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. Author manuscript; available in PMC: 2013 Dec 24.
Published in final edited form as: Cell Rep. 2013 Nov 14;5(4):10.1016/j.celrep.2013.10.015. doi: 10.1016/j.celrep.2013.10.015

Fig. 3. β-arr1 control of protein export explains enhanced δOR-VDCC inhibition.

Fig. 3

The increase in cell surface receptor number after 50 and 500nM SNC80 (Fig. 2C) could reflect β-arr1 control of δOR release to the plasma membrane. This was assessed by inhibiting protein export i. DRGs were pre-treated with Brefeldin A (Bref. A, 1μg/ml 30min pre-treatment) to inhibit protein release from the ER, and Exo1, a more specific inhibitor of protein release from the Golgi (0.8 and 3.2μg/ml, included in the intracellular recording solution). Both BrefA and Exo1 (0.8μg/ml) reduced the enhanced SNC80 inhibition of VDCCs in β-arr1−/− to +/+ levels but the higher dose of Exo1 (3.2μg/ml) reduced SNC80-inhibition in both −/− and +/+ neurons ii. Exo1 did not affect GABAB-VDCC inhibition, assessed by Baclofen (50 μM). All data are shown as mean±SEM, #p<0.05 vs untreated β-arr1+/+ or −/−. ***p<0.001 vs β-arr1+/+, n=6–12 per data point All exemplar currents depict the current before, during and after agonist application (1, 2 and 3) and the scale bars show time, 20ms, and current, 5nA on the x- and y-axes respectively. Columns in dark (β-arr1+/+) or light (β-arr1−/−) shades of grey indicate data shown in Fig 1.