Receptor binding profile suggests multiple mechanisms of action are responsible for ibogaine's putative anti-addictive activity.
Psychopharmacology – April 01, 1995
Source: PubMed
Summary
Ibogaine shows promise as a treatment for cocaine and opioid addiction, interacting with over 50 neurotransmitter receptors and ion channels at concentrations of 1-100 microM. Specifically, it affects mu, delta, and kappa opiate receptors, along with serotonin and muscarinic receptors. Notably, ibogaine also engages NMDA-associated ion channels, inhibiting key binding sites. This extensive interaction profile may contribute to its potential anti-addictive effects, suggesting a multifaceted approach to addressing substance use disorders.
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 microM. 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-alpha-benzoate binding (BTX-B), respectively. This broad spectrum of activity may in part be responsible for ibogaine's putative anti-addictive activity.