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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: J Pain. 2014 Jan 7;15(3):312–320. doi: 10.1016/j.jpain.2013.12.005

Figure 1. The prolongation of PGE2-induced hyperalgesia in primed male rats is dependent on αCaMKII.

Figure 1

Male rats that received intradermal injection of the PKCε activator ψεRACK (1 μg, panel A), activated αCaMKII (25 ng, panel B) or the ryanodine receptor agonist (1 μg, panel C) on the dorsum of the hind paw one (panels A and C) or two (panel B) weeks before were treated with intrathecal injection of ODN mismatch (clear bars) or antisense (black bars) for αCaMKII for 3 consecutive days. On the 4th day, vehicle or the αCaMKII inhibitor CaM2INtide (1 μg) was administered, 15 min prior to the injection of PGE2 (100 ng), at the same site. Mechanical nociceptive thresholds were evaluated 30 min and 4 h after PGE2, by the Randall-Selitto paw withdrawal test. We observed, in all cases, significant attenuation of the hyperalgesia induced by PGE2 at the 4th h in the groups pretreated with the antisense/CaM2INtide (panel A, F1,10 = 52.07, ***p < 0.0001; panel B, F1,10 = 68.83, ***p < 0.0001; panel C, F1,10 = 46.14, ***p < 0.0001), when compared to the mismatch/vehicle groups (two-way repeated measures ANOVA followed by Bonferroni post-test, n = 6 paws per group), indicating a role of αCaMKII in the prolongation of PGE2 hyperalgesia in the primed condition.