We examined the role of the γ2 subunit of G proteins (Gγ2) in the antinociception produced by c[D-Pen2, D-Pen5]enkephalin (DPDPE) in mice. DPDPE produced 84.0±9.0% antinociception in vehicle-treated mice. After intracerebroventricular (i.c.v.) treatment with an antisense phosphorothioate oligodeoxynucleotide to the Gγ2 subunit, DPDPE-mediated antinociception decreased to 24.4±7.4%. The mismatch phosphorothioate oligodeoxynucleotide-treated mice showed 65.1±10.3% antinociception, while the missense phosphorothioate oligodeoxynucleotide-treated mice showed 76.4±23.6% antinociception by DPDPE. The reduction of analgesia in antisense phosphorothioate oligodeoxynucleotide-treated mice was significant in comparison with vehicle-treated (P<0.001), mismatch phosphorothioate oligodeoxynucleotide-treated (P<0.01) and missense phosphorothioate oligodeoxynucleotide-treated (P<0.05) mice. These results suggest that the G protein γ2 subunit is involved in the transduction pathway leading to antinociception by DPDPE.
- DPDPE (c[D-Pen, D-Pen]enkephalin)
- G protein γ subunit
ASJC Scopus subject areas