Fig. 5: The interaction of SERBP1 and PCIF1 contributes to neuropathic pain.
a Schematic of virus injections and optical fiber implantation for activation of the optogenetic CRY2/CIBN system. b m6Am levels at 10 min after 1-h administration of blue light in wild-type mice injected 5 days previously in S1HL with Lenti-Pcif1-Cibn (Pci-Cibn) and Lenti-Serbp1-Cry2 (Ser-Cry2) or their controls Lenti-Cibn (Ctrl-Cibn) and Lenti-Cry2 (Ctrl-Cry2) (n = 10 mice). Pre, Pci-Cibn/Ser-Cry2-injected mice without blue light; Post, Pci-Cibn/Ser-Cry2-injected mice after 1-h blue light. Paw-withdrawal frequencies (PWF) to 0.07 g (c) and 0.4 g (d) von Frey filaments and paw-withdrawal latencies (PWL) to heat stimuli (e) on the contralateral side of mice injected as described in B. Behavioral tests were conducted 10 min after the end of 1 h blue light administration (n = 11 mice). f, g The level of PCIF1 protein (f) and m6Am (g) on day 7 after microinjection of AAV-DIO-shSerbp1 (shSerbp1) or AAV-DIO-scrambled-shRNA (Scr) in S1HL of CaMK2α-Cre mice preinjected with AAV-DIO-Pcif1 (Pcif1) or AAV-DIO-mCherry (mCherry) (F: n = 12 mice, G: n = 10 mice). Effect of SERBP1 downregulation on the contralateral mechanical (h, i) and heat (j) hypersensitivities induced by PCIF1 upregulation by DIO-Pcif1 (n = 10 mice). Red arrows, DIO-Pcif1 or DIO-mCherry injection. Blue arrows, DIO-shSerbp1 or DIO-mCherry injection. The data are represented as mean ± SEM. S1 samples from two mice were pooled to create one sample (b, f and g). Student’s unpaired t-test (two-tailed) was used for (b). Student’s paired t-test (two-tailed) was used for (c–e). One-way ANOVA followed with Tukey’s post hoc test was used for (f and g). Two-way ANOVA followed with Tukey’s post hoc test was used for (h–j).
