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Re: to all... flmm

Posted by Larry Hoover on August 29, 2004, at 21:09:25

In reply to Re: to all..., posted by flmm on August 29, 2004, at 18:46:09

> There is an implication that used correctly, MDMA possibly is safe, according to your post. I believe this is not the case and feel it is reckless to imply this.

Well, your position probably arises from a much-publicized paper in the prestigious journal Science, which was later subject to a much less-publicized full retraction. The study had used the wrong drug! The primates had received no MDMA at all! See the first abstract, along with a link I've added, which gives the full-text of the retraction.

Also, that prestigious researcher, Ricaurte, later gave MDMA to monkeys for eighteen months, as much as they wanted. Following two months of withdrawal, there was no change in brain neurotransmitter levels from normal levels. "Further, there were no measurable decrements in serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) or VMAT in any brain regions assayed."

There goes another myth.


Science. 2002 Sep 27;297(5590):2260-3.

Retraction in:
Ricaurte GA, Yuan J, Hatzidimitriou G, Cord BJ, McCann UD. Science. 2003 Sep 12;301(5639):1479.

Comment in:
Science. 2002 Sep 27;297(5590):2185-7.
Science. 2003 Jun 6;300(5625):1504-5; author reply 1504-5.

Severe dopaminergic neurotoxicity in primates after a common recreational dose regimen of MDMA ("ecstasy").

Ricaurte GA, Yuan J, Hatzidimitriou G, Cord BJ, McCann UD.

Department of Neurology, Johns Hopkins Bayview Medical Center, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.

The prevailing view is that the popular recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, or "ecstasy") is a selective serotonin neurotoxin in animals and possibly in humans. Nonhuman primates exposed to several sequential doses of MDMA, a regimen modeled after one used by humans, developed severe brain dopaminergic neurotoxicity, in addition to less pronounced serotonergic neurotoxicity. MDMA neurotoxicity was associated with increased vulnerability to motor dysfunction secondary to dopamine depletion. These results have implications for mechanisms of MDMA neurotoxicity and suggest that recreational MDMA users may unwittingly be putting themselves at risk, either as young adults or later in life, for developing neuropsychiatric disorders related to brain dopamine and/or serotonin deficiency.

Neuropsychopharmacology. 2004 Jul;29(7):1270-81.

Behavioral and neurochemical consequences of long-term intravenous self-administration of MDMA and its enantiomers by rhesus monkeys.

Fantegrossi WE, Woolverton WL, Kilbourn M, Sherman P, Yuan J, Hatzidimitriou G, Ricaurte GA, Woods JH, Winger G.

Department of Pharmacology, University of Michigan Medical School, Ann Arbor, MI 48101-0632, USA.

The effects of self-administered 3,4-methylenedioxymethamphetamine (MDMA) on behavior and neurochemistry have not been previously studied in laboratory primates. We investigated the capacity of MDMA and its enantiomers to maintain contingent responding over an extended duration, whether any decrements in the reinforcing effects of these compounds would be observed over time, whether such decrements would be MDMA-selective, and whether any neurochemical correlates could be identified. Animals were previously trained to self-administer cocaine, then exposed to periodic substitutions of various doses of racemic MDMA and its enantiomers; full dose-effect curves were generated for each MDMA compound repeatedly over the duration of the study. After approximately 18 months of MDMA self-administration, drug exposure was halted and after at least 2 months drug abstinence, animals were scanned using positron emission tomography (PET) with the vesicular monoamine transporter (VMAT) ligand dihydrotetrabenazine (DTBZ). Shortly thereafter, animals were euthanized, brains were dissected, and samples were assayed for brain monoamines and their metabolites using high-performance liquid chromatography (HPLC), and for VMAT using DTBZ binding. The reinforcing effects of racemic and R(-)-MDMA were reduced over a long series (months) of individual self-administration access periods; the reinforcing effects of S+-MDMA were more resistant to this effect, but were attenuated for one animal. The reinforcing effects of cocaine were not altered by chronic MDMA self-administration, nor was the VMAT binding potential as assessed by PET. Further, there were no measurable decrements in serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) or VMAT in any brain regions assayed. The reinforcing effects of MDMA are selectively attenuated by chronic MDMA self-administration, although this behavioral change appears to occur in the absence of any frank neurochemical correlates of toxicity. Copyright 2004 Nature Publishing Group




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