We examined the role of the gamma(2) subunit of G proteins (G gamma(2)) in
the antinociception produced by c[D-Pen(2),D- Pen(5)]enkephalin (DPDPE) in
mice. DPDPE produced 84.0 +/- 9.0% antinociception in vehicle-treated mice.
After intracerebroventricular (i.c.v.) treatment with an antisense phospho
rothioate oligodeoxynucleotide to the G gamma(2) subunit, DPDPE-mediated an
tinociception decreased to 24.4 +/- 7.4%. The mismatch phosphorothioate oli
godeoxynucleotide-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 antisen
se phosphorothioate oligodeoxynucleotide-treated mice was significant in co
mparison with vehicle-treated (P < 0.001), mismatch phosphorothioate oligod
eoxynucleotide-treated (P < 0.01) and missense phosphorothioate oligodeoxyn
ucleotide-treated (P < 0.05) mice. These results suggest that the G protein
gamma(2) subunit is involved in the transduction pathway leading to antino
ciception by DPDPE. (C) 2000 Published by Elsevier Science B.V. All rights
reserved.