Methamphetamine neurotoxicity and neuroinflammatory processes

Nicole A. Northrop, Bryan K. Yamamoto

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations

Abstract

Methamphetamine (Meth) is a widely abused psychostimulant known to cause neurotoxicity. Traditionally, the toxic effects of Meth were thought to be restricted to dopaminergic and serotonergic axon terminals, but more recently the targets of Meth have been found to include dopaminergic and GABAergic neurons, brain endothelial cells, and the liver. In addition to the neuronal and nonneuronal targets of Meth, mechanisms responsible for damage including oxidative stress, excitotoxicity, and mitochondrial dysfunction will be discussed. The focus of this chapter will be to integrate the known targets of Meth and mechanisms of Meth-induced damage with more recently identified neuroinflammatory markers found after exposure to Meth. Various inflammatory mediators and their temporal expression after Meth exposure will be reviewed as well as supporting evidence for the role of neuroinflammation in Meth-induced damage.

Original languageEnglish (US)
Title of host publicationNeuroinflammation and Neurodegeneration
PublisherSpringer New York
Pages443-462
Number of pages20
ISBN (Electronic)9781493910717
ISBN (Print)1493910701, 9781493910700
DOIs
StatePublished - Apr 1 2014

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Keywords

  • Cyclooxygenase (COX)
  • Cytokines
  • Methamphetamine
  • Microglia
  • Motor proteins
  • Neuroinflammation
  • Neurotoxicity
  • Striatum

ASJC Scopus subject areas

  • Medicine(all)
  • Neuroscience(all)

Cite this

Northrop, N. A., & Yamamoto, B. K. (2014). Methamphetamine neurotoxicity and neuroinflammatory processes. In Neuroinflammation and Neurodegeneration (pp. 443-462). Springer New York. https://doi.org/10.1007/978-1-4939-1071-7_21