLCHOLINE), Journal of cellular physiology, 167(2), 1996, pp. 277-284
Citations number
45
Categorie Soggetti
Physiology,"Cell Biology
ISSN journal
00219541
Volume
167
Issue
2
Year of publication
1996
Pages
277 - 284
Database
ISI
SICI code
0021-9541(1996)167:2<277:ROECRC>2.0.ZU;2-A
Abstract
Acetylcholine (ACh) caused repetitive transient Cl- currents activated by intracellular Ca2+ in single rat submandibular grand acinar cells. As the concentration of ACh increased the amplitude and the frequency of the transient Cl- currents increased. These responses occurred als o in the absence of extracellular Ca2+ but disappeared after several m inutes. Repetitive transient Cl- currents were restored by readmission of Ca2+ to the extracellular solution. The higher the concentration o f extracellular Ca2+ readmitted, the larger the amplitude of the trans ient Cl- currents. Ca2+ entry through a store-coupled pathway was dete cted by application of Ca2+ to the extracellular solution during a bri ef cessation of stimulation with ACh. In these experiments too, the hi gher the concentration of Ca2+, the larger the transient Cl- currents activated by Ca2+ released from the stores. The time course of decreas e in total charge movements of repetitive transient responses to ACh w ith removal of extracellular Ca2+ depended on a decrease in charge mov ements of each transient event rather than a decrease in frequency of the repetitive events. The decrease of charge movements of each transi ent event was due to a decrease in its amplitude rather than its durat ion. The results suggest that in this cell type an amplitude-modulated mechanism is involved in repetitive Ca2+ release and that Ca2+ entry is essential to maintain the repetitive release of Ca2+. The results f urther suggest that the magnitude of Ca2+ entry determines the number of unitary stores filled with Ca2+ which can synchronously respond to ACh. (C) 1996 Wiley-Liss, Inc.