Acetylcholine evokes an InsP3R1-dependent transient Ca 2+ signal in rat duodenum myocytes
Can. J. Physiol. Pharmacol.. 2008-09-01; 86(9): 626-632
Lire sur PubMed
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.
(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.
PMID: 18758512 [Indexed for MEDLINE]