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. Author manuscript; available in PMC: 2018 Jan 6.
Published in final edited form as: Neuroscience. 2016 Nov 5;340:384–397. doi: 10.1016/j.neuroscience.2016.10.064

Figure 8.

Figure 8

An antibody that activates TrkA causes thermal hyperalgesia. (A) Anti-TrkA antibody (20 µl/paw), when injected into the naïve rat plantar hind paw, led to a shortening of PWL, measured at 3–4 h, but prevented further shortening of PWL following NGF (500 ng/10 µl) (n=9). Significance (P<0.05) was only found for Dunn’s pair-wise comparison of 23h and 0.5h time points, applied after Friedman’s test. (B) Injection of control IgG, from naïve rat serum (20 µl/paw), 4 h before NGF (500 ng/10µl), neither changed PWL, nor affected thermal hyperalgesia from subsequently injected NGF (n=6). **P<0.01 vs. baseline after IgG, ILP (Friedman test followed by Dunn’s post hoc test). (C) Lack of effect of K252a on anti-TrkA antibody-induced thermal hyperalgesia. K252a (20 nmol/paw) was pre-injected 0.5h before the antibody (n=3). ^P<0.05 for baseline vs 24 h after antibody (two-tailed Wilcoxon Paired test). (D) Further reduction of PWL by i.pl. capsaicin, after the anti-TrkA antibody-induced hyperalgesia (n=6). ^P<0.05 vs. baseline ILP, naïve rats (two-tailed Wilcoxon test); +P<0.05 vs. value at 4h after TrkA ab. ILP (two-tailed Wilcoxon test).