Acetylcholine rescues two-cell block through activation of IP3 receptors and Ca 2+ /calmodulin-dependent kinase II in an ICR mouse strain

Seong Keun Cho, Sook Young Yoon, Chang Gi Hur, Hae Young Yang, Changyong Choe, Eun Jin Kim, Jung Soo Joo, Kee Ryeon Kang, Jae-Yong Park, Seong Geun Hong, Jaehee Han, Dawon Kang

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Acetylcholine (ACh) causes early activation events in mouse oocytes, but little is known about its precise role in the early embryonic development of mice. We aimed to determine whether and how ACh is capable of rescuing two-cell block in an in vitro culture system. ACh evoked different transient Ca 2+ patterns showing a higher Ca 2+ peak in the two-cell stage embryos (two-cells) than observed in mature oocytes. In early two-cells subjected to an in vitro two-cell block, xestospongin C (Xes-C), an IP3 receptor antagonist, significantly decreased the level of the ACh-induced Ca 2+ increase. The reduction in the ACh-induced Ca 2+ increase by Xes-C in late two-cells was lower than that in early two-cells. Furthermore, KN62 and KN93, both CaMKII inhibitors, were found to reduce the magnitude of the ACh-induced Ca 2+ increase in early two-cells. The addition of ACh to the culture medium showed an ability to rescue in vitro two-cell block. However, the addition of ACh together with both Xes-C and CaMKII inhibitors or with either inhibitor separately had no effect on the rescue of two-cell block. Long-term exposure of late two-cells to ACh decreased morula and early blastocyst development and ACh had a differential effect on early and late two-cells. These results indicate that ACh likely rescues the in vitro two-cell block through activation of IP3R- and/or CaMKII-dependent signal transduction pathways.

Original languageEnglish
Pages (from-to)1125-1136
Number of pages12
JournalPflugers Archiv European Journal of Physiology
Volume458
Issue number6
DOIs
Publication statusPublished - 2009 Jun 5
Externally publishedYes

Fingerprint

Inositol 1,4,5-Trisphosphate Receptors
Inbred ICR Mouse
Calcium-Calmodulin-Dependent Protein Kinases
Calmodulin
Acetylcholine
Phosphotransferases
Chemical activation
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Oocytes
Signal transduction
Morula
Blastocyst
Culture Media
Embryonic Development

Keywords

  • Acetylcholine
  • Calcium
  • Inositol 1,4,5-trisphosphate receptors
  • Pre-implantation embryo development

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

Cite this

Acetylcholine rescues two-cell block through activation of IP3 receptors and Ca 2+ /calmodulin-dependent kinase II in an ICR mouse strain . / Cho, Seong Keun; Yoon, Sook Young; Hur, Chang Gi; Yang, Hae Young; Choe, Changyong; Kim, Eun Jin; Joo, Jung Soo; Kang, Kee Ryeon; Park, Jae-Yong; Hong, Seong Geun; Han, Jaehee; Kang, Dawon.

In: Pflugers Archiv European Journal of Physiology, Vol. 458, No. 6, 05.06.2009, p. 1125-1136.

Research output: Contribution to journalArticle

Cho, Seong Keun ; Yoon, Sook Young ; Hur, Chang Gi ; Yang, Hae Young ; Choe, Changyong ; Kim, Eun Jin ; Joo, Jung Soo ; Kang, Kee Ryeon ; Park, Jae-Yong ; Hong, Seong Geun ; Han, Jaehee ; Kang, Dawon. / Acetylcholine rescues two-cell block through activation of IP3 receptors and Ca 2+ /calmodulin-dependent kinase II in an ICR mouse strain In: Pflugers Archiv European Journal of Physiology. 2009 ; Vol. 458, No. 6. pp. 1125-1136.
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AU - Cho, Seong Keun

AU - Yoon, Sook Young

AU - Hur, Chang Gi

AU - Yang, Hae Young

AU - Choe, Changyong

AU - Kim, Eun Jin

AU - Joo, Jung Soo

AU - Kang, Kee Ryeon

AU - Park, Jae-Yong

AU - Hong, Seong Geun

AU - Han, Jaehee

AU - Kang, Dawon

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N2 - Acetylcholine (ACh) causes early activation events in mouse oocytes, but little is known about its precise role in the early embryonic development of mice. We aimed to determine whether and how ACh is capable of rescuing two-cell block in an in vitro culture system. ACh evoked different transient Ca 2+ patterns showing a higher Ca 2+ peak in the two-cell stage embryos (two-cells) than observed in mature oocytes. In early two-cells subjected to an in vitro two-cell block, xestospongin C (Xes-C), an IP3 receptor antagonist, significantly decreased the level of the ACh-induced Ca 2+ increase. The reduction in the ACh-induced Ca 2+ increase by Xes-C in late two-cells was lower than that in early two-cells. Furthermore, KN62 and KN93, both CaMKII inhibitors, were found to reduce the magnitude of the ACh-induced Ca 2+ increase in early two-cells. The addition of ACh to the culture medium showed an ability to rescue in vitro two-cell block. However, the addition of ACh together with both Xes-C and CaMKII inhibitors or with either inhibitor separately had no effect on the rescue of two-cell block. Long-term exposure of late two-cells to ACh decreased morula and early blastocyst development and ACh had a differential effect on early and late two-cells. These results indicate that ACh likely rescues the in vitro two-cell block through activation of IP3R- and/or CaMKII-dependent signal transduction pathways.

AB - Acetylcholine (ACh) causes early activation events in mouse oocytes, but little is known about its precise role in the early embryonic development of mice. We aimed to determine whether and how ACh is capable of rescuing two-cell block in an in vitro culture system. ACh evoked different transient Ca 2+ patterns showing a higher Ca 2+ peak in the two-cell stage embryos (two-cells) than observed in mature oocytes. In early two-cells subjected to an in vitro two-cell block, xestospongin C (Xes-C), an IP3 receptor antagonist, significantly decreased the level of the ACh-induced Ca 2+ increase. The reduction in the ACh-induced Ca 2+ increase by Xes-C in late two-cells was lower than that in early two-cells. Furthermore, KN62 and KN93, both CaMKII inhibitors, were found to reduce the magnitude of the ACh-induced Ca 2+ increase in early two-cells. The addition of ACh to the culture medium showed an ability to rescue in vitro two-cell block. However, the addition of ACh together with both Xes-C and CaMKII inhibitors or with either inhibitor separately had no effect on the rescue of two-cell block. Long-term exposure of late two-cells to ACh decreased morula and early blastocyst development and ACh had a differential effect on early and late two-cells. These results indicate that ACh likely rescues the in vitro two-cell block through activation of IP3R- and/or CaMKII-dependent signal transduction pathways.

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KW - Calcium

KW - Inositol 1,4,5-trisphosphate receptors

KW - Pre-implantation embryo development

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