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 (opens in new tab)
Study at a glance
AI-extracted from the abstract| 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 Glutamate handling Brain chemistry Brain regions Support cells Neurotoxicity Neurotoxic effects |
| Citations | 14 |
| Key findings | 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.