Fig. 2
Chemogenetic activation of NAc D1R neurons increases wake and suppresses nest-building behavior and food intake. a Drawings of superimposed AAV injection sites in the NAc of D1R-Cre mice (n = 8, indicated with different colors). b Representative voltage traces recorded from an mCherry-expressing neuron during the application of CNO. CNO produced depolarization and firing in an hM3Dq-expressing neuron (left), and induced significant depolarization in hM3Dq-positive D1R neurons (right, n = 8 cells from 3 mice, paired t test; t7 = 5.8, P = 7 × 10−4). aCSF artificial cerebrospinal fluid. c Representative images of CNO-induced c-Fos (black)/mCherry (brown) colocalization in the NAc. Scale bars: 500 μm. Boxed regions in (c) are enlarged in the right panel. Scale bars: 10 μm. d, e Examples of relative EEG power, EEG/EMG traces, and hypnograms over 6 h following vehicle (d) or CNO (e) injection at 09:00. f Time course changes in wakefulness, NREM sleep, and REM sleep after administration of vehicle or CNO to mice expressing hM3Dq in NAc D1R neurons (n = 8, repeated-measures ANOVA; F1,14 = 11.9 (wake), 11.6 (NREM), 12.4 (REM); P = 0.004 (wake), 0.004 (NREM), 0.003 (REM)). g Total time spent in each stage for 2 h after vehicle or CNO injection (n = 8, paired t test). h EEG power density of wake during the 2 h after vehicle or CNO injection (n = 8, paired t test; not statistically significant). i Diagram of experiment. j Nesting score was assessed in 4 groups (n = 8 per group, Wilcoxon matched-pairs signed rank test: mCherry: Z = 0.6, P = 0.5; hM3Dq: Z = 2.3, P = 0.02). k Systemic application of CNO significantly reduced food consumption (n = 6 per group, paired t test). Data represent mean ± s.e.m. *P < 0.05, **P < 0.01
