Acetylcholine increases Ca2+ influx by activation of CaMKII in mouse oocytes

作者：Kang Dawon; Hur Chang Gi; Park Jae Yong; Han Jaehee; Hong Seong Geun^*

来源：Biochemical and Biophysical Research Communications, 2007, 360(2): 476-482.

DOI：10.1016/j.bbrc.2007.06.083

• acetylcholine
• T-type calcium channel
• CaMKII
• oocytes
• mice

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.

• 出版日期2007-8-24