[Ibogaine] Gallo Research Center studies cause and treatment of alcohol, drug addiction

Boris Leshinsky bleshins at bigpond.net.au
Thu Aug 11 23:48:03 EDT 2005


---- Eye of the Bhogi <freedomroot at gmail.com> wrote: 
> From the piece on Gallo funding of addiction research:  "But its side
> effects, including hallucinations, which made it popular in the 1960s
> drug culture, and evidence of toxicity to certain nerve cells in
> rodent studies have discouraged studies of its clinical potential
> against drug and alcohol addiction."
> 
> Howard or someone else scientific:  is the nerve cell toxicity related
> to the hallucinations?  What do we do to our nerves with chemical
> abuse anyway?  thanks, rachel

The nerve toxicity is related to dosage levels, apparently. Came across this trying to find an answer to my previous question.

In the study below, in rats, no observable damage* with a 25mg/kg dose.
At 50mg/kg 2 out 6 rats showed partial damage.
75mg/kg and 100mg/kg dosages caused more serious damage, area of damage apparently proportional to the dosage increase.
*Damage being "neurodegeneration of Purkinje cells and gliosis of Bergmann astrocytes in the cerebella"



"Toxicological Sciences 57, 95-101 (2000)
Copyright © 2000 by the Society of Toxicology
Neurotoxicology
A Dose-Response Study of Ibogaine-Induced Neuropathology in the Rat Cerebellum
Zengjun Xu*, Louis W. Chang*,{dagger}, William Slikker, Jr.{dagger},{ddagger}, Syed F. Ali{dagger},{ddagger}, Robert L. Rountree{ddagger} and Andrew C. Scallet{dagger},{ddagger},1

* Department of Pathology and {dagger} Department of Pharmacology & Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and {ddagger} Division of Neurotoxicology, National Center for Toxicological Research, Jefferson, Arkansas 72079

Ibogaine (IBO) is an indole alkaloid from the West African shrub, Tabernanthe iboga. It is structurally related to harmaline, and both these compounds are rigid analogs of melatonin. IBO has both psychoactive and stimulant properties. In single-blind trials with humans, it ameliorated withdrawal symptoms and interrupted the addiction process. However, IBO also produced neurodegeneration of Purkinje cells and gliosis of Bergmann astrocytes in the cerebella of rats given even a single dose (100 mg/kg, ip). Here, we treated rats (n = 6 per group) with either a single ip injection of saline or with 25 mg/kg, 50 mg/kg, 75 mg/kg, or 100 mg/kg of IBO. As biomarkers of cerebellar neurotoxicity, we specifically labeled degenerating neurons and axons with silver, astrocytes with antisera to glial fibrillary acidic protein (GFAP), and Purkinje neurons with antisera to calbindin. All rats of the 100-mg/kg group showed the same pattern of cerebellar damage previously described: multiple bands of degenerating Purkinje neurons. All rats of the 75-mg/ kg group had neurodegeneration similar to the 100-mg/kg group, but the bands appeared to be narrower. Only 2 of 6 rats that received 50 mg/kg were affected; despite few degenerating neuronal perikarya, cerebella from these rats did contain patches of astrocytosis similar to those observed with 75 or 100 mg/kg IBO. These observations affirm the usefulness of GFAP immunohistochemistry as a sensitive biomarker of neurotoxicity. None of the sections from the 25-mg/kg rats, however stained, were distinguishable from saline controls, indicating that this dose level may be considered as a no-observable-adverse-effect level (NOAEL).

Key Words: ibogaine; Purkinje neuron; Bergmann astrocyte; neurodegeneration; calbindin; GFAP; NOAEL; cerebellum."



Boris




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