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 (oocytesMII). 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.
|Number of pages||7|
|Journal||Biochemical and biophysical research communications|
|Publication status||Published - 2007 Aug 24|
- T-type calcium channel
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology