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Ibogaine alters synaptosomal and glial glutamate release and uptake.

M B Leal, T Emanuelli, L D Porciúncula, D O Souza, E Elisabetsky

Neuroreport February 12, 2001 DOI: 10.1097/00001756-200102120-00017 via PubMed

Summary

AI-generated from the abstract

Ibogaine, a compound proposed as a potential treatment for addiction, affects glutamate handling in brain cells. In mouse cortical synaptosomes, high concentrations of ibogaine (500–1000 µM) inhibited glutamate uptake and stimulated its release, while having no effect on rat synaptosomes or cerebellar synaptosomes. Additionally, ibogaine (1000 µM) nearly abolished glutamate uptake by cortical astrocyte cultures from both rats and mice. These results provide direct evidence that ibogaine alters glutamate handling in specific brain regions and support cells, linking its mechanism to neurotoxicity rather than therapeutic effects.

Study at a glance

Characteristics Laboratory experiment Peer reviewed
Population Cortical and cerebellar synaptosomes from mice and rats, and cortical astrocyte cultures from mice and rats
Intervention Ibogaine
Dose 2-1000 microM
Topics Addiction Ibogaine
Keywords Compound Addiction treatment Safer treatment development Brain messenger
Citations 14
Key finding Ibogaine at high concentrations inhibits glutamate uptake and stimulates glutamate release in mouse cortical synaptosomes, and nearly abolishes glutamate uptake in cortical astrocyte cultures, indicating glutamate involvement in ibogaine-induced neurotoxicity.

Abstract

Ibogaine has aroused expectations as a potentially innovative medication for drug addiction. It has been proposed that antagonism of the NMDA receptor by ibogaine may be one of the mechanisms underlying its antiaddictive properties; glutamate has also been implicated in ibogaine-induced neurotoxicity. We here report the effects of ibogaine on [3H]glutamate release and uptake in cortical and cerebellar synaptosomes, as well as in cortical astrocyte cultures, from mice and rats. Ibogaine (2-1000 microM) had no effects on glutamate uptake or release by rat synaptosomes. However, ibogaine (500-1000 microM) significantly inhibited the glutamate uptake and stimulated the release of glutamate by cortical (but not cerebellar) synaptosomes of mice. In addition, ibogaine (1000 microM) nearly abolished glutamate uptake by cortical astrocyte cultures from rats and mice. The data provide direct evidence of glutamate involvement in ibogaine-induced neurotoxicity.

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