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Neurotoxicity Research

, Volume 8, Issue 3–4, pp 199–206 | Cite as

Methamphetamine-induced neuronal apoptosis involves the activation of multiple death pathways. Review

  • Jean Lud Cadet
  • Subramaniam Jayanthi
  • Xiaolin Deng
Article

Abstract

The abuse of the illicit drug methamphetamine (METH) is a major concern because it can cause terminal degeneration and neuronal cell death in the brain. METH-induced cell death occurs via processes that resemble apoptosis. In the present review, we discuss the role of various apoptotic events in the causation of METH-induced neuronal apoptosisin vitro andin vivo. Studies using comprehensive approaches to gene expression profiling have allowed for the identification of several genes that are up-regulated or down-regulated after an apoptosis-inducing dose of the drug. Further experiments have also documented the fact that the drug can cause demise of striatal enkephalinergic neurons by cross-talks between mitochondria-, endo-plasmic reticulum- and receptor-mediated apoptotic events. These neuropathological observations have also been reported in models of drug-induced neuroplastic alterations used to mimic drug addiction (Nestler, 2001).

Keywords

Methamphetamine Neuronal apoptosis Mitochondria Endoplasmic reticulum Fas FasL 

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Copyright information

© Springer 2005

Authors and Affiliations

  • Jean Lud Cadet
    • 1
  • Subramaniam Jayanthi
    • 1
  • Xiaolin Deng
    • 1
  1. 1.Intramural Research Program, Department of Health and Human ServicesMolecular Neuropsychiatry Branch, NIH/NIDABaltimoreUSA

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