Fig. 1
ovBNST PKC-δ neurons regulate the anorexia induced by IL-1β or LPS. a–d Representative histology (a) and quantification (b–d) of Fos-like immunoreactivity in each ovBNST brain section after IP injection of saline, IL-1β, or LPS. One-way ANOVA with post-hoc Bonferroni t-test (F2,18 = 59.2, p < 0.001, b), unpaired t-test (IL-1β, t10 = 6.74, p < 0.001; LPS, t4 = 7.28, p = 0.002, c), n = 10 animals injected with saline, 6 animals injected with IL-1β, 3 animals injected with LPS. e Experiment procedure for feeding test after chemogenetic silencing of ovBNST PKC-δ neurons. f Expression of hM4Di in ovBNST PKC-δ neurons was achieved by stereotaxic injection of AAV-EF1α-FLEX-hM4Di-mCherry in ovBNST (up). Brain slice electrophysiological recording showed that the firing of ovBNST PKC-δ neurons expressing hM4Di-mCherry can be silenced by CNO (10 μM) (bottom). ac anterior commissure. g Food intake normalized to the body weight (% BW) in 24-h fasted animals after IP injection of different agents. Two-way ANOVA with post-hoc Bonferroni t-test showed a significant effect after CNO silencing of the ovBNST PKC-δ neurons. F(1,30) = 6.34 (IL-1β), F(1,18) = 7.11 (LPS), n = 4–13 animals (indicated below each group). Data are mean ± s.e.m. Scale bars, 100 µm. *p < 0.05, **p < 0.01, ***p < 0.001. Source data are provided as a separate file
