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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Neuropeptide regulation of adaptive immunity in the tibia fracture model of complex regional pain syndrome

Fig. 1

Neuropeptide signaling contributes to the development of evoked and spontaneous post fracture pain behaviors. Wildtype fracture (WT-FX) mice developed hind paw von Frey allodynia and hindlimb unweighting at 3 weeks post-fracture, compared to control wildtype no fracture (WT-NO FX) mice, but wildtype FX mice treated with the substance P (SP) tachykinin 1 receptor antagonist LY303870 (WT-FX + LY) had reduced allodynia (a) and unweighting (b). Substance P-deficient fracture mice (Tac1−/−-FX, panels c, d), and calcitonin gene-related peptide (CGRP) receptor-deficient fracture mice (RAMP1−/−-FX, panels e, f) also exhibited attenuated allodynia and unweighting after fracture. These results support the hypothesis that neuropeptide signaling contributes to the development and maintenance of pain behaviors after fracture. Measurements for a, c, and e represent the difference between the fracture side and contralateral paws, thus a negative value represents a decrease in mechanical nociceptive thresholds on the affected side. Measurements for b, d, f represent weight-bearing on the fracture hindlimb as a ratio to 50% of bilateral hindlimb loading, thus, a percentage lower than 100% represents hind paw unweighting. Data were analyzed using a one-way analysis of variance (ANOVA) with Bonferroni correction test for post hoc contrasts, error bars indicate SEM, n = 8 per cohort. *P < 0.05, **P < 0.01 vs. control WT-NO FX, #P < 0.05, ##P < 0.01 vs WT-FX

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