Fig. 3
From: An unsuspected role for organic cation transporter 3 in the actions of amphetamine

Amphetamine-induced efflux via OCT3 in an ex vivo system. a AMPH (10 µM) triggered efflux of pre-loaded [3H]MPP+ starting at t = 0 min from cultured rat superior cervical ganglia (SCG) cells in the absence or presence of cocaine (COC, 20 µM) or cocaine and D22 (COC 20 µM plus 0.1 µM D22, 1 µM D22, 10 µM D22, respectively). Addition of substances is indicated by black bars; Data are mean ± S.E.M., n = 9–12 independent observations per condition, *P < 0.05, (Bonferroni’s) compared to the control trace. b AMPH (10 µM) triggered efflux of [3H]MPP+ from SCGs (as in a) in the absence or presence of cocaine (20 or 100 µM, respectively) or cocaine (100 µM) and D22 (10 µM); * denotes statistical difference of COC 20 µM vs. the control trace; # denotes significance of COC 100 µM compared to the control trace and Φ indicates difference of COC 100 µM+10 µM D22 vs. all other groups (*, #, Φ, P < 0.05, Bonferroni’s). c AMPH-induced efflux of pre-loaded [3H]MPP+ starting at t = 0 min from HEK293 cells stably expressing human NET in the absence or presence of cocaine (COC; 20 µM). Black bars indicate addition of substances (*P < 0.05 (Bonferroni’s)). d AMPH (10 µM)-induced efflux of pre-loaded [3H]MPP+ from cultured SCGs (as in a) in the presence of desipramine (DES, 1 µM) and/or desipramine and corticosterone (CORT, 30 µM and 100 µM). For comparison, area under the curve (AUC) of the last five fractions in the presence of AMPH was calculated for each observation and analyzed by Kruskal–Wallis, followed by Dunn’s (*P < 0.05)