ArticlePflugers Archiv : European journal of physiology2003
Acetylcholine induces Ca2+ oscillations via m3/m4 muscarinic receptors in the mouse oocyte.
Article in Pflugers Archiv : European journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- The TRPV3 channel is a mediator of zinc influx and homeostasis in murine oocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ZneLife · 2023Article
- ZnbioRxiv : the preprint server for biology · 2023Article
- Characterization of an A-Type Muscarinic Acetylcholine Receptor and Its Possible Non-neuronal Role in the Oriental Armyworm,Frontiers in physiology · 2020Article
- Regulator of G-protein signaling 2 (RGS2) suppresses premature calcium release in mouse eggs.Development (Cambridge, England) · 2015Article
- Acetylcholine rescues two-cell block through activation of IP3 receptors and Ca2+/calmodulin-dependent kinase II in an ICR mouse strain.Pflugers Archiv : European journal of physiology · 2009Article
- FSH regulates acetycholine production by ovarian granulosa cells.Reproductive biology and endocrinology : RB&E · 2006Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in intracellular Ca2+ concentration are required for the activation of mammalian oocytes. They are caused mainly by Ca2+ release from the endoplasmic reticulum (ER) via Ins P3 receptors (Ins P3R). Several studies have reported that acetylcholine (ACh) is capable of triggering early activation events in mouse oocytes over-expressed with the m1 muscarinic ACh receptor (m1AChR). Here we examined which subtypes of the mAChR (m1 to m4) are involved in the generation of Ca2+ oscillations in native mouse oocytes. ACh (10 microM) elicited regular Ca2+ oscillations similar to those induced by sperm in their temporal characteristics. The Ca2+ oscillations were abolished by application with atropine, the mAChR inhibitor. Within 1 min after treatment of ACh, intracellular Fluo-3 fluorescence intensity increased from 794+/-119 to 2023+/-755 (increase to 250% of original value), indicating a strong rise of cytosolic Ca2+ concentration. 4-DAMP mustard and Tropicamide, specific antagonists of m3AChR and m4AChR, completely abolished ACh-induced Ca2+ oscillations. In the ovulated oocytes, the expression of m3/m4 AChR was clearly detected by RT-PCR analysis. Furthermore, ACh-induced Ca2+ oscillations were also abolished or decreased by PLC inhibitors (U73122 or D609) and an Ins P3-receptor antagonist (xestospongin C), confirming that ACh generates Ca2+ oscillations via the PLC-Ins P3 (PI) pathway. These results strongly suggest that m3/m4AChR is coupled to the generation of Ca2+ oscillations mainly via the PI pathway in mouse oocytes.
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