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Figure 1 | Molecular Pain

Figure 1

From: Transient inflammation-induced ongoing pain is driven by TRPV1 sensitive afferents

Figure 1

A. Hindpaw CFA produced lower paw withdrawal latencies within 24 hours (D1). Paw withdrawal latencies remained lower than pre-injury baseline (BL) 4 days following injury, but were higher than those observed 1 day following injury. *p < 0.05 vs. pre-injury thresholds (BL); #p < 0.05 vs. D1 thresholds, n = 7-8. B. Hindpaw CFA produced guarding behavior within 24 hours (D1). Guarding behavior remained elevated compared to pre-injury baselines (BL) 4 days following injury, but was significantly reduced compared to the D1 time-point. *p < 0.05 vs. pre-injury thresholds (BL); #p < 0.05 vs. D1 thresholds, n = 7-8. C. Spinal clonidine (10 μg) induced CPP selectively in CFA treated rats at day 1, but not day 4 post CFA, injection. No chamber preference is observed in saline treated rats indicating that this dose of spinal clonidine is not rewarding in the absence of injury. *p < 0.05 vs. saline paired chamber; #p < 0.05 vs. pre-conditioning, n = 7. D. Difference scores calculated as test time - preconditioning time spent in clonidine chamber confirm that CFA treated rats showed CPP 24 hrs, but not 4 days post CFA injection. *p < 0.05 vs. saline treated group. E. CFA decreased paw withdrawal latencies to radiant heat within 24 hours of injection (Post-CFA). Spinal clonidine (10 μg) attenuated, but did not fully reverse CFA-induced thermal hyperalgesia. This dose of spinal clonidine failed to induce antinociception in rats that received intraplantar saline, *p < 0.05 vs. post-CFA, #p < 0.05 vs. pre-CFA, n = 5-8. F. CFA-induced thermal hyperalgesia persisted through day 4 post-CFA. Spinal clonidine (10 μg) induced antihyperalgesia and antinociception, elevating paw withdrawal latencies above baseline values. *p < 0.05 vs. post-CFA, #p < 0.05 vs. pre-CFA, n = 5-8.

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