Ibogaine and cocaine abuse: pharmacological interactions at dopamine and serotonin receptors.
Brain research bulletin January 1, 1997 DOI: 10.1016/s0361-9230(96)00296-1 via PubMed
Summary
AI-generated from the abstractIbogaine, an indole alkaloid, may help treat drug dependence. Animal studies show it reduces some effects of stimulant drugs, like motor stimulation and self-administration. The mechanism likely involves dopamine, serotonin, NMDA, kappa, and/or sigma receptor sites, based on binding competition studies, though receptor affinity alone does not prove involvement. In vitro perfusion studies help clarify ibogaine's effects on neurotransmitter systems and their functional consequences. This review summarizes evidence for ibogaine's multiple effects, highlighting the potential importance of its action on serotonergic modulation of dopamine release.
Study at a glance
| Characteristics | Review Peer reviewed |
|---|---|
| Citations | 32 |
| Key finding | Ibogaine's multiple effects, particularly its action on serotonergic modulation of dopamine release, may be important for treating drug dependence. |
Abstract
Ibogaine is an indole alkaloid that has been of interest in recent years due to its putative efficacy in the treatment of drug dependence. For the most part, animal data have shown attenuation of some of the effects of stimulant drugs, for example, motor stimulation and self-administration. The mechanism of this inhibition of drug-induced behavior seems to suggest the action of the dopamine, serotonin, NMDA, kappa, and/or sigma receptor sites, as indicated by the affinity of ibogaine to receptor selective ligands in binding competition studies. However, affinity for receptors does not in itself indicate their involvement. In vitro perfusion studies have proven a useful model to study the effect of ibogaine on neurotransmitter systems and the functional effects of such interactions. This review summarizes these data and the support of multiple effects of ibogaine, and the potential importance of its action on serotonergic modulation of dopamine release.