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Fig. 1 | BMC Biology

Fig. 1

From: Control of glutamate release by complexes of adenosine and cannabinoid receptors

Fig. 1

Modulation by A2AR ligands on CB1R-mediated G protein activation in the A2AR-CB1R heteromer. a–e CODA-RET experiments, where two complementary halves of Rluc (cRluc and nRluc) are respectively fused to the A2AR and CB1R and YFP is fused to the α-subunit of Gi. HEK-293T cells were transiently transfected with cDNAs of A2AR-cRluc (3.33 μg), CB1R-nRluc (1.67 μg), Gαi1-YFP (5 μg), and non-fused β1 and γ2 subunits (4.5 μg and 5 μg, respectively). a Concentration-response curves of the effect of the selective CB1R agonist CP55940 on the ligand-induced BRET changes, which are determined by changes in the interaction of the A2AR-CB1R heteromer with Gi, in the presence (blue plot) and absence (red plot) of the non-selective adenosine agonist NECA (10 μM). Data are means ± S.E.M. of triplicate BRET ratio values of a representative experiment. b, c EC50 and Emax values of 12 independent experiments performed in triplicate, expressed as means ± S.E.M.; the EC50 and Emax values were obtained by non-linear regression fitting to a sigmoidal concentration-response curve and analyzed statistically with a paired t-test (*: p < 0.05, compared with the absence of NECA). d, e Modification by NECA (1 and 10 μM), caffeine (CAFF, 1 and 3 mM) and NECA (10 μM) plus caffeine (3 mM) on the effect of an EC50 concentration of CP55940 (2 μM); values are means ± S.E.M. (n = 10–11 with triplicates) of the percentage of the effect of CPP55940 alone and analyzed statistically with repeated measures ANOVA, followed by Dunnett’s multiple comparison test (**: p < 0.01, compared with CPP55940 alone)

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