Mechanisms for the coupling of cannabinoid receptors to intracellular calcium mobilization in rat insulinoma β-cells
Experimental Cell Research. 2007-08-15; 313(14): 2993-3004
DOI: 10.1016/j.yexcr.2007.05.012
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1. Exp Cell Res. 2007 Aug 15;313(14):2993-3004. doi: 10.1016/j.yexcr.2007.05.012.
Epub 2007 May 18.
Mechanisms for the coupling of cannabinoid receptors to intracellular calcium
mobilization in rat insulinoma beta-cells.
De Petrocellis L(1), Marini P, Matias I, Moriello AS, Starowicz K, Cristino L,
Nigam S, Di Marzo V.
Author information:
(1)Endocannabinoid Research Group, Institute of Cybernetics, National Research
Council, Via Campi Flegrei 34, Comprensorio Olivetti, 80078 Pozzuoli, Naples,
Italy.
In RIN m5F rat insulinoma beta-cells, agonists at cannabinoid CB(1) receptors
modulate insulin release. Here we investigated in these cells the effect of the
activation of cannabinoid CB(1) and CB(2) receptors on intracellular Ca(2+)
([Ca(2+)](i)). The CB(1) agonist arachidonoyl-chloro-ethanolamide (ACEA), and
the CB(2) agonist JWH133, elevated [Ca(2+)](i) in a way sensitive to the
inhibitor of phosphoinositide-specific phospholipase C (PI-PLC), U73122 (but not
to pertussis toxin and forskolin), and independently from extracellular Ca(2+).
PI-PLC-dependent Ca(2+) mobilization by ACEA was entirely accounted for by
activation of inositol-1,3,4-phosphate (IP(3)) receptors on the endoplasmic
reticulum (ER), whereas the effect of JWH133 was not sensitive to all tested
inhibitors of IP(3) and ryanodine receptors. ACEA, but not JWH133, significantly
inhibited the effect on [Ca(2+)](i) of bombesin, which acts via G(q/11)- and
PI-PLC-coupled receptors in insulinoma cells. The endogenous CB(1) agonists,
anandamide and N-arachidonoyldopamine, which also activate transient receptor
potential vanilloid type 1 (TRPV1) receptors expressed in RIN m5F cells,
elevated [Ca(2+)](i) in the presence of extracellular Ca(2+) in a way sensitive
to both CB(1) and TRPV1 antagonists. These results suggest that, in RIN m5F
cells, CB(1) receptors are coupled to PI-PLC-mediated mobilization of
[Ca(2+)](i) and might inhibit bombesin signaling.
DOI: 10.1016/j.yexcr.2007.05.012
PMID: 17585904 [Indexed for MEDLINE]