Ibogaine affects brain energy metabolism.
Roman Paškulin, Polona Jamnik, Marko Živin, Peter Raspor, Borut Strukelj
European Journal of Pharmacology December 15, 2006 DOI: 10.1016/j.ejphar.2006.09.008 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal experimental study Peer reviewed |
|---|---|
| Population | Rat brains |
| Intervention | Ibogaine |
| Dose | 20 mg/kg body weight i.p. |
| Duration | 24 and 72 hours |
| Topics | Addiction Ibogaine |
| Keywords | Addiction treatment Addiction recovery Substance abuse treatment Drug rehabilitation Anti-addiction therapy Detoxification Relapse prevention Detoxify Reverse tolerance Neurobiology Brain health Brain function Neural mechanisms Brain metabolism Enzymes Cellular changes Energy metabolism Cellular energy Bioenergetics Mitochondrial function Atp production Cellular respiration Metabolic pathways Energy production |
| Citations | 24 |
| Key findings | Ibogaine treatment induced enzymes of glycolysis and the TCA cycle in rat brains, suggesting its anti-addiction effect may be mediated by increased energy metabolism. |
Abstract
Ibogaine is an indole alkaloid present in the root of the plant Tabernanthe iboga. It is known to attenuate abstinence syndrome in animal models of drug addiction. Since the anti-addiction effect lasts longer than the presence of ibogaine in the body, some profound metabolic changes are expected. The aim of this study was to investigate the effect of ibogaine on protein expression in rat brains. Rats were treated with ibogaine at 20 mg/kg body weight i.p. and subsequently examined at 24 and 72 h. Proteins were extracted from whole brain and separated by two-dimensional (2-D) electrophoresis. Individual proteins were identified by matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS). Enzymes of glycolysis and tricarboxylic acid (TCA) cycle namely glyceraldehyde-3-phosphate dehydrogenase, aldolase A, pyruvate kinase and malate dehydrogenase were induced. The results suggest that the remedial effect of ibogaine could be mediated by the change in energy availability. Since energy dissipating detoxification and reversion of tolerance to different drugs of abuse requires underlying functional and structural changes in the cell, higher metabolic turnover would be favourable. Understanding the pharmacodynamics of anti-addiction drugs highlights the subcellular aspects of addiction diseases, in addition to neurological and psychological perspectives.