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Iboga Effect on Receptors


Hello! Please help me collect all the info we have on the effect Iboga compounds have on nerve receptors, i.e. which compounds do what to which receptors.

As far as I know, ibogaine has antagonistic activity at the NMDA receptors. What else do we have?

Though ibogaine does not appear to affect binding at dopamine receptors or transporters, it has been found to reduce extracellular levels of dopamine in the nucleus accumbens. Ibogaine effects on dopamine metabolites appear to be inconsistent. When measurements are taken shortly after administration (within 2 hours), or when high concentrations are used (greater than 100 uM), increases in dihydroxyphenyl-acetic acid (DOPAC) and homovanilic acid (HVA) are seen. However, when lower concentrations are used (e.g. 10 uM) or measurements are taken after a longer period of time (up to a week), dopamine brain concentrations remain unchanged, and metabolite concentrations decrease.

Sershen et al. (1994) reported that ibogaine's effects on dopaminergic function are largely regulated by its interactions with serotonin receptors. This was inferred from their finding that ibogaine inhibited the ability of the 5-HT1b agonist CGS-12066A to increase stimulation induced dopamine release in rat and mouse striatal slices. It has also been demonstrated that ibogaine increased the ability of the 5-HT3 agonist phenylbiguanide to produce stimulation evoked dopamine release in mouse striatal slices. Taken together, these findings support the notion that ibogaine's effects on serotonin have a role in determining its dopaminergic effects, but the specific nature of this role has yet to be determined.

Ibogaine has been found to increase 5-HT concentrations in both the nucleus accumbens and striatum of the rat). However, Benwell et al. (1996) found that ibogaine reduced serotonin levels in the medial prefrontal cortex. Furthermore, studies of ibogaine's specific actions at serotonin receptors have been inconclusive. Deecher et al. (1992) found that ibogaine did not displace ligands acting at 5-HT1a, 5-HT1b, 5-HT1c, 5-HT1d, 5-HT2, or 5-HT3 receptors, while Repke et al. (1994) found that it did inhibit binding of 5-HT1a, 5-HT2a, and 5-HT3 ligands with low affinity (>100, 12.5, and >100 uM). Additionally, Sweetnam et al. showed that ibogaine inhibits radioligand binding to both 5-HT2 and 5-HT3 receptors, with considerably higher affinity (approximately 4 uM), while Helsley et al. (1998) found that ibogaine bound to 5-HT2 receptors with low affinity in vitro ( > 40 uM), but occupied this receptor in vivo following systemic administration.

It is postulated that ibogaine may act as a reversible inhibitor of serotonin transporters, as concluded from the observation that it inhibited transporters in the isolated kidney cells of pigs. Sershen et al. (1994) found that, at doses of 40-50 mg/kg, ibogaine decreased levels of 5-hydroxyindoleacetic acid [5-HIAA] in the frontal cortex, hippocampus and olfactory tubercle of the mouse. Ibogaine was also found to decrease 5-HIAA levels in the nucleus accumbens and striatum of the rat, but to increase 5-HIAA levels in the medial prefrontal cortex.



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