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. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Cell Signal. 2014 Nov 17;27(3):716–726. doi: 10.1016/j.cellsig.2014.11.006

Figure 7. Effects of CRIP1a on CB1R-mediated inhibition of cAMP accumulation.

Figure 7

(A) cAMP levels in WT, empty vector Control, and XS or KD clones were determined by incubating cells with vehicle or 1 μM forskolin for 4 min (a time within the linear range of stimulation). (B-D) Dose-response curves for cannabinoid agonist inhibition of cAMP accumulation, using forskolin as an adenylyl cyclase activator, was determined in N18TG2 WT, Control vector, CRIP1a XS, and CRIP1a KD cells with either mAEA (B), WIN55212-2 (C), or CP55940 (D). Background levels (cAMP accumulation in the absence of FSK) were subtracted from all values and represented less than 10% of FSK-stimulated cAMP accumulation (A). Data were normalized such that 100% was equal to cAMP in WT cells treated with forskolin only, while 0% was equal to cAMP in cells treated with vehicle only. *p<0.05 indicates significant difference between WT and CRIP1a KD in the EC50 values calculated from nonlinear regression fitting of CP55940 concentration-effect curves and two-way ANOVA.