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Figure 3 | Molecular Pain

Figure 3

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

Figure 3

Runx1F/F;Nav1.8Cre mice showed impaired inflammatory pain but largely unaffected heat pain or neuropathic pain. (A) Mechanical thresholds measured by Von Frey filaments in control mice (n = 10) and L-CKO mice (n = 12). No difference was observed (p > 0.05). (B) Heat sensitivity measured using the hot plate assay. Controls, n = 10. Mutants, n = 12. No difference was observed (p > 0.05). (C) Neuropathic pain (SNI model). No difference was observed in mechanical allodynia over the examined time course (controls, n = 10; mutants, n = 12) (p > 0.05, ANOVA). (D, E) Inflammatory Pain (CFA model), (D) Measurement of mechanical allodynia using Von Frey filaments. Controls showed an 84 ± 3% drop in mechanical threshold two days after CFA injection (n = 9, ***p < 0.001), while mutants showed only a 33 ± 8% drop (n = 14, **p < 0.01). This difference in mechanical sensitivity drop was highly significant (†††p < 0.001). (E) Measurement of heat hyperalgesia using the Hargreaves apparatus. Controls (n = 8) were strongly sensitized (70 ± 4% drop in latency, ***p < 0.001) while mutants (n = 8) showed no significant sensitization (p > 0.05). The difference in latency between controls and mutants post-CFA was highly significant (†††p < 0.001). Error bars indicate standard errors of the mean (SEM).

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