Cocaine and inhibition of nitric oxide synthesis produce opioid-mediated antinociception

  • Forman L
  • Tringo L
  • Sun M
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Abstract

Cocaine and nitric oxide are known to influence the perception of pain. The present study sought to determine if the endogenous opioid peptide system participates in cocaine-induced antinociception and antinociception produced by antagonism of nitric oxide. Pain perception was measured using the hot plate test. Administration of cocaine (25 mg/kg) to male rats resulted in a significant increase in reaction time in the hot plate test, which was reversed by treatment with 3, 10, and 30 mg/kg of the opiate antagonist, naloxone. In rats that were not treated with cocaine, doses of 30 and 60 mg/kg of naloxone significantly reduced hot plate reaction time. Treatment of animals with the nitric oxide synthase inhibitor, N(ω)nitro-L-arginine, produced a significant increase in response time to the hot plate, which was reversed by administration of naloxone. These data indicate that antinociception produced in the rat by cocaine appears to have a supraspinal component and to involve activation of endogenous opioid peptide activity in the brain. The results also suggest a tonic inhibition of endogenous opioid peptide activity by nitric oxide, which when antagonized, results in diminished response to pain.

Author-supplied keywords

  • Antinociception
  • Cocaine
  • Hot plate
  • Naloxone
  • Nitric oxide
  • Opioid peptides

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Authors

  • L. J. Forman

  • L. Tringo

  • M. Sun

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