Fig. 3

TLR4-deleted mice are partially protected against HFD-induced food-reward behavioural dysregulations and neuroinflammation. Wild-type and TLR4 KO mice were monitored for 8 weeks on CT or HFD. (A) Experimental plan of Experiment 3. (B) Body weight gain evolution in grams before behavioural tests (n = 15–17/group). (C) Mean daily HFD intake in kcal before behavioural tests in WT_HFD and KO_HFD-fed mice (n = 10–12/group). (D) 2-Food-choice paradigm: HFHS diet-based food intake in grams in WT_CT, KO_CT, WT_HFD and KO_HFD-fed mice (n = 10–12/group). (E) Operant conditioning test showing the number of active lever presses during the four progressive ratio (PR) sessions and (F) the breakpoint during the PR4 session by WT_CT, KO_CT, WT_HFD and KO_HFD-fed mice (n = 8–12/group). (G) NAc relative mRNA expression of ionized calcium-binding adapter (Iba1), glial fibrillary acidic protein (Gfap), cluster of differentiation 45 (Cd45), tumour necrosis factor alpha (Tnfa), interleukin 1 beta (Il1b) and interleukin 6 (Il6) measured by real-time qPCR in CT and HFD-fed mice (n = 10–16/group). (H) DS relative mRNA expression of ionized calcium-binding adapter (Iba1), glial fibrillary acidic protein (Gfap), cluster of differentiation 45 (Cd45), tumour necrosis factor alpha (Tnfa), interleukin 1 beta (Il1b) and interleukin 6 (Il6) was measured by real-time qPCR in CT and HFD-fed mice (n = 10–16/group). The results were obtained from 2 independent experiments. The data are shown as the means ± SEMs. P values were obtained after two-way repeated-measures ANOVA followed by Bonferroni post hoc correction (B, E), after unpaired Student’s t-test (C), and after one-way ANOVA followed by the Holm‒Sidak post hoc test (D, F, G, H). Different letters indicate significant differences at p values < 0.05 between WT_CT, KO_CT, WT_HFD and KO_HFD