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.
Comparable studies
Other preclinical and animal studies on ibogaine for addiction, most cited first.
| Study | Year | Design | Participants |
|---|---|---|---|
| Glial Cell Line-Derived Neurotrophic Factor Mediates the Desirable Actions of the Anti-Addiction Drug Ibogaine against Alcohol Consumption Rats | 2005 | Experimental study | |
| Effects of ibogaine on acute signs of morphine withdrawal in rats: independence from tremor. Morphine-dependent rats | 1992 | Randomized controlled trial | |
| Autoregulation of glial cell line-derived neurotrophic factor expression: implications for the long-lasting actions of the anti-addiction drug, Ibogaine. Dopaminergic-like SHSY5Y cell line | 2006 | In vitro cell culture study | |
| A dose-response study of ibogaine-induced neuropathology in the rat cerebellum. Rats | 2000 | Dose-response study | n = 30 |
| Oral noribogaine shows high brain uptake and anti-withdrawal effects not associated with place preference in rodents. Mice and rats | 2016 | Experimental study with three experiments |
Citations in the library
Cites 10
- Treatment of acute opioid withdrawal with ibogaine. The American Journal on Addictions 1999
- Ibogaine possesses a selective affinity for sigma 2 receptors. Life Sciences 1995
- Medication Development of Ibogaine as a Pharmacotherapy for Drug Dependencea. Annals of the New York Academy of Sciences May 1, 1998
- Receptor binding profile suggests multiple mechanisms of action are responsible for ibogaine's putative anti-addictive activity. Psychopharmacology April 1, 1995
- Mechanisms of Antiaddictive Actions of Ibogainea. Annals of the New York Academy of Sciences May 1, 1998
and 5 more in the library