Acetylcholine evokes an InsP3R1-dependent transient Ca 2+ signal in rat duodenum myocytes

Nicolas Fritz, Fabrice Dabertrand, Jean Mironneau, Nathalie Macrez, Jean-Luc Morel
Can. J. Physiol. Pharmacol.. 2008-09-01; 86(9): 626-632
DOI: 10.1139/Y08-067

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1. Can J Physiol Pharmacol. 2008 Sep;86(9):626-32. doi: 10.1139/y08-067.

Acetylcholine evokes an InsP3R1-dependent transient Ca2+ signal in rat duodenum

Fritz N(1), Dabertrand F, Mironneau J, Macrez N, Morel JL.

Author information:
(1)Division of Molecular Neurobiology, Department of Medical Biochemistry and
Biophysics, Karolinska Institutet, Stockholm, Sweden.

In smooth muscle myocytes, agonist-activated release of calcium ions (Ca2+)
stored in the sarcoplasmic reticulum (SR) occurs via different but overlapping
transduction pathways. Hence, to fully study how SR Ca2+ channels are activated,
the simultaneous activation of different Ca2+ signals should be separated. In rat
duodenum myocytes, we have previously characterized that acetylcholine (ACh)
induces Ca2+ oscillations by binding to its M2 muscarinic receptor and activating
the ryanodine receptor subtype 2. Here, we show that ACh simultaneously evokes a
Ca2+ signal dependent on activation of inositol 1,4,5-trisphosphate (InsP3)
receptor subtype 1. A pharmacologic approach, the use of antisense
oligonucleotides directed against InsP3R1, and the expression of a specific
biosensor derived from green-fluorescent protein coupled to the pleckstrin
homology domain of phospholipase C, suggested that the InsP3R1-dependent Ca2+
signal is transient and due to a transient synthesis of InsP3 via M3 muscarinic
receptor. Moreover, we suggest that both M2 and M3 signalling pathways are
modulating phosphatidylinositol 4,5-bisphosphate and InsP3 concentration, thus
describing closely interacting pathways activated by ACh in duodenum myocytes.

DOI: 10.1139/y08-067
PMID: 18758512 [Indexed for MEDLINE]

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