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J E Nagel

2 papers in the library · 40 citations · publishing 1996-1998

Papers

Ibogaine acts at the nicotinic acetylcholine receptor to inhibit catecholamine release.

Brain research June 22, 1998 S J Mah, Y Tang, P E Liauw et al. 20 citations

Ibogaine, at low concentrations below 10 microM, selectively inhibits catecholamine release triggered by nicotinic acetylcholine receptor activation in cultured bovine chromaffin cells, while not affecting release caused by membrane depolarization or sodium channel activation. This inhibition is not reversed by kappa opioid receptor antagonists, indicating the effect is not mediated through kappa opioid receptors. The inhibition by low-dose ibogaine is rapidly reversible, whereas higher doses produce inhibition lasting at least 19 hours after removal. These findings suggest ibogaine acts at the nicotinic acetylcholine receptor, relevant to its potential anti-addictive effects and development of treatments for nicotine addiction.

Ibogaine selectively inhibits nicotinic receptor-mediated catecholamine release.

European journal of pharmacology December 19, 1996 A S Schneider, J E Nagel, S J Mah 20 citations

Low 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.