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

Figure 5.

Figure 5.

Role of Gαi1 in systemic AD fentanyl- and morphine-induced analgesia and priming. Rats received intrathecal injections of AS-ODN (120 μg in 20 μl/d, i.t.) or SE-ODN (120 μg in 20 μl/d, i.t.) against Gαi1 mRNA, daily for 3 consecutive days. On the fourth day, 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 Gαi1 AS-ODN increased analgesia induced by systemic AD fentanyl (A), while it decreased AD morphine-induced analgesia (B), compared with their respective Gαi1 SE-ODN-treated groups (A: t(10) = 3.24, ** p = 0.0088; B: t(10) = 4.81, *** p = 0.0007, when the analgesia in the Gαi1 AS-ODN-treated and the SE-ODN-treated groups is compared at 1 h after systemic AD fentanyl and morphine; unpaired Student's t test). At the end of the fourth day, rats again received intrathecal Gαi1 AS-ODN or SE-ODN. Five days after systemic AD fentanyl and morphine administration, at which time the mechanical nociceptive threshold was not different from preopioid baselines (C: SE-ODN-treated group: t(5) = 0.39, p = 0.71; AS-ODN-treated group that received systemic AD fentanyl: t(5) = 1.4, p = 0.22; D: SE-ODN-treated group: t(5) = 1.0, p = 0.36; AS-ODN-treated group that received systemic AD morphine: t(5) = 0.58, p = 0.59, 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. Prolongation of PGE2-induced hyperalgesia was not affected by treatment with Gαi1 AS-ODN in both AD fentanyl-treated (C) and morphine-treated (D) groups of rats (C: F(1,10) = 1.28, p = 0.28; D: F(1,10) = 0.13, p = 0.72, when the hyperalgesia in the Gαi1 SE-ODN-treated and the AS-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). These findings support the suggestion that Gαi1 plays a role in analgesia, but not in hyperalgesic priming, produced by AD fentanyl and morphine (n = 6 paws/6 rats/group).