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. 2016 Nov 28;174(1):57–69. doi: 10.1111/bph.13652

Figure 5.

Figure 5

Phα1β and its recombinant form (CTK 01512–2) reduce TRPA1 channel‐dependent hyperalgesia in a model of neuropathic pain induced by BTZ. At day 7 after treatment with BTZ (1 mg·kg−1, i.p.), mechanical hyperalgesia and cold hyperalgesia are increased (BL, basal level threshold at day 0 before BTZ). Time course and dose–response curve of i.t. administration of Phα1β (10–100 pmol per site), CTK 01512–2 (100 pmol per site) and the selective TRPA1 channel antagonist, HC‐030031 (HC, 30 nmol per site) on mechanical (A) and cold (B) hyperalgesia evoked by BTZ (1 mg·kg−1, i.p.) at day 7 after treatment. Time course of the effect of the i.pl. administration of CTK 01512–2 (300 pmol per paw), ω‐conotoxin MVIIA (300 pmol per paw) and HC‐030031 (HC, 300 nmol per paw) on mechanical (C) and cold (D) hyperalgesia evoked by BTZ (1 mg·kg−1, i.p.) at day 7 after treatment. Dose–response curves were performed 0.5 h after AITC treatment. Each point and column represents the mean of six mice, and vertical lines show the SEM. Statistical analysis was performed using one‐way or two‐way ANOVA followed by Student–Newman–Keuls post hoc test or by Bonferroni's post hoc test respectively. *P < 0.05, significantly different from BTZ/PBS; # P < 0.05, significantly different from BL values.