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. 2022 May 6;8(18):eabm2545. doi: 10.1126/sciadv.abm2545

Fig. 6. Elevated TNFα mediates Gpr56 cKO–induced MGE proliferation deficits.

Fig. 6.

(A) TNFα mRNA was significantly elevated in E14.5 microglia isolated from Gpr56 cKO and MIA fetal brains. IL-17a–neutralizing antibodies significantly attenuated microglial TNFα mRNA elevation in MIA-treated fetal brains. n = 5 to 8. ACTB, actin beta. (B) Representative images of BrdU and Nkx2.1 in ex vivo culture slices. (C) The percentage of BrdU+ cells in the MGE were significantly decreased in Gpr56 cKO slices compared to control slices under PBS treatment. In control slices, TNFα treatment significantly decreased the percentage of BrdU+ progenitors in the MGE, while treatment with TNFR1-neutralizing antibodies had no effect (P > 0.99). In Gpr56 cKO slices, TNFR1-neutralizing antibody treatment significantly increased MGE proliferation, while TNFα treatment did not alter MGE proliferation (P > 0.99). Control: n = 5; cKO: n = 6. Unpaired t test for (A) and two-way ANOVA and Bonferroni’s post hoc test for (C). *P < 0.05, **P < 0.01, and ***P < 0.001. Data are presented as means ± SEM.