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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51 Citations
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51 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

Long-Term Changes in the Antinociceptive Potency of Morphine or Dexmedetomidine After a Single Treatment

Long-term changes in the antinociceptive potency of morphine or dexmedetomidine after single treatment in different heat pain tests indicate a delayed type of acute tolerance to morphine.

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.

Opioid pathways activation mediates the activity of nicorandil in experimental models of nociceptive and inflammatory pain.

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.
...

References

SHOWING 1-10 OF 22 REFERENCES

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.

Naltrindole, an opioid δ antagonist, blocks the enhancement of morphine-antinociception induced by a CCKB antagonist in the rat

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.

Opioid receptor types and antinociceptive activity in chronic inflammation: bothe κ- and μ-opiate agonistic effects are enhanced in arthritic rats

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.

The results demonstrated that a CCK antagonist directed to the central CCK type B receptor potentiates the analgesic effects of opioids and nonopioid drugs at the spinal level, thus supporting the notion that CCK in the central nervous system may be an endogenous, physiological opioid antagonist.

Modulation of ~-mediated antinociception by ~ agonists: characterization with antagonists

Cholecystokinin antagonists selectively potentiate analgesia induced by endogenous opiates

Differential effects of leucine and methionine enkephalin on morphine-induced analgesia, acute tolerance and dependence.

Results suggest that leucine enkephalin may be an important and potent physiological modulator of narcotic efficacy and enhance the development of acute tolerance and dependence produced by a single dose of morphine.

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.