SUPRASPINAL DELTA-RECEPTOR SUBTYPE ACTIVITY OF HEROIN AND 6-MONOACETYLMORPHINE IN SWISS WEBSTER MICE

被引:26
作者
RADY, JJ
TAKEMORI, AE
PORTOGHESE, PS
FUJIMOTO, JM
机构
[1] VET ADM MED CTR,COLL MED,RES SERV 151,MILWAUKEE,WI 53295
[2] UNIV MINNESOTA,MINNEAPOLIS,MN 55455
关键词
HEROIN; DELTA(1) OPIOID RECEPTORS; 6-MONOACETYLMORPHINE; DELTA SUBTYPE;
D O I
10.1016/0024-3205(94)00486-2
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The purpose of this study was to determine which delta (delta) opioid receptor subtype, delta(1) or delta(2), 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 delta 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 delta opioid receptor and the availability of selective antagonists. 7-Benzylidenenaltrexone (BNTX) antagonizes the antinociception induced by delta(1) opioid receptor agonists without affecting that induced by delta(2) receptor agonists. Naltriben (NTB) selectively inhibits delta(2)- but not delta(1)-induced antinociception. In the present study BNTX and NTB were administered i.c.v. with heroin and MAM to determine the delta receptor subtype responsible for inhibition of the tail-flick response in Swiss Webster mice. The ED(50) for heroin-induced antinociception was increased 19-fold by BNTX and was not altered by NTB administration. On the other hand, the ED(50) value of MAM was increased 3-fold by NTB and was not altered antinociception induced by by BNTX administration. These results suggest that heroin activated supraspinal delta(1) receptors and MAM acted on supraspinal delta(2) receptors to produce antinociception in Swiss Webster mice.
引用
收藏
页码:603 / 609
页数:7
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