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. 2017 Dec 20;43(4):900–911. doi: 10.1038/npp.2017.284

Figure 3.

Figure 3

Amphetamine in adolescence recruits miR-218 to downregulate Dcc mRNA and protein expression in the VTA. (a) Left panel: timeline of antimiR-218 (amiR-218) or scramble (Scr) sequence microinfusions, amphetamine (AMPH) or saline treatment, and experimental procedures. Right panel: schematic representation of the mechanism of action of antagomiRs. (b) Behavioral activity during the 90 min test performed after each treatment injection, #significantly different from saline-treated mice, p<0.05. (c) AMPH upregulates miR-218 in Scr-treated mice, but not in those treated with antimiR-218. MiR-218 levels are significantly reduced following antimir-218 infusion, regardless of drug exposure *significantly different from the other groups, p<0.01; +significantly different from Scr-Saline, p<0.05). AntimiR-218 infusion abolishes AMPH-induced downregulation of Dcc mRNA and DCC protein expression in the VTA; *significantly different from the rest of the groups, p<0.05. (d) Robo1 expression in the VTA is not altered by AMPH treatment or by antimiR-218 microinfusion. (e) AMPH in adolescence induces a significant shift in the Dcc:Robo1 mRNA expression ratio in the VTA with a predominance of Robo1 mRNA in amphetamine vs saline groups. This effect is abolished when miR-218 degradation is induced; +significantly different from Scramble-Saline, p<0.05. All data are shown as mean±SEM.