Fig. 5: IL-17A improves cerebellar PC excitability and ASD-like behaviors in Fmr1-KO mice.

a, b Whole-cell patch-clamp recordings showing that IL-17A bath incubation (10 ng/mL, 10 min) increased the spontaneous firing rates of PCs in Fmr1-KO mice. This effect was blocked by co‑application of the NF‑κB inhibitor PDTC (1.64 ng/mL, 10 min), with no significant difference observed between the Fmr1‑KO + PDTC and Fmr1‑KO + PDTC + IL‑17 A groups (WT, n = 9 cells from 4 mice; Fmr1-KO/Fmr1-KO + IL-17A, n = 5 cells from 3 mice; Fmr1-KO + PDTC /Fmr1‑KO + PDTC + IL‑17 A, n = 5 cells from 3 mice). c-e Bath incubation with IL-17A (10 ng/mL, 10 min) reduced the amplitude of sIPSCs in PCs, but did not affect their frequency in Fmr1-KO mice. The effect of IL‑17 A on sIPSC amplitude was abolished in the presence of PDTC (1.64 ng/mL, 10 min) (WT, n = 7 cells from 2 mice; Fmr1-KO/Fmr1-KO + IL-17A, n = 6 cells from 2 mice; Fmr1-KO + PDTC /Fmr1‑KO + PDTC + IL‑17 A, n = 6 cells from 3 mice). f Schematic diagram illustrating the protocol for behavioral assessment: IL-17A (50 ng/side) or vehicle was microinjected into cerebellar Crus I 4 h prior to testing. g, h Microinjection of IL-17A into Crus I significantly improved social interaction time and the social preference index with stranger mice (WT, n = 8 mice; Fmr1-KO, n = 12 mice; Fmr1-KO + IL-17A, n = 8 mice), and reduced the number of buried marbles in Fmr1-KO mice. (WT, n = 7 mice; Fmr1-KO, n = 5 mice; Fmr1-KO + IL-17A, n = 8 mice). Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, n.s. indicates not significant.