Role of extracellular Ca2+ in acetylcholine-induced repetitive Ca2+ release in submandibular gland acinar cells of the rat

• Published in: Journal of cellular physiology Vol. 167; no. 2; pp. 277 - 284
• Main Authors: Zhang, W., Fukushi, Y., Nishiyama, A., Wada, J., Kamimura, N., Mio, Y., Wakui, M.
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.05.1996
• Subjects: Acetylcholine - pharmacology; Animals; Calcium - metabolism; Calcium - pharmacology; Cell Membrane - metabolism; Cell Membrane - ultrastructure; Chloride Channels - drug effects; Chloride Channels - metabolism; Patch-Clamp Techniques; Periodicity; Rats; Submandibular Gland - cytology; Submandibular Gland - physiology
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/(SICI)1097-4652(199605)167:2<277::AID-JCP11>3.0.CO;2-5

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 also in the absence of extracellular Ca2+ but disappeared after several minutes. Repetitive transient Cl− currents were restored by readmission of Ca2+ to the extracellular solution. The higher the concentration of extracellular Ca2+ readmitted, the larger the amplitude of the transient Cl− currents. Ca2+ entry through a store‐coupled pathway was detected by application of Ca2+ to the extracellular solution during a brief cessation of stimulation with ACh. In these experiments too, the higher the concentration of Ca2+, the larger the transient Cl− currents activated by Ca2+ released from the stores. The time course of decrease in total charge movements of repetitive transient responses to ACh with removal of extracellular Ca2+ depended on a decrease in charge movements of each transient event rather than a decrease in frequency of the repetitive events. The decrease of charge movements of each transient event was due to a decrease in its amplitude rather than its duration. 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 further suggest that the magnitude of Ca2+ entry determines the number of unitary stores filled with Ca2+ which can synchronously respond to ACh. © 1996 Wiley‐Liss, Inc.