Acetylcholine increases Ca2+ influx by activation of CaMKII in mouse oocytes |
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Authors: | Kang Dawon Hur Chang-Gi Park Jae-Yong Han Jaehee Hong Seong-Geun |
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Institution: | Department of Physiology, College of Medicine and Institute of Health Sciences, Gyeongsang National University, Jinju 660-751, Republic of Korea. |
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Abstract: | IP3-induced Ca2+ release is the primary mechanism that is responsible for acetylcholine (ACh)-induced Ca2+ oscillation. However, other mechanisms remain to explain intracellular Ca2+ elevation. We here report that ACh induces Ca2+ influx via T-type Ca2+ channel by activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII), and the ACh-induced Ca2+ influx facilitates the generation of Ca2+ oscillation in the mouse ovulated oocytes (oocytes(MII)). ACh increased Ca2+ current by 50+/-21%, and produced Ca2+ oscillation. However, the currents and Ca2+ peaks were reduced in Ca2+ -free extracellular medium. ACh failed to activate Ca2+ current and to produce Ca2+ oscillation in oocytes pretreated with KN-93, a CaMKII inhibitor. KN-92, an inactive analogue of KN93, and PKC modulators could not prevent the effect of ACh. These results show that ACh increases T-type Ca2+ current by activation of CaMKII, independent of the PKC pathway, in the mouse oocytes. |
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Keywords: | Acetylcholine T-type calcium channel CaMKII Oocytes Mice |
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