Effects of ibogaine and noribogaine on phosphoinositide hydrolysis.
Brain research August 26, 1996 DOI: 10.1016/0006-8993(96)00688-9 via PubMed
Summary
AI-generated from the abstractThe antiaddictive compound ibogaine and its primary metabolite noribogaine were tested for their effects on phosphoinositide hydrolysis in rat brain tissue. Ibogaine did not alter phosphoinositide turnover in striatal or hippocampal slices, but noribogaine caused a concentration-dependent increase in the generation of inositol phosphates. This increase was not due to neurotransmitter release, as it was unaffected by tetrodotoxin, cadmium, or omega-conotoxin. The results suggest that noribogaine's stimulation of phosphoinositide hydrolysis may contribute to the behavioral effects of ibogaine.
Study at a glance
| Characteristics | Laboratory experiment Peer reviewed |
|---|---|
| Population | Rat striatal and hippocampal slices |
| Interventions | ibogaine noribogaine |
| Citations | 7 |
| Key finding | Noribogaine, but not ibogaine, stimulates phosphoinositide hydrolysis in rat brain slices independently of neurotransmitter release. |
Abstract
The effects of the antiaddictive compound, ibogaine, and its primary metabolite, noribogaine (12-hydroxyibogamine), on phosphoinositide hydrolysis were investigated. Although ibogaine did not alter phosphoinositide turnover in either striatal or hippocampal slices, noribogaine elicited a concentration-dependent increase in the generation of [3H]inositol phosphates. This stimulation was not altered by inclusion of tetrodotoxin, cadmium or omega-conotoxin indicating that the increased production of [3H]inositol phosphates was not secondary to a release of one or more neurotransmitters. The present study indicates a stimulation of phosphoinositide hydrolysis by noribogaine may be involved in the behavioral effects of ibogaine.