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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: J Pain. 2017 Jan 9;18(5):574–582. doi: 10.1016/j.jpain.2016.12.017

Fig. 2. AMP-induced mechanical hyperalgesia in primed male and female rats is dependent on its conversion to adenosine and activation of A1 adenosine receptors.

Fig. 2

Male (left panel) and female (right panel) rats received an intradermal injection of ryanodine (100 ng in males and 1 pg in females) on the dorsum of both hind paws. One week later, the ecto-5′nucleotidase inhibitor AMPCP (1 μg, gray symbols) was injected in the left paws, and the A1 adenosine receptor antagonist DPCPX (1 μg, black symbols) was injected in the right paws, at the same site as ryanodine. The control groups, represented by the white symbols, are the same primed groups shown in Fig. 1. After 10 min, AMP (1 μg) was injected in all paws and the mechanical nociceptive threshold evaluated, 10, 20 and 30 min later. While in primed paws AMP induced significant hyperalgesia (control groups), in the groups pretreated with AMPCP or DPCPX the AMP-induced hyperalgesia was markedly attenuated (males: AMPCP, F1,10 = 32.22, *p = 0.0002; DPCPX, F1,10 = 65.62, ****p < 0.0001; females: AMPCP, F1,10 = 14.96, **p = 0.0031; DPCPX, F1,10 = 27.07, ***p = 0.0004, when the inhibitors groups are compared to the control groups, two-way repeated measures ANOVA followed by the Bonferroni post-hoc test) demonstrating that the mechanical hyperalgesia induced by AMP in primed rats is dependent on its conversion to adenosine. (N = 6 paws per group)