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

slowone at hush.ai slowone at hush.ai
Sat Aug 13 21:29:54 EDT 2005

"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."

I.e. the only known form of ibogaine-induced nerve damage is the 
result of a cascade of effects. I wonder if ablation of the 
inferior olive would affect ibogaine's ability to interrupt 
addiction. Addiction interruption could even be the result of a 
different cascade of effects (rather than directly caused by the 
ibogaine). Someday science may sort these things out.. hopefully in 
my lifetime. Thanks for posting this, Howard.

On Thu, 11 Aug 2005 12:42:43 -0700 HSLotsof at aol.com wrote:
>Administration of a non-NMDA antagonist, GYKI 52466, increases 
>Purkinje cell degeneration caused by ibogaine.
>O'Hearn E, Molliver ME
>Department of Neurology, The Johns Hopkins University School of 
>Baltimore, MD 21205, USA. eohearn at jhmi.edu
>Ibogaine is a tremorigenic hallucinogen that has been proposed for 

>use in treating addiction. We previously reported that ibogaine, 
>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 
>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, 
>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) 
>mediate Purkinje cell excitation by climbing fibers, we 
>hypothesized that 
>(GYKI-52466), which 
>antagonizes non-NMDA receptors, may have a neuroprotective effect 
>by blocking 
>glutamatergic excitation at climbing fiber synapses. To test this 
>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 
>  /]=--------------------------------------------------------------

> [%] Ibogaine List Commands: 
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