The purpose of this study was to determine which delta (δ) opioid receptor subtype, δ1 or δ2, was involved in producing the antinociceptive action of heroin and 6-monacetylmorphine (MAM) in Swiss Webster mice. Previous work from this laboratory established that heroin and MAM, given intracerebroventricularly (i.c.v.) in Swiss Webster mice, produce antinociception through activation of supraspinal δ receptors. Naltrindole, but not naloxone or nor-binaltorphimine, antagonizes the inhibitory action of heroin and MAM in the tail-flick test. Recent literature documents the occurence of subtypes of the δ opioid receptor and the availability of selective antagonists. 7-Benzylidenenaltrexone (BNTX) antagonizes the antinociception induced by δ1 receptor agonists without affectingthat induced by δ2 receptor agonists. Naltriben (NTB) selectively inhibits δ2- but not δ1-induced antinociception. In the present study BNTX and NTB were administered i.c.v. with heroin and MAM to determine the δ receptor subtype responsible for inhibition of the tail-flick response in Swiss Webster mice. The ED50 for heroin-induced antinociception was increased 19-fold by BNTX and was not altered by NTB administration. On the other hand, the ED50 value of MAM was increased 3-fold by NTB and was not altered b by BNTX administration. These results suggest that heroin activated supraspinal δ1 receptors and MAM acted on supraspinal δ2 receptors to produce antinociception in Swiss Webster mice.
- delta subtype
- δ opioid receptors