The pharmacology of ibogaine is quite complex, affecting many different neurotransmitter systems simultaneously.Because of its fairly low potency at any of its target sites, ibogaine is used in doses anywhere from 5 mg/kg of body weight for a minor effect to 30 mg/kg in the cases of strong polysubstance addiction. It is unknown whether doses greater than 30 mg/kg in humans produce effects that are therapeutically beneficial, medically risky, or simply prolonged in duration. In animal neurotoxicity studies, there was no observable neurotoxicity of ibogaine at 25 mg/kg, but at 50 mg/kg, one-third of the rats had developed patches of neurodegeneration, and at doses of 75 mg/kg or above, all rats showed a characteristic pattern of degeneration of Purkinje neurons, mainly in the cerebellum. While caution should be exercised when extrapolating animal studies to humans, these results suggest that neurotoxicity of ibogaine is likely to be minimal when ibogaine is used in the 10–20 mg/kg range typical of drug addiction interruption treatment regimes, and indeed death from the other pharmacological actions of the alkaloids is likely to occur by the time the dose is high enough to produce consistent neurotoxic changes.