ArticleNaunyn-Schmiedeberg's archives of pharmacology1995
Differential calcium signalling by m2 and m3 muscarinic acetylcholine receptors in a single cell type.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 34 citations in OpenAlex.
- The signaling and selectivity of α-adrenoceptor agonists for the human α2A, α2B and α2C-adrenoceptors and comparison with human α1 and β-adrenoceptors.Pharmacology research & perspectives · 2022Article
- Muscarinic Acetylcholine Receptors in the Retina-Therapeutic Implications.International journal of molecular sciences · 2021Review
- cAMP guided his way: a life for G protein-mediated signal transduction and molecular pharmacology-tribute to Karl H. Jakobs.Naunyn-Schmiedeberg's archives of pharmacology · 2019Review
- Desensitization of cAMP Accumulation via Human β3-Adrenoceptors Expressed in Human Embryonic Kidney Cells by Full, Partial, and Biased Agonists.Frontiers in pharmacology · 2019Article
- Lack of specificity of commercially available antisera against muscarinergic and adrenergic receptors.Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
- Propiverine and metabolites: differences in binding to muscarinic receptors and in functional models of detrusor contraction.Naunyn-Schmiedeberg's archives of pharmacology · 2006Article
- Extracts from Rhois aromatica and Solidaginis virgaurea inhibit rat and human bladder contraction.Naunyn-Schmiedeberg's archives of pharmacology · 2004Article
- Gender comparison of muscarinic receptor expression and function in rat and human urinary bladder: differential regulation of M2 and M3 receptors?Naunyn-Schmiedeberg's archives of pharmacology · 2003Article
- Sphingosine kinase-mediated Ca2+ signalling by G-protein-coupled receptors.The EMBO journal · 1998Article
- Calcium signalling by G protein-coupled sphingolipid receptors in bovine aortic endothelial cells.Naunyn-Schmiedeberg's archives of pharmacology · 1996Article
- A role for Rho in receptor- and G protein-stimulated phospholipase C. Reduction in phosphatidylinositol 4,5-bisphosphate by Clostridium difficile toxin B.Naunyn-Schmiedeberg's archives of pharmacology · 1996Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have compared muscarinic acetylcholine receptor (mAChR) coupling to phospholipase C (PLC) and increases in cytoplasmic Ca2+ concentration [Ca2+]i in human embryonic kidney (HEK) cells, stably expressing either the human m3 or m2 receptor subtype. In m3 mAChR-expressing cells, carbachol stimulated inositol phosphate (InsP) formation and increased [Ca2+]i with EC50 values of about 2 microM and 30 nM, respectively. Maximal inositol 1,4,5-trisphosphate (InsP3) production (about fourfold) was rapid (15 s) and stable for 2 min. Maximal increases in [Ca2+]i were 300-350 nM and mainly, almost 90%, due to influx of extracellular Ca2+. The efficacy of pilocarpine for stimulating InsP and Ca2+ responses was not significantly different from that of carbachol. All m3 mAChR-mediated responses were pertussis toxin (PTX)-insensitive. In m2 mAChR-expressing cells, carbachol stimulated InsP formation and increased [Ca2+]i with EC50 values of about 20 microM and 7 microM, respectively. Maximal InsP formation was only 10-15% of that observed in m3 mAChR-expressing cells, whereas maximal elevations of [Ca2+]i were similar in both cell types. Formation of InsP3 was rapid (15 s to 2 min) and about twofold above basal. In contrast to m3 mAChR activation, [Ca2+]i increases induced by m2 mAChR activation were exclusively due to Ca2+ mobilization from intracellular stores. The efficacy of pilocarpine for stimulating InsP and Ca2+ responses was 50% and 20% of the efficacy of carbachol, respectively. PTX treatment did not affect m2 mAChR-induced PLC stimulation, but reduced the m2 mAChR-mediated increases in [Ca2+]i to 50%. In conclusion, m3 and m2 mAChRs stably expressed in HEK cells can induce similar cellular responses; however, they do so by activating apparently distinct signalling pathways. While coupling of m2 mAChR to PLC occurs in a PTX-insensitive manner, coupling to mobilization of Ca2+ from intracellular stores is partly PTX-sensitive and this may occur at least partly independent of PLC activation.
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