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. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: J Neuroimmune Pharmacol. 2012 Mar 28;7(4):856–865. doi: 10.1007/s11481-012-9351-6

Fig. 1. AEA inhibits agonist mediated βarr2-GFP distribution in U2OS cells co-expressing GPR55E and βarr2-GFP.

Fig. 1

(A) (i–iv) Cells were pre-incubated with increasing concentrations of the antagonist (AEA) for 15 min prior to agonist application (3 μM LPI or 30 μM SR141716A). The response was normalized to the averaged response obtained by the agonist. Data are mean ± SEM from three independent experiments performed in duplicate (*P<0.05, **P<0.01, ***P<0.001). (a) AEA inhibition of LPI. (b) AEA inhibition of SR141716A. (c) Representative images, captured with confocal microscopy at 40x magnification depicting βarr2-GFP recruitment pattern are illustrated. Cells treated with vehicle and 30 μM AEA show that βarr2-GFP is homogenously distributed in the cytoplasm. Treatment with 3 μM LPI and 30 μM SR141716A resulted in cytosolic distribution βarr2-GFP which was largely attenuated following treatment with AEA.