Attempted reversal of cocaine-induced antinociceptive effects with naloxone, an opioid antagonist.
We attempted to reverse the behavioral and neuronal antinociceptive effects of cocaine with naloxone, an opioid antagonist. Cocaine (20 mg/kg i.p.) produced a strong analgesic effect in the formalin test and in the tail pinch test. These cocaine-induced analgesic effects could be reversed by naloxone at a very high dose (10 mg/kg) but not at a dose (1 mg/kg) which was sufficient to attenuate morphine (10 mg/kg)-induced analgesia. Naloxone alone at a dose of 10 mg/kg did not produce significant effects. In general, nociceptively evoked responses in medial thalamic neurons were suppressed by cocaine (20 mg/kg), and this suppression was attenuated by naloxone (10 mg/kg). The results suggest that opioid receptors which are not involved in mediating morphine-induced analgesia and which have a low sensitivity to naloxone are involved in cocaine-induced central analgesia.
Pertovaara
A
A
Department of Physiology, University of Helsinki, Finland.
Mecke
E
E
Carlson
S
S
D000700:Analgesics / Q000037:antagonists & inhibitors*; D000818:Animals; D003042:Cocaine / Q000037:antagonists & inhibitors*; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects*; D010147:Pain Measurement; D051381:Rats; D011919:Rats, Inbred Strains; D011957:Receptors, Opioid / Q000187:drug effects*; D013788:Thalamus / Q000166:cytology / Q000187:drug effects*
D000700:Analgesics; D011957:Receptors, Opioid; D009270:Naloxone; D003042:Cocaine