The role of oxidative stress, metabolic compromise, and inflammation in neuronal injury produced by amphetamine-related drugs of abuse

Bryan K. Yamamoto, Jamie Raudensky

Research output: Contribution to journalReview article

98 Scopus citations

Abstract

Methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) are amphetamine derivatives with high abuse liability. These amphetamine-related drugs of abuse mediate their effects through the acute activation of both dopaminergic and serotonergic neurons. Long-term abuse of these amphetamine derivatives, however, results in damage to both dopaminergic and serotonergic terminals throughout the brain. This toxicity is mediated in part by oxidative stress, metabolic compromise, and inflammation. The overall objective of this review is to highlight experimental evidence that METH and MDMA increase oxidative stress, produce mitochondrial dysfunction, and increase inflammation that converge and culminate in the long-term toxicity to dopaminergic and serotonergic neurons.

Original languageEnglish (US)
Pages (from-to)203-217
Number of pages15
JournalJournal of Neuroimmune Pharmacology
Volume3
Issue number4
DOIs
StatePublished - Dec 1 2008
Externally publishedYes

Keywords

  • Inflammation
  • MDMA
  • Matrix metalloproteinase
  • Methamphetamine
  • Mitochondrial dysfunction
  • Oxidative stress

ASJC Scopus subject areas

  • Neuroscience (miscellaneous)
  • Immunology and Allergy
  • Immunology
  • Pharmacology

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