Fig. 2
Cocaine-induced FRD in NAcSh D1R-MSNs is neither prevented by DA receptor antagonists nor altered by a non-selective monoamine uptake inhibitor. (a) Bottom: Summary bar graph showing the number of spikes elicited at 280 pA for all groups. Cocaine-induced FRD (COC, 3 μM, 1 h) is not blocked by DARs antagonists (D1R: SCH23390, SCH, 2 μM; D2R: Sulpiride, SULP, 10 μM). For the sake of visual clarity, we did not present the whole input–output curves but only the number of spikes at 280 pA, however, see Supplementary Fig. S3 for the complete curves (SAL, n = 17 cells/9 mice; COC, 9 cells/4 mice; SCH, 8 cells/3 mice; SCH + COC, n = 8 cells/3 mice; SULP, n = 12 cells/6 mice; SULP + COC, 9 cells/3 mice, SULP + SCH, 10 cells/3 mice; SULP + SCH + COC, 9 cells/4 mice). Top: Sample traces. (b) Left: Prior in vivo administration of SCH (0.01 mg/kg, i.p) does not prevent in vivo cocaine-induced FRD (15 mg/kg, i.p., five once-daily) (SAL-SAL, n = 18 cells/4 mice; SAL-COC, 15 cells/4 mice; SCH-SAL, 16 cells/4 mice; SCH + COC, n = 17 cells/4 mice). Right: Sample traces. (c) Left: Indatraline (Inda, 30 nM) does not alter firing rate in NAcSh MSNs, and cocaine-induced FRD remains unaffected by Inda (SAL, n = 7 cells/4 mice; COC, 8 cells/3 mice; Inda, 9 cells/4 mice; Inda + COC, n = 10 cells/3 mice). Right: Sample traces. In (a), one-way ANOVA, ****p < 0.0001. Post-hoc tests showed that none of the groups with COC is different from one another other; and that all other groups (SAL, SCH, SULP, and SCH + SULP) were different from COC but not different from one another other. ****p < 0.0001. In (b), two-way ANOVA, ***p < 0.001. Post-hoc tests showed that SAL-SAL is not different from SCH-SAL group, but both SAL-SAL and SCH-SAL are different from SAL-COC and SCH-COC. **p < 0.001. In c, two-way ANOVA, p < 0.05. Post-hoc tests showed that SAL is different from groups with cocaine, but not different from indatraline. **p < 0.01, ***p < 0.001. Calibration: 200 ms, 50 mV. Data are represented as mean ± SEM
