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. 2022 Feb 16;42(7):1196–1210. doi: 10.1523/JNEUROSCI.1982-21.2021

Figure 6.

Figure 6.

Role of Gαi2 in analgesia and hyperalgesic priming induced by systemic analgesic dose fentanyl and morphine. Rats received injections of AS-ODN (120 μg/20 μl/d, i.t.) or SE-ODN (120 μg/20 μl/d, i.t.) against Gαi2 mRNA, daily for 3 consecutive days. Approximately 17 h after the third injection of ODNs, AD fentanyl (A: 0.03 mg/kg, s.c.) or morphine (B: 3 mg/kg, s.c.) was administered and the mechanical nociceptive threshold was evaluated 1 h later. Treatment with Gαi2 AS-ODN increased analgesia induced by AD fentanyl (A); however, it did not affect analgesia induced by AD morphine (B), when compared with the SE-ODN-treated group (A: t(10) = 5.07, ***p = 0.0005; B: t(10) = 0.96, p = 0.36, when the analgesia in the Gαi2 AS-ODN-treated and the SE-ODN-treated groups is compared at 1 h after systemic AD fentanyl and morphine, respectively; unpaired Student's t test). Rats again received Gαi2 AS-ODN or SE-ODN later on the fourth day. Five days after AD opioids, at which time mechanical nociceptive threshold was not different from preopioid baselines (C: SE-ODN-treated group: t(5) = 2.5, p = 0.06; AS-ODN-treated group that received AD fentanyl: t(5) = 0.67; p = 0.53; D: SE-ODN-treated group: t(5) = 1.0, p = 0.36; AS-ODN-treated group that received AD morphine: t(5) = 0.12, p = 0.91, when the mechanical nociceptive threshold is compared before and 5 d after systemic AD opioids; paired Student's t test), PGE2 (100 ng/5 μl, i.d.) was administered and the mechanical nociceptive threshold was evaluated 30 min and 4 h later. In both the Gαi2 AS-treated and SE-ODN-treated groups, the prolongation of PGE2-induced hyperalgesia was present 5 d after systemic AD fentanyl and morphine (C and D, respectively; C: F(1,10) = 0.68, p = 0.43; D: F(1,10) = 2.84, p = 0.12, when the hyperalgesia in the Gαi2 AS-ODN-treated and the SE-ODN-treated groups is compared at the fourth hour after intradermal PGE2 administration; two-way repeated-measures ANOVA followed by Bonferroni's post hoc test). Our data support the suggestion that the Gαi2 subunit plays a role in analgesia produced by AD fentanyl, but not morphine; also, hyperalgesic priming produced by AD fentanyl and morphine is not Gαi2 dependent (n = 6 paws/6 rats/group).