Abstract
The intracerebroventricular (i.c.v.) injection to mice of antisera directed against different sequences G i3α, impaired the antinociception produced by the selective ligands of δ opioid receptors DPDPE and [D-Ala 2]-Deltorphin II, when studied 24 h later in the tail-flick test. Likewise, the potency of the μ/δ ligands DADLE, etorphine and β-endorphin-(1–31) was also reduced. Antinociception due to the μ-agonists morphine and DAMGO was slightly altered by this treatment. The selective δ antagonist ICI 174864 significantly reduced the antinociceptive activity of these opioids to the same extent observed after giving anti-G i3α antisera. In animals treated with the antisera, ICI 174864 failed to reduce the antinociceptive effect that remained. It is concluded that G i3 is the type of transducer protein regulated by δ opioid receptors to produce supraspinal antinociception in mice.
Published Version
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