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

Dawon Kang, Chang Gi Hur, Jae Yong Park, Jaehee Han, Seong Geun Hong

Research output: Contribution to journalArticle

14 Citations (Scopus)

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 (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.

Original languageEnglish
Pages (from-to)476-482
Number of pages7
JournalBiochemical and biophysical research communications
Volume360
Issue number2
DOIs
Publication statusPublished - 2007 Aug 24

Keywords

  • Acetylcholine
  • CaMKII
  • Mice
  • Oocytes
  • T-type calcium channel

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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