Annals of the New York Academy of Sciences
September 1, 2000
S D Glick, I M Maisonneuve, K K Szumlinski
89 citations
18-Methoxycoronaridine (18-MC), a safer iboga alkaloid, reduces self-administration of morphine, cocaine, ethanol, and nicotine in rats without affecting nondrug reward, unlike ibogaine. Both compounds block opioid withdrawal and dopamine release in the nucleus accumbens, but only ibogaine raises serotonin levels and enhances cocaine-induced dopamine. Ibogaine causes tremors and cerebellar damage at high doses; 18-MC does not. 18-MC has lower affinity for NMDA, sigma-2, sodium channels, and serotonin transporter than ibogaine. The findings suggest 18-MC has a narrower action profile and a substantially better therapeutic index than ibogaine.
Pharmacology, biochemistry, and behavior
January 1, 2001
K K Szumlinski, R E Haskew, M Y Balogun et al.
28 citations
Pretreatment with ibogaine or its synthetic derivative 18-methoxycoronaridine reversed the behavioral disinhibition and increased corticosterone levels caused by a low dose of methamphetamine in rats. Methamphetamine alone increased open-arm entries in the elevated plus maze and raised plasma corticosterone, suggesting behavioral disinhibition rather than anxiety reduction. Both iboga compounds blocked these effects without altering general locomotion, indicating a potential mechanism for their anti-addictive properties through modulation of neuroendocrine stress responses.
Psychopharmacology
August 1, 2000
K K Szumlinski, M Y Balogun, I M Maisonneuve et al.
28 citations
Ibogaine and 18-methoxycoronaridine (18-MC), compounds being studied as potential treatments for addiction, increased the behavioral effects of methamphetamine in rats. Rats given methamphetamine daily for seven days and then pretreated with 18-MC showed more movement in response to methamphetamine than those given a placebo. Both ibogaine and 18-MC also intensified repetitive, stereotypic behaviors caused by higher doses of methamphetamine. These results match earlier findings with cocaine, suggesting the iboga agents interact with brain pathways that control hyperactivity from repeated stimulant use. The authors propose this enhancement may partly explain how these agents reduce drug self-administration.
Behavioural brain research
December 1, 1997
J R Blackburn, K K Szumlinski
22 citations
Ibogaine may reduce dopamine activity only in animals or people previously exposed to addictive drugs, not in drug-naive ones. In three experiments with male Long Evans rats, 40 mg/kg ibogaine did not decrease preference for a sweet glucose + saccharin solution, nor did it attenuate conditioned flavor preference. However, ibogaine significantly lowered amphetamine-induced locomotion in rats that had received four prior doses of amphetamine, but not in drug-naive rats. The findings suggest ibogaine can reduce sensitized dopamine activity back toward baseline levels, potentially lowering drug craving in addiction.
European journal of pharmacology
June 16, 2000
K K Szumlinski, I M Maisonneuve, S D Glick
19 citations
Ibogaine, given to rats 19 hours before a cocaine challenge, reversed a key brain change caused by repeated cocaine use: the sensitized dopamine response in the nucleus accumbens. While ibogaine did not alter the dopamine increase from a single cocaine dose, it eliminated the amplified dopamine release that normally occurs in cocaine-sensitized animals. This effect on neuroadaptation may underlie ibogaine's proposed anti-addictive properties.
Psychopharmacology
July 1, 1999
K K Szumlinski, I M Maisonneuve, S D Glick
14 citations
Ibogaine pretreatment amplifies the stimulating effects of cocaine on movement in rats, but the effect depends on the animals' prior cocaine history. In rats previously treated with cocaine for five days and then withdrawn for two weeks, ibogaine increased movement responses to lower cocaine doses (5 and 10 mg/kg) while decreasing the response to a higher dose (40 mg/kg). In rats with no prior cocaine history, ibogaine only enhanced movement responses across all cocaine doses. Chronic cocaine exposure alone also augmented movement responses compared to acute exposure. The findings show a complex interplay between ibogaine, cocaine dose, and prior drug history.
Pharmacology, biochemistry, and behavior
July 1, 1999
K K Szumlinski, I M Maisonneuve, S D Glick
14 citations
A single injection of ibogaine, given 19 hours before a cocaine challenge, more strongly amplifies cocaine-induced movement in rats that have a history of chronic cocaine use than in rats without prior cocaine exposure. The effect grows larger after a second ibogaine treatment but disappears within 24 hours when ibogaine is no longer given. Tolerance to cocaine's stimulant effects appeared in rats that received only cocaine without ibogaine. These results show that ibogaine heightens sensitivity to cocaine's psychomotor effects, and the size of this enhancement depends on the animal's past experience with both ibogaine and cocaine.
Toxicon : official journal of the International Society on Toxinology
January 1, 2001
K K Szumlinski, I M Maisonneuve, S D Glick
9 citations
No approved therapy exists for stimulant addiction, but ibogaine and its synthetic analog 18-methoxycoronaridine (18-MC) reduce stimulant self-administration in animals. Early findings suggested these agents paradoxically enhance dopamine release and motor behaviors, leading to the hypothesis that they increase sensitivity to stimulant effects. However, recent observations show 18-MC does not affect acute cocaine-induced dopamine, and both ibogaine and 18-MC block sensitized dopamine levels from chronic cocaine. This positive relationship between iboga pretreatment and reversal of dopamine sensitization indicates these agents may attenuate self-administration by reversing neuroadaptations linked to craving and compulsive drug-seeking.