Ibogaine alters synaptosomal and glial glutamate release and uptake.
Neuroreport – February 12, 2001
Source: PubMed
Summary
Ibogaine, a compound explored for addiction treatment, significantly impacts brain chemistry. New research reveals how it affects glutamate, a key brain messenger. The investigation found that high doses of ibogaine notably altered glutamate handling, inhibiting its uptake and stimulating its release in specific mouse brain regions and in support cells from both rats and mice. This vital insight clarifies glutamate's involvement in ibogaine's potential neurotoxic effects, advancing our understanding for safer treatment development.
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.