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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Nat Neurosci. 2014 Jul 27;17(9):1240–1248. doi: 10.1038/nn.3767

Figure 7. Local CEA inhibitory circuits mediate feeding inhibition by PKC-δ+ neurons.

Figure 7

a. Schematic illustrating combined in vivo light and drug delivery to CEA. b, IPSC of PKC-δ− neurons by optogenetic activation of PKC-δ+ neurons is blocked by bicuculline. c, Food intake in 24 h fasted animals photostimulated and infused with ACSF or 0.2 mM bicuculline. n = 7 mice in each group. Two-way ANOVA (F(1, 12) = 0.869, p = 0.37) with post-hoc Bonferroni t-test indicated that ChR2 induced feeding inhibition is blocked by bicuculline. d. CEl PKC-δ−, but not PKC-δ+, neurons are silenced following CEl injection of Cre-out rAAV-eNpHR3.0 (schematic). e. Silencing of CEl PKC-δ− neurons reduces food intake in 24 h fasted animals. n = 9 mice in each group. Paired t-test, t(16) = 3.46, p = 0.0030. See Methods and Supplementary Fig. 9 for additional details. f-h. Food intake in 24 h fasted (g) or fed (h) animals after activation of PKC-δ− neurons (f). n = 10 (control) and 9 (activation) animals. Unpaired t-test, t(17) = 0.458, p = 0.65 (g); t(17) = 0.39, p = 0.70 (h). Box plots show mean (+), median, quartiles (boxes), and range (whiskers). i. Food intake in 24 h fasted animals treated with CCK while activating CEl PKC-δ− neurons using Cre-out ChR2. Unpaired t-test, t(17) = 2.64, p = 0.0093 (saline + activation vs. CCK + activation); t(15) = 2.78, p = 0.014 (CCK + control vs. CCK + activation). Values are means ± s.e.m.. n.s., not significant; *p < 0.05; ** p < 0.01; *** p < 0.001.