Abstract
In RIN m5F rat insulinoma β-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.
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