Brain research
September 19, 1994
S D Glick, M E Kuehne, J Raucci et al.
189 citations
Several iboga alkaloids and the related harmala alkaloid harmaline reduce morphine and cocaine self-administration in rats in a dose-dependent manner (2.5-80 mg/kg) during the hour after treatment. Some alkaloids, including ibogaine, tabernanthine, desethylcoronaridine, and the R-isomers of coronaridine and ibogamine, also decrease intake the following day. In some rats, a single injection or two to three weekly injections produce persistent decreases lasting several days, with R-ibogamine showing the most consistent long-term effects. The study also assessed the tremor-inducing and neurotoxic potential of these compounds and their effects on dopamine levels in brain reward regions.
European journal of pharmacology
June 18, 1991
I M Maisonneuve, R W Keller, S D Glick
127 citations
Ibogaine, a substance claimed to reduce drug craving, alters brain dopamine systems for longer than it remains in the body. In rats, an acute injection of ibogaine decreased dopamine levels in the striatum, increased them in the prefrontal cortex, and had no effect in the nucleus accumbens. Nineteen hours later, dopamine remained lower in the striatum, and metabolite levels were reduced across all three brain regions. When given 19 hours before a low dose of morphine, ibogaine prevented the usual dopamine increase caused by morphine. A high dose of morphine alone did not raise dopamine, making it unclear whether ibogaine blocked or enhanced the low-dose effect. Overall, ibogaine produces lasting changes in brain dopamine systems and alters their response to morphine.
Brain research
March 13, 1992
I M Maisonneuve, K L Rossman, R W Keller et al.
86 citations
Ibogaine, a compound proposed for treating addiction to opiates and stimulants, produces both immediate and lasting changes in brain dopamine levels. One hour after a single injection, dopamine decreased by 50% while its metabolite HVA increased by 37–100% in the striatum, nucleus accumbens, and prefrontal cortex. Nineteen hours later, another metabolite, DOPAC, was reduced in the nucleus accumbens and striatum, and striatal DOPAC remained low after a week. No significant neurochemical changes were present after one month. Ibogaine pretreatment also reduced the stimulatory effect of morphine on movement when morphine was given 19 hours or a week later, but not after a month. These findings suggest ibogaine's effects on dopamine systems coincide with a sustained dampening of morphine-induced motor activity.
Brain research
May 1, 1992
I M Maisonneuve, R W Keller, S D Glick
53 citations
Ibogaine, a substance proposed for treating stimulant addiction, was tested in rats. When given 19 hours before D-amphetamine, ibogaine increased the rise in extracellular dopamine in the striatum and nucleus accumbens and enhanced the motor-stimulating effects of D-amphetamine across several doses. These results suggest ibogaine might increase the reinforcing efficacy of D-amphetamine, but because high doses of D-amphetamine can be aversive, the potentiation could also reduce reinforcing efficacy.
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.