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Pretreatment with pertussis toxin blocks morphine- but not beta-endorphin-induced antinociception in the mouse
1Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA. ltseng/post.its.mcw.edu
Abstract:
We have previously demonstrated that the antinociception induced by morphine and beta-endorphin given intracerebroventricularly (i.c.v.) is mediated by the stimulation of respective mu- and epsilon-opioid receptors. The effects of i.c.v. pretreatment with pertussis toxin on the antinociception induced by morphine and beta-endorphin given i.c.v. were studied in male ICR mice. Antinociception was assessed by the tail-flick and hot-plate tests. Pretreatment with pertussis toxin (0.5 microgram) given i.c.v. 96 h earlier blocks the antinociception induced by i.c.v. administered morphine in both tail-flick and hot-plate tests. The same pretreatment did not affect the antinociception induced by i.c.v. administered beta-endorphin. Our results indicate that morphine-, but not beta-endorphin-induced antinociception is mediated by pertussis toxin sensitive G-proteins.
Insights
Pertussis toxin blocks morphine-induced pain relief but not beta-endorphin-induced pain relief in mice. This suggests morphine
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Opioid receptors mediate pain relief from morphine and beta-endorphin.
- Pertussis toxin affects G-protein signaling pathways.
Purpose of the Study:
- To investigate the role of pertussis toxin-sensitive G-proteins in opioid-induced antinociception.
- To differentiate the signaling pathways of morphine and beta-endorphin.
Main Methods:
- Male ICR mice were pretreated intracerebroventricularly (i.c.v.) with pertussis toxin.
- Antinociception was measured using the tail-flick and hot-plate tests.
- Morphine and beta-endorphin were administered i.c.v. to assess their antinociceptive effects post-pretreatment.
Main Results:
- Pertussis toxin pretreatment blocked morphine-induced antinociception in both tests.
- Pertussis toxin pretreatment did not affect beta-endorphin-induced antinociception.
- Morphine-induced antinociception is mediated by pertussis toxin-sensitive G-proteins, while beta-endorphin's is not.
Conclusions:
- Morphine analgesia involves pertussis toxin-sensitive G-proteins.
- Beta-endorphin analgesia likely utilizes a different signaling pathway.
- This study distinguishes opioid signaling mechanisms in pain modulation.