Ibogaine selectively inhibits nicotinic receptor-mediated catecholamine release.
European journal of pharmacology – December 19, 1996
Source: PubMed
Summary
Ibogaine shows promise as an anti-addictive drug by selectively inhibiting catecholamine release. In experiments with cultured chromaffin cells, low concentrations (1-10 microM) reduced nicotinic receptor-mediated catecholamine release by a significant margin. At higher doses (100 microM), ibogaine further inhibited other stimulated release pathways. These findings indicate that ibogaine may act specifically on the nicotinic acetylcholine receptor, potentially targeting the ion channel site, which could be crucial for developing treatments for addiction.
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.