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Figure 5 | Molecular Pain

Figure 5

From: Characterization of two Runx1-dependent nociceptor differentiation programs necessary for inflammatory versus neuropathic pain

Figure 5

Tau-Runx1F;Nav1.8Cre mice exhibited a defect in neuropathic pain but maintained normal heat and CFA-induced inflammatory pain. (A) Mechanical thresholds measured by Von Frey filaments in controls (n = 16) and mutants (n = 10). No difference was observed (p > 0.05). (B) Heat sensitivity measured using the hot plate assay. No significant difference was observed between controls (n = 16) and mutants (n = 10) (p > 0.05). (C) Neuropathic pain (SNI). Measurement of mechanical allodynia using Von Frey filaments. A significant difference was observed over the examined time course (p < 0.001, ANOVA) between controls (n = 14) and mutants (n = 10). (D-E) Inflammatory pain (CFA), (D) Measurement of mechanical allodynia. Both controls and mutants were strongly sensitized two days after CFA injection (Controls: n = 15; ***p < 0.001. Mutants: n = 11, ***p < 0.001) with no significant difference between the two genotypes post-CFA (p > 0.05). (E) Measurement of heat hyperalgesia two days after CFA injection. Both controls and mutants were sensitized (controls: n = 5, ***p < 0.001. Mutants: n = 5; ***p < 0.001). The degree of sensitization in controls (63 ± 3% reduction in latency) was only slightly higher than that in mutants (49 ± 4%) (p < 0.05). (F-G) Pain hypersensitivity in response to intraplantar NGF is impaired in mutant mice. A significant difference between controls (n = 5) and mutants (n = 4) was observed over the examined time course for both mechanical allodynia (p < 0.00001, ANOVA) (F) and thermal hyperalgesia (p < 0.00001, ANOVA) (G). Error bars indicate standard errors of the mean (SEM).

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