Figure 2. Chemogenetic Activation of DRN^Vgat Neurons Suppresses Energy Expenditure.

(A) Experimental schema and representative IHC for DRN^Vgat neurons infected with excitatory DREADD hM3D(Gq).

(B) Representative thermal images of iBAT (control or Vgat:hM3D(Gq)) before and after injection of CNO. Chemogenetic activation of DRN^Vgat neurons suppresses iBAT thermogenesis.

(C and D) Short- and long-term changes in iBAT and core temperature after chemogenetic activation of DRN^Vgat neurons. (C) Activation of DRN^Vgat neurons significantly suppresses iBAT (treatment: p < 0.0001) and core temperature (treatment: p < 0.0001). Two-way repeated measures (RM) ANOVA comparing control and treated groups (n = 7–8 mice per group). (D) Average iBAT and core temperature at 0–3 h post-CNO injection. iBAT (p < 0.0001) and core (p < 0.0001) temperatures remain significantly suppressed 3 h post-CNO injection. Two-way RM ANOVA comparing t = 0 and t = 3 h post-CNO injection (n = 7–8 mice per group).

(E) Chemogenetic activation of DRN^Vgat neurons suppresses locomotor activity (treatment: p < 0.001), oxygen consumption (treatment: p < 0.01), carbon dioxide production (treatment: p < 0.001), and total energy expenditure (treatment: p < 0.01). Two-way RM ANOVA comparing control and treated groups after CNO injection (n = 7–8 mice per group).

(F) Molecular profiling of iBAT after chemogenetic activation of DRN^Vgat neurons. Genes tested: Cidea (p > 0.05), Dio2 (p < 0.001), Prdm16 (p > 0.05), Ucp1 (p < 0.01). Unpaired t tests comparing treatments (n = 4–5 samples per group).

Scale bar, 100 μm. **p < 0.01, ***p < 0.001, ****p < 0.0001. Data are presented as mean ± SEM.

See also Figure S2.