Fig. 4: Effect of chronic chemogenetic manipulations of D2-neurons and D1-neurons of the NAc in a wheel-running/high-fat free-feeding choice procedure. | Nature Communications

Fig. 4: Effect of chronic chemogenetic manipulations of D2-neurons and D1-neurons of the NAc in a wheel-running/high-fat free-feeding choice procedure.

From: Nucleus accumbens D1- and D2-expressing neurons control the balance between feeding and activity-mediated energy expenditure

Fig. 4

A Experimental design. B–D Food consumption over time (B; Two-way RM ANOVA; Interaction F(18, 207) = 4.489, p = 0.0001; Post-hoc D2 Gq vs D2 WT: Day 3 p = 0.0091, Day25 p = 0.0330; Post-hoc D2 Gq vs D2 Gi: Day 1 p = 0.0256, Day24 p = 0.0197, Day25 p = 0.0312), variation in wheel running (C; Two-way RM ANOVA; Interaction F(34, 318) = 3.536, p = 0.0001; Post-hoc D2 Gi vs D2 WT: Day1 p = 0.0272; Post-hoc D2 Gq vs D2 WT: Day11 p = 0.0305, Day13 p = 0.0038, Day15 p = 0.0208, Day19 p = 0.0328, Day21 p = 0.0145, Day23 p = 0.0228) and variation in total and fat mass (D; One way ANOVA; Fat Mass variation CNO period F(2.00, 10.99) = 5.966, p = 0.0176; Post-hoc D1 WT vs D1 Gi p = 0.0026; Post-hoc D1 WT vs D1 Gq p = 0.0447; Total mass variation CNO removal F(2, 23) = 12.67, p = 0.0002; Post-hoc D2 WT vs D2 Gq p = 0.0002; Post-hoc D2 Gi vs D2 Gq p = 0.0040; Fat Mass variation CNO removal F(2, 23) = 8.537, p = 0.0017; Post-hoc D2 WT vs D2 Gq p = 0.0020; Post-hoc D2 Gi vs D2 Gq p = 0.0184) were measured under chronic D2-neurons inhibition (D2 Gi) and activation (D2 Gq) compared to WT controls, as well as after CNO cessation. E–G Food consumption over time (E; Two-way RM ANOVA; Interaction F(14, 222) = 6.702, p = 0.0001; Post-hoc D1 Gq vs D1 WT: Day1 p = 0.0183, Day7 p = 0.0411; Post-hoc D1 Gq vs D1 Gi: Day1 p = 0.0022, Day5 p = 0.0096, Day24 p = 0.0082; One-way ANOVA mean D10-D22 F(2, 32) = 6.579, p = 0.0040; Post-hoc D1 Gq vs D1 WT p = 0.0152, D1 Gq vs D1 Gi p = 0.0084), variation in wheel running (F; Two-way RM ANOVA; Virus effect F(2, 28) = 11.07 p = 0.0003, Interaction F(34, 471) = 3.334, p = 0.0001; Post-hoc D1 Gi vs D1 WT: Day1 p = 0.0299, Day17 p = 0.0187, Day21 p = 0.0174, Day25 p = 0.0223, Day29 p = 0.009, Day31 p = 0.0325; Post-hoc D1 Gq vs D1 WT: Day3 p = 0.0223, Day5 p = 0.0129, Day7 p = 0.0218, Day9 p = 0.0213, Day11 p = 0.0086, Day13 p = 0.0290, Day15 p = 0.0285) and variation in total and fat mass (G; One way ANOVA; Total mass variation CNO period F(2.00, 20.08) = 3.861, p = 0.0381; Post-hoc D1 Gi vs D1 Gq p = 0.0826; Fat Mass variation CNO period F(2, 32) = 3.492, p = 0.0425; Post-hoc D1 Gi vs D1 Gq p = 0.0463) were measured under chronic D1-neurons inhibition (D1 Gi) and activation (D2 Gq) compared to WT controls, as well as after CNO cessation. D2 WT n = 9; D2 Gi n = 8; D2 Gq n = 9; D1 WT n = 12; D1 Gi n = 11; D1 Gq n = 12. $: 0.05<p < 0.1; *: p < 0.05; **: p < 0.01; Error bars = s.e.m. Detailed statistics are displayed in Supplementary Table 2. Source data are provided as a Source Data file.

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