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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Pain. 2015 Oct;156(10):1852–1863. doi: 10.1097/j.pain.0000000000000204

Figure 5. Substance P deficient (SP KO) and CGRP RAMP1 receptor deficient (RAMP1 KO) fracture (FX) mice had reduced hindpaw allodynia, unweighting, warmth, and edema, compared to wildtype (WT) fracture mice.

Figure 5

WT fracture mice exhibited hind paw von Frey allodynia (A), unweighting (B), warmth (C) and edema (D) at 3 weeks post-fracture. The SP deficient fracture mice had attenuated hind paw allodynia (A) and unweighting (B), and failed to develop hind paw warmth (C) or edema (D). Similarly, the RAMP1 receptor deficient fracture mice had no von Frey allodynia (A), attenuated unweighting (B), and no warmth (C), but the development of post-fracture hindpaw edema was unaffected by the loss of CGRP signaling (D), compared to WT FX mice. Values are means ± SE, n=8 per cohort. One-way ANOVA (p < 0.001) with Bonferroni post hoc testing ** P< 0.01 and *** P< 0.001 for WT FX, SP KO FX, or RAMP1 KO FX vs WT Control, ## p< 0.01 and ### p< 0.001 for SP KO FX, or RAMP1 KO FX vs WT FX.