Cocaine: Evidence for Supraspinal, Dopamine-Mediated, Non-Opiate Analgesia

Brain Res. 1989 Feb 13;479(2):306-12. doi: 10.1016/0006-8993(89)91633-8.

Abstract

Cocaine (25 mg/kg i.p.) produces analgesia in the rat within 5 min and for a duration of 90 min as determined by the formalin test or for 30 min as determined by the hot plate test. Cocaine analgesia is unaffected by doses of naloxone that are sufficient to attenuate morphine analgesia in both tests. Chlorpromazine (3 mg/kg i.p.), SCH 23390 (100 micrograms/kg i.p.; a D1 dopamine receptor antagonist), and eticlopride (75 micrograms/kg i.p.; a D2 dopamine receptor antagonist) each attenuate cocaine analgesia in both tests at doses that alone do not affect performance in either test. Measurements of blood pressure and heart rate indicate that cocaine analgesia is not due to the activation of baroreceptor reflex afferents. We conclude that cocaine is a supraspinally acting, dopamine-mediated, non-opiate analgesic in the rat.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Analgesia*
  • Animals
  • Benzazepines / pharmacology
  • Blood Pressure / drug effects
  • Brain / drug effects
  • Brain / physiology*
  • Chlorpromazine / pharmacology
  • Cocaine / metabolism
  • Cocaine / pharmacology*
  • Heart Rate / drug effects
  • Male
  • Naloxone / pharmacology
  • Pain / metabolism
  • Rats
  • Rats, Inbred Strains
  • Receptors, Dopamine / drug effects
  • Receptors, Dopamine / physiology*
  • Salicylamides / pharmacology

Substances

  • Benzazepines
  • Receptors, Dopamine
  • Salicylamides
  • Naloxone
  • Cocaine
  • eticlopride
  • Chlorpromazine