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. 2023 Nov 22;8(22):e169554. doi: 10.1172/jci.insight.169554

Figure 5. Npff/Npy1r-INs do not contribute to nerve injury–induced mechanical and cold allodynia.

Figure 5

(A) Strategy for selectively targeting Npff/Npy1r-INs in NpffCre mice with intraspinal injections of the Cre-dependent virus AAV8-hSyn-DIO-hM4DGi-mCherry. (B) AAV transfection in NpffCre mice (large image) and FISH confirmation of Npy1r and Npff expression in transfected cells (insert). Scale bar: 10 μm. (C) Experimental timeline of chemogenetic reflexive behavioral testing at both pre- and post-SNI time points. (D and E) Chemogenetic inhibition of NPFF-INs with CNO (3 mg/kg) does not change mechanical sensitivity when conducted either before (3-way repeated measures [RM] ANOVA: drug × virus × side, F1,20 = 0.7875, P = 0.3854) or after SNI (3-way RM ANOVA: drug × virus × side, F1,20 = 0.6462, P = 0.4309) (n = 6 mice/group). (F and G) Chemogenetic inhibition of NPFF-INs with CNO (3 mg/kg) does not change cold sensitivity pre-SNI (3-way RM ANOVA: drug × virus × side, F1,20 = 1.215, P = 0.2834) or post-SNI (3-way RM ANOVA: drug × virus × side, F1,20 = 0.1615, P = 0.6920) (n = 6 mice/group). Data shown as mean ± SEM.