Receptor binding profile suggests multiple mechanisms of action are responsible for ibogaine’s putative anti-addictive activity
Bauer, C., Collins, J. L., Ferkany, J., Lancaster, J., Perschke, S., Snowman, A., Sweetnam, P. M.
This in vitro (cells) study (1995) on ibogaine revealed the mechanisms of action to be at the mu, delta, kappa, opiate, serotonin 2 and 3, muscarinic 1 and 2 receptors, and de dopamine, norepinephrine, and serotonin reuptake sites. Ibogaine also interacted with NMDA associated and sodium ion channels.
Abstract
The indole alkaloid ibogaine (NIH 10567, Endabuse) is currently being examined for its potential utility in the treatment of cocaine and opioid addiction. However, a clearly defined molecular mechanism of action for ibogaine's putative anti-addictive properties has not been delineated. Radioligand binding assays targeting over 50 distinct neurotransmitter receptors, ion channels, and select second messenger systems were employed to establish a broad in vitro pharmacological profile for ibogaine. These studies revealed that ibogaine interacted with a wide variety of receptors at concentrations of 1-100 µM. These included the mu, delta, kappa, opiate, 5HT2, 5HT3, and muscarinic1 and 2 receptors, and the dopamine, norepinephrine, and serotonin uptake sites. In addition, ibogaine interacted with N-methyl-D-aspartic acid (NMDA) associated ion and sodium ion channels as determined by the inhibition of [3H]MK-801 and [3H]bactrachotoxin A 20-α-benzoate binding (BTX-B), respectively. This broad spectrum of activity may in part be responsible for ibogaine's putative anti-addictive activity.