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Kappa- and delta-opioids block sympathetically dependent hyperalgesia
1Department of Anatomy, University of California, San Francisco 94143-0724.
Summary
Peripheral kappa- and delta-opioid agonists effectively block bradykinin-induced hyperalgesia. This pain relief stems from actions on sympathetic nerve terminals, mediated by inhibitory G-proteins.
Area of Science:
- Neuroscience
- Pharmacology
- Pain Research
Background:
- Prostaglandin E2 (PGE2) directly induces hyperalgesia, blocked by mu-opioids.
- Kappa- and delta-opioid receptors are present on sympathetic postganglionic neuron (SPGN) terminals.
- SPGN terminals mediate bradykinin (BK)-induced hyperalgesia via PGE2 production.
Purpose of the Study:
- To investigate the antinociceptive effects of kappa- and delta-opioids on BK-induced hyperalgesia.
- To determine the role of SPGN terminals in mediating these effects.
Main Methods:
- Intradermal injection of BK to induce mechanical hyperalgesia.
- Administration of kappa- (U50,488H), delta- (DPDPE), and mu- (DAMGO) opioid agonists.
- Use of pertussis toxin to assess involvement of inhibitory G-proteins.
Main Results:
- BK-induced mechanical hyperalgesia was blocked by kappa-, delta-, and mu-opioid agonists.
- Pertussis toxin administration prevented the inhibitory effects of all tested opioid agonists.
- This indicates the involvement of inhibitory G-proteins in the analgesic mechanism.
Conclusions:
- Peripheral analgesic effects of kappa- and delta-opioid agonists on BK hyperalgesia are mediated by actions on SPGN terminals.
- These effects are dependent on the activation of inhibitory G-proteins.