European journal of pharmacology
April 3, 1991
S D Glick, K Rossman, S Steindorf et al.
195 citations
Ibogaine, a naturally occurring alkaloid, reduced intravenous morphine self-administration in rats. The drug caused an acute decrease in morphine intake in the hour after treatment, but this was linked to abnormal motor behavior (whole body tremors). A more notable aftereffect occurred a day later, when ibogaine should have been fully eliminated from the body and no obvious signs of exposure remained. Some rats showed a persistent decrease in morphine intake for days or weeks after a single injection; others required two or three weekly injections before showing such changes, and a few rats were resistant to prolonged aftereffects. The aftereffect was not due to conditioned aversion. Ibogaine also acutely suppressed bar-pressing for water but showed no aftereffect on that behavior, suggesting some specificity for morphine reinforcement.
Neuropharmacology
May 1, 1992
S D Glick, K Rossman, N C Rao et al.
121 citations
Ibogaine, a compound reported to suppress narcotic withdrawal in humans, was tested in morphine-dependent rats. Rats received morphine for five days, then ibogaine (20, 40, or 80 mg/kg) or saline 30 minutes before naltrexone-precipitated withdrawal. Doses of 40 and 80 mg/kg significantly reduced four withdrawal signs: wet-dog shakes, grooming, teeth chattering, and diarrhea. Three other signs—weight loss, burying, and flinching—were unaffected. Ibogaine caused head and body tremors lasting 2-3 hours, which might have interfered with withdrawal expression. In a second experiment, ibogaine given 4 hours before naltrexone, when tremors were absent, still significantly reduced the same four withdrawal signs, indicating a genuine anti-withdrawal effect.
Brain research
November 19, 1993
S D Glick, K Rossman, S Wang et al.
38 citations
Ibogaine, given systemically, alters dopamine and its metabolites in brain reward regions. When applied directly to the striatum and nucleus accumbens, high concentrations (200-400 µM) mimicked the acute effects of systemic ibogaine, lowering dopamine and raising metabolite levels, while a low concentration (10 µM) reproduced the persistent effect of lowering DOPAC. This suggests ibogaine acts directly on dopaminergic nerve terminals and that long-lasting effects may stem from persisting low ibogaine levels. Locally applied ibogaine also enhanced amphetamine's effect on dopamine, and systemic ibogaine pretreatment enhanced locally applied amphetamine's effect, indicating a pharmacodynamic mechanism contributes to their interaction. The relevance to ibogaine's anti-addictive claims remains unclear.