Causes and consequences of methamphetamine and MDMA toxicity

Maria S. Quinton, Bryan K. Yamamoto

Research output: Contribution to journalReview article

151 Scopus citations

Abstract

Methamphetamine (METH) and its derivative 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) are 2 substituted amphetamines with very high abuse liability in the United States. These amphetamine-like stimulants have been associated with loss of multiple markers for dopaminergic and serotonergic terminals in the brain. Among other causes, oxidative stress, excitotoxicity and mitochondrial dysfunction appear to play a major role in the neurotoxicity produced by the substituted amphetamines. The present review will focus on these events and how they interact and converge to produce the monoaminergic depletions that are typically observed after METH or MDMA administration. In addition, more recently identified consequences of METH or MDMA-induced oxidative stress, excitotoxicity, and mitochondrial dysfunction are described in relation to the classical markers of METH-induced damage to dopamine terminals.

Original languageEnglish (US)
Article number38
Pages (from-to)E337-E347
JournalAAPS Journal
Volume8
Issue number2
DOIs
StatePublished - May 12 2006
Externally publishedYes

Keywords

  • Blood-brain barrier
  • Excitotoxicity
  • Glutamate
  • Mitochondrial dysfunction
  • Oxidative stress
  • Substituted amphetamines

ASJC Scopus subject areas

  • Pharmaceutical Science

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