The increase in morphine antinociceptive potency produced by carrageenan-induced hindpaw inflammation is blocked by naltrindole, a selective δ-opioid antagonist

@article{Ossipov1995TheII,
  title={The increase in morphine antinociceptive potency produced by carrageenan-induced hindpaw inflammation is blocked by naltrindole, a selective $\delta$-opioid antagonist},
  author={Michael H. Ossipov and Carl J Kovelowski and Frank Porreca},
  journal={Neuroscience Letters},
  year={1995},
  volume={184},
  pages={173-176}
}
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52 Citations
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Results Citations
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52 Citations

Effects of spinal cholecystokinin receptor antagonists on morphine antinociception in a model of visceral pain in the rat.

Data indicate that CCK, acting at the CCK(B) receptor, is involved in modulating morphine antinociception following a noxious visceral stimulus, however, CCK receptor antagonists no longer enhance morphine ant inociceptive effects after instillation of intracolonic TNBS, suggesting that visceral inflammation may lead to a reduction in spinal CCK release.

The analgesic effects of supraspinal mu and delta opioid receptor agonists are potentiated during persistent inflammation.

  • R. HurleyD. Hammond
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 2000
Results indicate that peripheral inflammatory injury alters the pharmacology of excitatory and inhibitory inputs that modulate the activity of RVM neurons in such a manner as to enhance the effects of opioid agonists in this region.

The Analgesic Effects of Supraspinal μ and δ Opioid Receptor Agonists Are Potentiated during Persistent Inflammation

Results indicate that peripheral inflammatory injury alters the pharmacology of excitatory and inhibitory inputs that modulate the activity of RVM neurons in such a manner as to enhance the effects of opioid agonists in this region.

Contribution of Endogenous Enkephalins to the Enhanced Analgesic Effects of Supraspinal μ Opioid Receptor Agonists after Inflammatory Injury

It is suggested that persistent inflammatory injury increased the release in the RVM of opioid peptides with preferential affinity for the δ opioid receptor, which can interact in a synergistic or additive manner with an exogenously administered μ opioid receptor agonist.

Effects of opioid receptor antagonists on the effects of i.v. morphine on carrageenin evoked c-Fos expression in the superficial dorsal horn of the rat spinal cord

Involvement of Gi/o proteins and GIRK channels in the potentiation of morphine-induced spinal analgesia in acutely inflamed mice

Differences in the transduction mechanism activated by MOR at postsynaptic level, probably related with GIRK channels activity, could participate in the potentiation of morphine-induced spinal analgesia in acutely inflamed mice.

Further evidence for the interaction of μ- and δ-opioid receptors in the antinociceptive effects of the dual inhibitor of enkephalin catabolism, RB101(S) A spinal c-Fos protein study in the rat under carrageenin inflammation

Opioid Pharmacology of Acute and Chronic Pain

This work has suggested that neuropathic pain states are thought to be associated with increased spinal CCK content and, accordingly, reduced antinociceptive potency and efficacy of morphine, and that spinal levels of dynorphin are also Thought to be increased in conditions of chronic pain.

Synergy between the antinociceptive effects of morphine and NSAIDs.

The synergy between morphine and NSAIDs could be related to different pathways of pain transmission, probably related to the different intracellular signal transduction mechanisms of action of opioid and non-opioid agents.

Persistent pain model reveals sex difference in morphine potency.

These studies demonstrate sex-based differences in the effects of morphine on thermal hyperalgesia in a model of persistent inflammatory pain.
...

References

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Cholecystokinin as a factor in the enhanced potency of spinal morphine following carrageenin inflammation

It is proposed that in normal animals, morphine may produce a maximal stimulation of the release of CCK such that exogenous CCK is unable to reduce further the analgesic effects under these conditions.

Activation of spinal delta-1 or delta-2 opioid receptors reduces carrageenan-induced hyperalgesia in the rat.

Although NTB distinguishes between delta-1 and delta-2 opioid receptors, high doses may not effectively distinguish between delta and mu receptors, consistent with characterization of NTB as a selective delta- 2 receptor antagonist.

PD134308, a selective antagonist of cholecystokinin type B receptor, enhances the analgesic effect of morphine and synergistically interacts with intrathecal galanin to depress spinal nociceptive reflexes.

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Cholecystokinin antagonists selectively potentiate analgesia induced by endogenous opiates

The analgesic effects of morphine, but not those of the enkephalinase inhibitor thiorphan, are enhanced in arthritic rats

Modulation of mu-mediated antinociception by delta agonists in the mouse: selective potentiation of morphine and normorphine by [D-Pen2,D-Pen5]enkephalin.

Opioid δ-receptor involvement in supraspinal and spinal antinociception in mice

Subcutaneous formalin induces a segmental release of Met-enkephalin-like material from the rat spinal cord

Cholecystokinin and its antagonist lorglumide respectively attenuate and facilitate morphine-induced inhibition of C-fiber evoked discharges of dorsal horn nociceptive neurons