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Journal of Neuroscience, Vol 11, 928-932, Copyright © 1991 by Society for Neuroscience

ARTICLE

Kappa- and delta-opioids block sympathetically dependent hyperalgesia

YO Taiwo and JD Levine
Department of Anatomy, University of California, San Francisco 94143- 0724.

Direct hyperalgesia induced by prostaglandin E2 (PGE2) can be blocked by mu- but not delta- or kappa-opioids. However, there is evidence that kappa- and delta-opioid receptors are located on sympathetic postganglionic neuron (SPGN) terminals, which mediate bradykinin (BK) hyperalgesia via SPGN-terminal-dependent production of PGE2. Therefore, we evaluated the antinociceptive effect of delta- and kappa-opioids on BK hyperalgesia. We demonstrate that the mechanical hyperalgesia induced by intradermal injection of BK can be blocked by the kappa- opioid agonist trans-3,4-dichloro-N-methyl-N[2-(-pyrrolidinyl)cyclo- hexyl] benzeneacetamide (U50,488H) and by the delta-opioid agonist (D- Pen2,5)-enkephalin (DPDPE), as well as the mu-opioid agonist Tyr-D-Ala- Gly-NMe-Phe-Gly-ol(DAMGO). Pertussis toxin prevented the inhibition of BK-induced hyperalgesia by U50,488H, DPDPE, or DAMGO. We conclude that the observed peripheral analgesic effects of kappa- and delta-opioid agonists result from actions upon SPGN terminals and that these effects are mediated by inhibitory G-proteins.

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