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. 2018 Jul 6;141(8):2312–2328. doi: 10.1093/brain/awy177

Figure 6.

Figure 6

GTN evokes PMA via NADPH oxidase dependent mechanism. (A) Representative images of TRPA1, NOX1, NOX2 and NOX4 staining in mouse trigeminal ganglion. (B) The unselective NOX inhibitor, apocynin (APO; 100 mg/kg), the selective (C) NOX2 (gp91ds-tat peptide, gp91; 10 mg/kg) or the selective NOX1 (ML171; 60 mg/kg) (i.p., all pre-GTN) do not affect PMA evoked by systemic (i.p.) GTN (10 mg/kg). (C) APO (100 mg/kg), gp91 (10 mg/kg) or ML171 (60 mg/kg) (i.p., all post-GTN) partially reduce PMA. The combination of gp91 and ML171 (i.p., post-GTN) reverses PMA measured 2 h after GTN. (D) In situ proximity ligation assays (PLAs) for TRPA1: NOX2 in mouse trigeminal ganglion labelled with NeuN. Veh = the vehicle of GTN. Dash (‐) indicates vehicles of treatments. Error bars indicate mean ± SEM, 7–8 mice per group. ***P < 0.001 versus vehicle. ###P < 0.001 versus GTN; one-way ANOVA with Bonferroni post hoc correction.