Journal
NEUROPSYCHOBIOLOGY
Volume 60, Issue 3-4, Pages 119-129Publisher
KARGER
DOI: 10.1159/000253548
Keywords
3,4-Methylenedioxymethamphetamine; 5-Hydroxytryptamine; Serotonin; Dopamine; Hyperthermia; Metabolism; Neurotoxicity
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Funding
- Ministerio de Educacion y Ciencia [SAF2005-07919-C02-02]
- Ministerio de Sanidad y Consumo (PNSD)
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Administration of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) to various experimental animals has been shown to induce a selective damage to serotonergic axon terminals. While a great consensus appears to exist regarding the causative role of reactive oxygen species (ROS) in the mechanisms underlying MDMA toxicity, the source of free radicals is still a matter of debate. While some authors support dopamine metabolism/oxidation inside 5-hydroxytryptamine (5-HT) terminals as the key factor responsible for ROS formation and final 5-HT terminal degeneration, others believe it is MDMA metabolism into pro-oxidant compounds. Although at first sight both hypotheses appear to contend with each other, it may not be the case. This mini-review was therefore undertaken to try to reconcile both hypotheses and to address the dilemma of the causality of MDMA neurotoxicity. Copyright (C) 2009 S. Karger AG, Basel
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