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Related Experiment Videos

Dynorphin-independent spinal cannabinoid antinociception.

L R Gardell1, M H Ossipov, T W Vanderah

  • 1Department of Pharmacology, College of Medicine, University of Arizona Health Sciences Center, 85724 Tucson, AZ, USA Department of Anesthesiology, College of Medicine, University of Arizona Health Sciences Center, Tucson, AZ, USA.

Pain
|December 7, 2002
PubMed
Summary

Spinal cannabinoid agonists, like delta 9-tetrahydro-cannabinol (Delta(9)-THC), reduce pain directly via cannabinoid receptors. This occurs without needing dynorphin release or kappa opioid receptor activation, as shown in prodynorphin knockout mice.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Pain Research

Background:

  • Spinal antinociception from cannabinoid agonists is hypothesized to involve dynorphin release acting on kappa opioid receptors.
  • Alternatively, cannabinoids may act directly on spinal cannabinoid receptors to inhibit pain signaling.

Purpose of the Study:

  • To investigate the mechanism of spinal antinociception induced by cannabinoid agonists.
  • To determine if dynorphin release and kappa opioid receptor activation are required for cannabinoid-mediated pain relief.

Main Methods:

  • Used prodynorphin knockout mice and wild-type littermates to assess antinociceptive effects of spinal delta 9-tetrahydro-cannabinol (Delta(9)-THC) and WIN 55,212-2.
  • Administered kappa opioid receptor antagonist (nor-binaltorphimine) and cannabinoid receptor antagonist (SR141716A) to evaluate receptor involvement.

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  • Constructed antinociceptive dose-response curves.

    • Main Results:

    • Delta(9)-THC and WIN 55,212-2 were equally effective in both prodynorphin knockout and wild-type mice.
    • Kappa opioid receptor antagonist (nor-BNI) did not affect cannabinoid-induced antinociception but blocked U50,488H-induced effects.
    • Cannabinoid receptor antagonist (SR141716A) blocked the antinociceptive actions of both Delta(9)-THC and WIN 55,212-2.

    Conclusions:

    • Spinal cannabinoid-mediated antinociception likely occurs through direct activation of cannabinoid receptors.
    • Dynorphin release and subsequent kappa opioid receptor activation are not required for this antinociceptive effect.