Skip to main content
. Author manuscript; available in PMC: 2016 Sep 29.
Published in final edited form as: Cell Rep. 2015 Sep 10;12(12):1997–2008. doi: 10.1016/j.celrep.2015.08.041

Figure 2. Cocaine-Induced Increase in NAc DA Transients Require CB1R Activation in VTA.

Figure 2

(A) Voltammetric current (encoded in color) plotted against the applied carbon-fiber electrode potential (ordinate) and the acquisition time (abscissa). Traces above color plots represent current (normalized to concentration) from the potential where DA is oxidized (~+0.6 V in green), when animals are given an i.v. bolus of cocaine (1 mg/kg), preceded by intra-VTA vehicle infusion.

(B) Systemic effects of cocaine are attenuated following CB1R blockade in VTA (250 ng rimonabant [Rbt] in 500 μl, unilateral and ipsilateral to the recording electrode).

(C) Effects of all treatments on NAc DA transient frequency (F(4,31) = 29.14, p < 0.0001, one-way ANOVA; n = 12 rats). Baseline indicates the frequency of DA transients without intracranial or systemic injections. In other groups the intra-VTA injection is indicated first, followed by the i.v. injection (e.g., intracranial Veh\intra-VTA Veh). Note that Rbt alone (Rbt/Veh) did not alter DA transient frequency, and Rbt significantly reduced the effect of i.v. cocaine on DA transients (Rbt/cocaine, ***p < 0.0001, Bonferroni post hoc test).