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. Author manuscript; available in PMC: 2018 Sep 1.
Published in final edited form as: Psychopharmacology (Berl). 2017 Jun 30;234(18):2761–2776. doi: 10.1007/s00213-017-4673-y

Figure 3. HCRTr1 blockade decreases the amplitude of, and blocks cocaine-induced increases in, spontaneous phasic DA amplitude.

Figure 3

(A) Diagram of the experimental set-up and timeline for freely-moving FSCV experiments measuring spontaneous DA transients. Green hashed segments illustrate the 1-min time points for which post hoc analysis was performed. Example voltammetric color plots and raw data traces of spontaneous phasic DA events following treatment with (B) Vehicle, (C) 10 mg/kg, or (D) 20 mg/kg RTIOX-276. For each panel, data is shown during baseline (left), pretreatment (middle), and cocaine (right) collections. Effects of (E) Vehicle, (F) 10 mg/kg, or (G) 20 mg/kg RTIOX-276 on the frequency of spontaneous phasic DA transients. Two-way repeated measures ANOVA with Time and Drug as the repeated measures variables indicated no significant effects of Time (F (14,98) = 0.9, p = 0.59), Drug (F (2,14) = 1.9, p = 0.17) and Time x Drug interaction (F(28,196) = 1.0, p = 0.43) following RTIOX-276 treatment. Effects of (H) Vehicle, (I) 10 mg/kg, or (J) 20 mg/kg RTIOX-276 on the amplitude of spontaneous phasic DA transients. Two-way repeated measures ANOVA with Time and Drug as the repeated measures variables indicated that there was a significant effect of Time (F (14,98) = 8.7, p < 0.001), Drug (F (2,14) = 13.5, p < 0.001) and Time x Drug interaction (F(28,196) = 2.1, p < 0.002) following RTIOX-276 treatment. Grouped data are presented as mean ± SEM. Holm-Bonferroni post hoc tests: *p < 0.05, **p < 0.01.