Journal
CELL CALCIUM
Volume 54, Issue 2, Pages 111-119Publisher
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.ceca.2013.05.004
Keywords
Ca2+ signaling; Ca2+ oscillation; Muscarinic acetylcholine receptor
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Funding
- Ministry of Education, Science and Culture of Japan [20220007]
- ICORP-SORST of JST
- Grants-in-Aid for Scientific Research [20220007] Funding Source: KAKEN
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We examined ACh-induced [Ca2+](i) dynamics in pancreatic acinar cells prepared from mAChR subtype-specific knockout (KO) mice. ACh did not induce any [Ca2+](i) increase in the cells isolated from M1/M3 double KO mice. In the cells from M3KO mice, ACh (0.3-3 mu M) caused a monotonic [Ca2+](i) increase. However, we found characteristic oscillatory [Ca2+](i) increases in cells from M1KO mice in lower concentrations of ACh (0.03-0.31 mu M). We investigated the receptor specific pattern of [Ca2+](i) increase in COS-7 cells transfected with M1 or M3 receptors. ACh induced the oscillatory [Ca2+](i) increase in M3 expressing cells, but not in cells expressing M1, which exhibited monotonic [Ca2+](i), increases. IP3 production detected in fluorescent indicator co-transfected cells was higher in M1 than in M3 expressing cells. From the examination of four types of M1/M3 chimera receptors we found that the carboxyl-terminal region of M3 was responsible for the generation of Ca2+ oscillations. The present results suggest that the oscillatory Ca2+ increase in response to M3 stimulation is dependent upon a moderate IP3 increase, which is suitable for causing Ca2+-dependent IP3-induced Ca2+ release. The C-terminal domain of M3 may contribute as a regulator of the efficiency of Gq and PLC cooperation. (C) 2013 Elsevier Ltd. All rights reserved.
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