The analgesic activity of paracetamol is prevented by the blockade of cannabinoid CB1 receptors

Eur J Pharmacol. 2006 Feb 15;531(1-3):280-1. doi: 10.1016/j.ejphar.2005.12.015. Epub 2006 Jan 24.

Abstract

The mechanism of the analgesic activity of paracetamol (acetaminophen), one of the most widely used drugs for the treatment of pain, is still not clear. Here we show that in rats, using the hot plate test, the analgesic effect of paracetamol is prevented by two antagonists at cannabinoid CB1 receptors (AM281 and SR141716A) at doses that prevent the analgesic activity of the cannabinoid CB1 agonist HU210. Our present results suggest that paracetamol-induced antinociception involves the cannabinoid system.

MeSH terms

  • Acetaminophen / pharmacology*
  • Analgesics, Non-Narcotic / pharmacology*
  • Animals
  • Dose-Response Relationship, Drug
  • Dronabinol / analogs & derivatives
  • Dronabinol / pharmacology
  • Male
  • Morpholines / pharmacology
  • Nociceptors / drug effects
  • Nociceptors / physiology
  • Pain Measurement / methods
  • Pain Threshold / drug effects
  • Piperidines / pharmacology
  • Pyrazoles / pharmacology
  • Rats
  • Rats, Wistar
  • Receptor, Cannabinoid, CB1 / agonists
  • Receptor, Cannabinoid, CB1 / antagonists & inhibitors
  • Receptor, Cannabinoid, CB1 / physiology*
  • Rimonabant

Substances

  • Analgesics, Non-Narcotic
  • Morpholines
  • Piperidines
  • Pyrazoles
  • Receptor, Cannabinoid, CB1
  • Acetaminophen
  • Dronabinol
  • HU 211
  • Rimonabant
  • AM 281