Ibogaine selectively inhibits nicotinic receptor-mediated catecholamine release.
A S Schneider, J E Nagel, S J Mah
European journal of pharmacology December 19, 1996 DOI: 10.1016/s0014-2999(96)00815-1 via PubMed
Summary
AI-generated from the abstractLow concentrations of ibogaine (1-10 microM) selectively inhibit nicotinic receptor-mediated catecholamine release in cultured chromaffin cells, while higher concentrations (100 microM) block additional modes of release. This suggests ibogaine acts at the nicotinic acetylcholine receptor, possibly at the ion channel site, clarifying one mechanism underlying its putative anti-addictive properties.
Study at a glance
| Characteristics | In vitro experimental study Peer reviewed |
|---|---|
| Population | Cultured chromaffin cells |
| Intervention | Ibogaine |
| Dose | 1-10 µM, 100 µM |
| Citations | 20 |
| Key finding | Low concentrations of ibogaine selectively inhibit nicotinic receptor-mediated catecholamine release, indicating action at the nicotinic acetylcholine receptor ion channel. |
Abstract
The effects of ibogaine, a putative anti-addictive drug, on stimulated catecholamine release were examined in cultured chromaffin cells to clarify its mechanism(s) of action. Low concentrations of ibogaine (1-10 microM) had a selective inhibitory action on nicotinic receptor-mediated catecholamine release, while higher concentrations (100 microM) inhibited additional modes of stimulated catecholamine release. These results suggest a selective inhibitory action of ibogaine at the nicotinic acetylcholine receptor, possibly at the receptor ion channel site.