Brain research
May 6, 1996
S D Glick, M E Kuehne, I M Maisonneuve et al.
118 citations
A novel synthetic compound, 18-methoxycoronaridine (MC), reduces morphine and cocaine self-administration in rats without the tremors and cerebellar toxicity seen with ibogaine. In acute tests, MC decreased drug intake but did not affect bar-press responding for water. In some rats, a single 40 mg/kg dose of MC produced prolonged decreases in morphine or cocaine intake lasting days or weeks. MC showed no tremorigenic effect, and a high dose of 100 mg/kg caused no cerebellar toxicity. Like ibogaine, MC lowered extracellular dopamine levels in the nucleus accumbens. MC appears to be a safer ibogaine-like agent potentially useful for treating addiction.
Pharmacology, biochemistry, and behavior
October 1, 1997
A H Rezvani, D H Overstreet, Y Yang et al.
78 citations
A single injection of 18-methoxycoronaridine (18-MC), a nontoxic ibogaine analogue, dose dependently reduced alcohol consumption and preference in alcohol-preferring rats, while water intake increased correspondingly. Only the highest dose (40 mg/kg) also decreased food intake. The mechanism by which 18-MC suppresses alcohol intake is not yet fully understood but may involve modulation of neurotransmitters that regulate alcohol consumption.
European journal of pharmacology
August 8, 1996
R T Layer, P Skolnick, C M Bertha et al.
48 citations
Ibogaine, a psychoactive alkaloid, is more potent than its analogs at blocking NMDA receptors, a brain target linked to addiction. In lab tests, ibogaine inhibited [3H]MK-801 binding to NMDA receptors most strongly (Ki ≈ 1.2 µM), while similar compounds like O-desmethylibogaine were less potent (Ki ≈ 5.5 µM) and O-t-butyl-O-desmethylibogaine much weaker (Ki ≈ 179 µM). In morphine-dependent mice, only ibogaine reduced withdrawal jumping triggered by naloxone, suggesting its anti-addictive effects stem from NMDA receptor antagonism.
Psychopharmacology
October 1, 1998
S D Glick, I M Maisonneuve, K E Visker et al.
45 citations
Two animal experiments tested whether ibogaine and its synthetic version 18-methoxycoronaridine (18-MC) can block nicotine's effects in rats. Pretreatment with 18-MC significantly reduced nicotine-induced dopamine release in the brain's reward center, the nucleus accumbens. In a self-administration test, both compounds decreased rats' preference for nicotine for at least 24 hours. While ibogaine initially suppressed both nicotine and water intake, 18-MC selectively reduced nicotine consumption without affecting water intake. The results suggest 18-MC could be a prototype for a new smoking cessation treatment.
European journal of pharmacology
October 8, 1997
I M Maisonneuve, K E Visker, G L Mann et al.
20 citations
Ibogaine and two related compounds (noribogaine and 18-methoxycoronaridine) both inhibit and later enhance cocaine-induced hyperactivity in rats, depending on timing. When given 1 hour before cocaine, all three agents reduced the hyperactivity caused by cocaine. When given 19 hours before cocaine, they instead amplified it. These opposite, time-dependent effects explain conflicting findings in earlier research and were not caused by the drugs' own effects on movement.