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18-Methoxycoronardine attenuates nicotine-induced dopamine release and nicotine preferences in rats.

Stanley D Glick, Isabelle M Maisonneuve, K E Visker, K A Fritz, Upul K. Bandarage, Martin E. Kuehne

Psychopharmacology October 1, 1998 DOI: 10.1007/s002130050716 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Preclinical animal study Peer reviewed
Population Awake and freely moving rats
Interventions Ibogaine 18-methoxycoronaridine (18-MC)
Dose 40 mg/kg, i.p.
Duration At least 24 hours
Keywords Nicotine addiction treatment Smoking cessation Quit smoking Tobacco dependence treatment Anti-smoking therapy Treatments Drug discovery Pharmaceutical research New drug development Therapeutic compounds 18-methoxycoronardine 18-mc Neuropharmacology Brain research Dopamine system Dopamine surge Preclinical research Animal studies Rat experiments In vivo research Rats
Citations 45
Key points 18-MC attenuated nicotine-induced dopamine release in the nucleus accumbens and selectively reduced nicotine self-administration in rats without affecting water intake.

Abstract

Two studies were conducted to assess, in vivo, potential anti-nicotinic effects of the iboga alkaloid ibogaine and its synthetic congener 18-methoxycoronaridine (18-MC). As previously demonstrated for ibogaine, using microdialysis, pretreatment (19h beforehand) with 18-MC (40 mg/kg, i.p.) significantly attenuated nicotine-induced dopamine release in the nucleus accumbens of awake and freely moving rats. In an oral model of nicotine self-administration, both ibogaine and 18-MC decreased rats' preferences for nicotine for at least 24 h. Acutely, during the first hour after administration, ibogaine depressed responding for water as well as for nicotine; however, during this same time, 18-MC reduced nicotine intake without affecting responding for water. The results suggest that 18-MC might be the prototype of a new treatment for smoking.