The partial opioid agonist, buprenorphine, protects against lethal effects of cocaine.

Abstract

Buprenorphine (0.3-3.0 mg/kg) produced dose-dependent protection against the lethal effects of cocaine in mice. The (+)-enantiomer of buprenorphine did not protect up to doses over 100 times greater than the lowest effective dose of its (-)-enantiomer. The protective effects were also produced by the opioid agonists morphine and methadone, but not by the opioid antagonist, naltrexone. Low doses of naltrexone (0.3-1.0 mg/kg) blocked the protective effects of buprenorphine. Protection conferred by buprenorphine was not observed in CXBK mice, a recombinant inbred strain relatively devoid of mu-opioid receptors. Thus, buprenorphine appears to protect against the lethal effects of cocaine by a process mediated by mu-opioid receptors. The present results should provide some additional safety assurance in future clinical trials with buprenorphine, especially in outpatient trials where cocaine abuse may continue along with treatment.

• Authors: J M Witkin, R E Johnson, J H Jaffe, S R Goldberg, N A Grayson, K C Rice, J L Katz
• Journal: Drug and alcohol dependence (Drug Alcohol Depend) Vol. 27 Issue 2 Pg. 177-84 (Mar 1991) ISSN: 0376-8716 [Print] Ireland
• PMID: 1647294 (Publication Type: Journal Article)

Chemical References

• Receptors, Opioid
• Receptors, Opioid, mu
• Buprenorphine
• Naltrexone
• Morphine
• Cocaine
• Methadone

Topics

• Animals
• Brain (drug effects)
• Buprenorphine (pharmacology)
• Cocaine (toxicity)
• Dose-Response Relationship, Drug
• Methadone (pharmacology)
• Mice
• Mice, Inbred Strains
• Morphine (pharmacology)
• Naltrexone (pharmacology)
• Receptors, Opioid (drug effects)
• Receptors, Opioid, mu
• Seizures (chemically induced, prevention & control)