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Acetylcholine‐ and caffeine‐evoked repetitive transient Ca(2+)‐activated K+ and C1‐ currents in mouse submandibular cells.
Author(s) -
Smith P M,
Gallacher D V
Publication year - 1992
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1992.sp019077
Subject(s) - caffeine , acetylcholine , chemistry , patch clamp , agonist , ibmx , biophysics , endocrinology , medicine , membrane potential , forskolin , biology , biochemistry , receptor
1. Resting and acetylcholine‐induced membrane currents were measured in single mouse submandibular acinar cells using the patch‐clamp whole‐cell current recording technique. 2. Micromolar ACh activated a large, sustained outward, Ca(2+)‐dependent K+ current and a single transient inward Ca(2+)‐dependent C1‐current. 3. Nanomolar ACh induced a series of transients in both the K+ and C1‐ currents; C1‐ current activation was now observed throughout the period of agonist application. We consider this repetitive transient current activation better able to support sustained fluid and electrolyte secretion than the response elicited by a high dose of agonist. 4. Repetitive K+ and C1‐ current transients were also induced by 1 mM‐caffeine, consistent with caffeine‐induced Ca2+ release from the Ca(2+)‐sensitive Ca2+ stores which are thought to comprise part of the pathway for activation of secretion. 5. The ACh‐induced current transients were inhibited by 10 mM‐caffeine, 100 microM‐IBMX and 10 microM membrane‐permeable cyclic AMP. Therefore, it seems likely that caffeine is able to inhibit agonist‐induced calcium mobilization via a cyclic AMP‐dependent pathway.