Interactions between ibogaine, a potential anti-addictive agent, and morphine: an in vivo microdialysis study.
I M Maisonneuve, R W Keller, S D Glick
European journal of pharmacology June 18, 1991 DOI: 10.1016/0014-2999(91)90634-3
Summary
Ibogaine may significantly alter brain chemistry in ways that impact drug cravings. In a study with 40 mg/kg of ibogaine, extracellular dopamine (DA) levels dropped by 19 hours post-injection in the striatum and were lower across all examined brain regions. When administered before morphine, ibogaine blocked the typical rise in DA levels caused by morphine in the striatum, prefrontal cortex, and nucleus accumbens. These findings suggest that ibogaine influences dopamine systems well beyond its presence in the body, potentially affecting addiction treatment strategies.
Abstract
Ibogaine, an indolalkylamine, has been claimed to be effective in abolishing drug craving in heroin and cocaine addicts. The present study used in vivo microdialysis to determine the effects of ibogaine on extracellular levels of dopamine (DA) and its metabolites and the effects of ibogaine pretreatment on morphine stimulation of brain DA systems. Acutely, ibogaine (40 mg/kg i.p.) decreased extracellular DA levels in the striatum, increased them in the prefrontal cortex and had no significant effects in the nucleus accumbens. Nineteen hours after ibogaine injection. DA levels were still decreased in the striatum and the metabolite levels were lower in all three regions. When injected 19 h prior to a morphine challenge (5 mg/kg i.p.), ibogaine (40 mg/kg, i.p.) prevented the rise in DA levels in all three regions normally observed after a morphine injection. A high dose of morphine (30 mg/kg i.p.), administered alone, produced no increase in extracellular DA levels; it is therefore unclear whether ibogaine antagonized or potentiated the effects of the lower dose of morphine. Regardless of the nature of this interaction, it appears that ibogaine affects brain DA systems for a period of time that exceeds its elimination from the body and, during this time, alters the responses of these systems to morphine.