Among recent proposals for ibogaine mechanisms of action is activation of the glial cell line-derived neurotrophic factor (GDNF) pathway in the ventral tegmental area (VTA) of the brain. The work has principally been accomplished in preclinical ethanol research, where 40 mg/kg of ibogaine caused increases of RNA expression of GDNF in keeping with reduction of ethanol intake in the rat, absent neurotoxicity or cell death.
Ibogaine is a noncompetitive antagonist at α3β4 nicotinic receptors, binding with moderate affinity. Several other α3β4 antagonists are known, and some of these, such as bupropion (Wellbutrin or Zyban), and mecamylamine, have been used for treating nicotine addiction. This α3β4 antagonism correlates quite well with the observed effect of interrupting addiction. Co-administration of ibogaine with other α3β4 antagonists such as 18-MC, dextromethorphan or mecamylamine had a stronger anti-addictive effect than when it was administered alone. Since α3β4 channels and NMDA channels are related to each other and their binding sites within the lumen bind a range of same ligands (e.g. DXM, PCP), some older sources suggested that ibogaine’s anti-addictive properties may be (partly) due to it being an NMDA receptor antagonist. However, ligands, like 18-MC, selective for α3β4- vs. NMDA-channels showed no drop-off in activity.
It is suspected that ibogaine’s actions on the opioid and glutamatergic systems are also involved in its anti-addictive effects. Persons treated with ibogaine report a cessation of opioid withdrawal signs generally within an hour of administration.
Ibogaine is a weak 5HT2A receptor agonist, and although it is unclear how significant this action is for the anti-addictive effects of ibogaine, it is likely to be important for the hallucinogenic effects. Ibogaine is also a sigma2 receptor agonist.
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