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Neurotox Res. 2005 Nov;8(3-4):199-206.

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

Author information

  • 1Molecular Neuropsychiatry Branch, NIH/NIDA, Intramural Research Program, Department of Health and Human Services, 5500 Nathan Shock Drive, Baltimore, MD 21224, USA. JCADET@intra.nida.nih.gov

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 apoptosis in vitro and in 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-, endoplasmic 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).

PMID:
16371314
[PubMed - indexed for MEDLINE]
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