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

HSLotsof at aol.com HSLotsof at aol.com
Thu Aug 11 15:42:43 EDT 2005

In a message dated 8/11/05 10:00:11 AM, freedomroot at gmail.com writes:

<< 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 >>

This should help.  Howard

Neuroscience. 2004;127(2):373-83.   
Administration of a non-NMDA antagonist, GYKI 52466, increases excitotoxic 
Purkinje cell degeneration caused by ibogaine.

O'Hearn E, Molliver ME
Department of Neurology, The Johns Hopkins University School of Medicine, 
Baltimore, MD 21205, USA. eohearn at jhmi.edu
Ibogaine is a tremorigenic hallucinogen that has been proposed for clinical 
use in treating addiction. We previously reported that ibogaine, administered 
systemically, produces degeneration of a subset of Purkinje cells in the 
cerebellum, primarily within the vermis. Ablation of the inferior olive affords 
protection against ibogaine-induced neurotoxicity leading to the interpretation 
that ibogaine itself is not directly toxic to Purkinje cells. We postulated that 
ibogaine produces sustained excitation of inferior olivary neurons that leads 
to excessive glutamate release at climbing fiber terminals, causing 
subsequent excitotoxic injury to Purkinje cells. The neuronal degeneration induced by 
ibogaine provides an animal model for studying excitotoxic injury in order to 
analyze the contribution of glutamate receptors to this injury and to evaluate 
neuroprotective strategies. Since non-N-methyl-D-aspartate (NMDA) receptors 
mediate Purkinje cell excitation by climbing fibers, we hypothesized that 
1-4-aminophenyl-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI-52466), which 
antagonizes non-NMDA receptors, may have a neuroprotective effect by blocking 
glutamatergic excitation at climbing fiber synapses. To test this hypothesis, 
rats were administered systemic ibogaine plus GYKI-52466 and the degree of 
neuronal injury was analyzed in cerebellar sections. The results indicate that 
the AMPA antagonist GYKI-52466 (10 mg/kg i.p. x 3) does not protect against 
Purkinje cell injury at the doses used. Rather, co-administration of GYKI-52466 
with ibogaine produces increased toxicity evidenced by more extensive Purkinje 
cell degeneration. Several hypotheses that may underlie this result are 
discussed. Although the reason for the increased toxicity found in this study is not 
fully explained, the present results show that a non-NMDA antagonist can 
produce increased excitotoxic injury under some conditions. Therefore, caution 
should be exercised before employing glutamate antagonists to reduce the risk of 
neuronal damage in human clinical disorders. Moreover, the contribution of 
different glutamate receptors to excitotoxic injury is complex and merits further 

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