Figure 8.

Protein translation inhibitor reverses priming when it is administered at the terminal of the nociceptor, but not at its cell body. The effect of the protein translation inhibitor cordycepin on priming was evaluated in rats that had received intraganglion (i.gl.) injection of 8-bromo cAMP (10 μg) 2 weeks before. The average paw-withdrawal thresholds before and 2 weeks after 8-bromo cAMP (when the experiments were performed) were 121.6 ± 1.4 and 120.0 ± 1.4 g, respectively; no significant (NS) difference between these two values was observed (t₍₁₇₎ = 1.062, p = 0.3032, NS; paired Student's t test, data not shown). Rats were then divided into a control group (white bars) and two experimental groups, one that received cordycepin intradermally on the dorsum of the hindpaw (1 μg, gray bars) and the other that received i.gl. injection to the DRG (10 μg, black bars). Fifteen minutes later, PGE₂ (100 ng) was injected into the dorsum of the hindpaw, and the paw-withdrawal threshold was evaluated 30 min and 4 h later. We observed that, while PGE₂-induced hyperalgesia was still significant at the fourth hour in the control group and the experimental group that received cordycepin in the DRG (p > 0.05, when both groups are compared), in the group that received cordycepin in the paw it was significantly attenuated at the fourth hour (***p < 0.001, when compared with the control group), indicating a role of protein translation in the terminal of the nociceptor, but not in the DRG, in hyperalgesic priming (two-way repeated-measures ANOVA followed by Bonferroni post-test; N = 6 paws per group).