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. 2023 Apr 20;16:1153870. doi: 10.3389/fnmol.2023.1153870

Figure 4.

Figure 4

Cingulate FMRP is necessary for the development of peripheral hypersensitivity after nerve injury (A) PWT tests after CPN ligation in Fmr1 WT and KO mice (Two-way RM ANOVA, interaction: F(1;11) = 4.90, p < 0.05, Time: F(1;11) = 6.50, p < 0.05, WT vs. KO: F(1;11) = 10.37, p < 0.01; Sham: WT vs. KO, p > 0.05; WT: n = 8, KO: n = 5; “**” indicates p < 0.01). (B) Upper schematics of lentivirus vectors engineered shRNA to knock down Fmr1 and eGFP Ctrl. Lower experimental paradigm for behavioral testing after injection of Fmr1-shRNA virus into ACC. (C) Illustration of bilateral expression of lenti-Fmr1 shRNA virus in ACC of Fmr1 WT mice (scale bar, 200 μm). (D) PWT tests in Fmr1 WT mice conducted at BL, after virus injection of either Fmr1 Ctrl or shRNA in ACC, further after CPN ligation (Two-way RM ANOVA, interaction: F(3;30) = 1.43, p > 0.05, Time: F(3;30) = 19.10, p < 0.01, Ctrl vs. shRNA: F(1;30) = 8.24, p < 0.05, n = 6/group; “*” indicates p < 0.05). (E) Upper schematics of AAV8 vector engineered to overexpress Fmr1 and an eGFP Ctrl. Lower experimental paradigm for behavioral testing. (F) PWTs in Fmr1 KO mice detected at BL, after virus injection of either Fmr1 Ctrl or OE in ACC, further after CPN ligation (Two-way RM ANOVA, interaction: F(4;72) = 12.36, p < 0.01, Time: F(4;72) = 16.11, p < 0.01, Ctrl vs. OE: F(1;72) = 102.31, p < 0.01, n = 10/group; “**” indicates p < 0.01). Data are represented as mean ± SEM; ns, not significant.