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

Ron Davis rwd3 at cox.net
Sat Aug 13 23:53:17 EDT 2005

now you're making sense to a senseless fool.  KOKO the Kenai Klown.  All bs 
aside,  one day,  b/4 i lose it all, i hope to thank the wild bunch for 
doing the core stuff i can't which I am certain will play into significant 
stuff I am unable to understand at the moment but will soon be revealed to 
me.  thank you.  need all the help I can get at the momenent. i'm a factory 
fluke right now. rd in real time
----- Original Message ----- 
From: <slowone at hush.ai>
To: <ibogaine at mindvox.com>
Sent: Saturday, August 13, 2005 8:29 PM
Subject: Re: [Ibogaine] Gallo Research Center studies cause and treatment of 
alcohol, drug addiction

> "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
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