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. 2017 Feb 13;8:22. doi: 10.3389/fpsyt.2017.00022

Figure 6.

Figure 6

Transient pan-neuronal knockdown of Dop1R1 and Dop1R2 during development recapitulates arousal defects in adult animals. (A) Timeline of experiment, as in Figure 1, except that the heat treatment produces knockdown of D1 or D2 receptors. (B) Average responsiveness (white bars, mm/s ± SEM) or sleep duration (black bars, min ± SEM) during the day and night for treated nSyb-Gal4/UAS-Dop1R1/R2 RNAi or D2 RNAi; tubulin (tub)-Gal80TS animals (N = 132, 66, and 75, respectively) compared to nSyb-Gal4/+; tub-Gal80TS genetic controls, set as zero (N = 228). (C) Daytime sleep intensity (% reactive ± SEM) for the same flies as in (B). (D) Nighttime sleep intensity (% reactive ± SEM) for the same flies as in (B). (E) Relative gene expression (±SEM) for Dop1R1 in pupae and adults following developmental knockdown. (F) Relative gene expression (±SEM) for Dop1R2 in pupae and adults following developmental knockdown. Fold change compared to either genetic control (1 or 2) is shown. ***P < 0.001; **P < 0.01; *P < 0.05, by one-way ANOVA, adjusted for multiple comparisons by a Post Hoc Tukey’s test.