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Fig. 6 | Microbiome

Fig. 6

From: The gut metabolite indole-3-propionic acid activates ERK1 to restore social function and hippocampal inhibitory synaptic transmission in a 16p11.2 microdeletion mouse model

Fig. 6

IPA enhanced ERK1/2 phosphorylation in hippocampus of 16p11.2\({}^{+/-}\) mice. A Schematic of the 16p11.2 deletion region and the synonymous region in mouse chromosome 7. B Heat map of 23 expressed genes within 16p11.2 fragment in mouse hippocampus (n = 3 per group). C Protein-protein interaction (PPI) network of differential genes (screening criteria, p < 0.05) in the hippocampus of WT and 16p11.2\({}^{+/-}\) mice. Nodes were size-scaled by degree. D Mapk3 expression was decreased in the hippocampus of 16p11.2\({}^{+/-}\) mice as assessed by RT-qPCR, and IPA could not increase its expression (n = 4 per group. Two-way ANOVA). E The representative Western blots showed IPA promoted the phosphorylation of ERK1/2 in hippocampus of 16p11.2\({}^{+/-}\) mice. F-I Quantification of Western blot analysis showed that IPA did not change the expression levels of ERK1 (F) and ERK2 (G) in the hippocampus of 16p11.2\({}^{+/-}\) mice, but significantly increased the phosphorylation level of ERK1/2 (H, I) (WT + Vehicle: n = 8 mice; WT + IPA: n = 8 mice; 16p11.2\({}^{+/-}\) + Vehicle: n = 8 mice; 16p11.2\({}^{+/-}\) + IPA: n = 7 mice. Two-way ANOVA). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, and n.s.: not significant. Detailed statistical information is presented in Additional file 2: Table S1

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