Figure 2.

Activation of α7 nACh receptors attenuates signs of established inflammatory hypersensitivity. The rats were injected with either (A, B, C) carrageenan (2% in saline, 100 µL, s.c.) or (D, E, F) CFA (50% in saline, 100 µL, s.c.) into the plantar surface of the hind paw. They were then administered either drug or vehicle at the time (t) indicated before measurement of a post-treatment response. (A, D) Effects of diclofenac (1–30 mg·kg⁻¹ and 3–30 mg·kg⁻¹ p.o., t =−60 min) and vehicle (10% HBCD) on paw pressure threshold (g) in response to mechanical stimulation of the ipsilateral hind paw as an index of mechanical hyperalgesia. Pre- and post-inflammation baseline (BL) values are indicated with dashed lines. In subsequent experiments, diclofenac (10 mg·kg⁻¹) was included as a positive control and data expressed as a % of diclofenac-mediated anti-hyperalgesia. Effects of (B, E) compound B (3–30 mg·kg⁻¹ and 10, 30 mg·kg⁻¹, s.c., t =−30 min) and vehicle (0.9% NaCl/0.5% glucose) and (C, F) PNU-120596 (0.3–30 mg·kg⁻¹ and 10, 30 mg·kg⁻¹ i.p., t =−30 min) and vehicle (15% MBCD) on mechanical hyperalgesia. All groups n= 8–16 rats. All data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 versus corresponding vehicle group (one-way anova followed by Bonferroni's t-test, and where appropriate, sub-analysis by Student's t-test).