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Journal of Pharmacology and Experimental Therapeutics

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Abstract

Heroin acts on different opioid receptors than morphine in Swiss Webster and ICR mice to produce antinociception.

J J Rady, S C Roerig and J M Fujimoto
Journal of Pharmacology and Experimental Therapeutics February 1991, 256 (2) 448-457;
J J Rady
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S C Roerig
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J M Fujimoto
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Abstract

The opioid receptor types involved in supraspinal and spinal heroin-induced analgesia in Swiss Webster and ICR mice were determined by intracerebroventricular (i.c.v.) and intrathecal (i.t.) administration of opioid agonists and antagonists. Also, comparisons were made with morphine. Antinociception was measured by changes in tail-flick latency. In Swiss Webster mice, i.c.v. heroin like [D-Pen2-D-Pen5]enkephalin, a delta receptor opioid agonist, activated supraspinal delta opioid receptors as evidenced by inhibition of analgesia by coadministration of naltrindole, a delta receptor antagonist. Lack of effect of i.t. yohimbine and methysergide vs. i.c.v. heroin indicated that spinal descending noradrenergic and serotonergic systems were not involved. Heroin and [D-Pen2-D-Pen5]enkephalin were also matched in producing additive interactions with i.t. opioids. Also, i.c.v. heroin like [D-Pen2-D-Pen5]enkephalin did not activate a dynorphin-mediated antianalgesic system. In ICR mice, i.c.v. heroin receptor selectivity matched that of i.c.v. Tyr-D-Ala2-Gly-NMePhe4-Gly-ol5, a selective mu receptor opioid agonist. Analgesia was inhibited by pretreatment with i.c.v. beta-funaltrexamine, a nonequilibrium mu receptor antagonist. Intrathecal administration of methysergide inhibited i.c.v. heroin-induced analgesia whereas i.t. yohimbine had no effect, which indicated that a descending serotonergic system but not a noradrenergic system was involved. Low doses of i.t. naloxone and nor-binaltorphimine increased the analgesic effect. This effect was consistent with activation of an antianalgesic system by i.c.v. heroin, which was mediated by dynorphin A in the spinal cord. Desensitization of the antianalgesic system also resulted in increased analgesia. In both Swiss Webster and ICR mice, i.t. heroin-induced analgesia involved spinal mu receptors like those stimulated by Tyr-D-Ala2-Gly-NMePhe4-Gly-ol5. Analgesia was inhibited by i.t. naloxone. In both strains, i.t. heroin, like i.t. Tyr-D-Ala2-Gly-NMePhe4-Gly-ol5, produced an additive interaction with i.t. clonidine. In conclusion, the supraspinal receptors activated by heroin are different between Swiss Webster and ICR mice. In both strains, the receptor selectivities assigned to heroin did not match those for morphine. Heroin did not act by being biotransformed to morphine.

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Journal of Pharmacology and Experimental Therapeutics
Vol. 256, Issue 2
1 Feb 1991
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Abstract

Heroin acts on different opioid receptors than morphine in Swiss Webster and ICR mice to produce antinociception.

J J Rady, S C Roerig and J M Fujimoto
Journal of Pharmacology and Experimental Therapeutics February 1, 1991, 256 (2) 448-457;

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Abstract

Heroin acts on different opioid receptors than morphine in Swiss Webster and ICR mice to produce antinociception.

J J Rady, S C Roerig and J M Fujimoto
Journal of Pharmacology and Experimental Therapeutics February 1, 1991, 256 (2) 448-457;
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