Journal
NEUROTOXICITY RESEARCH
Volume 8, Issue 3-4, Pages 199-206Publisher
SPRINGER
DOI: 10.1007/BF03033973
Keywords
methamphetamine; neuronal apoptosis; mitochondria; endoplasmic reticulum; Fas; FasL
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Funding
- Intramural NIH HHS Funding Source: Medline
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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).
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