期刊
NEUROTOXICITY RESEARCH
卷 8, 期 3-4, 页码 199-206出版社
SPRINGER
DOI: 10.1007/BF03033973
关键词
methamphetamine; neuronal apoptosis; mitochondria; endoplasmic reticulum; Fas; FasL
资金
- Intramural NIH HHS Funding Source: Medline
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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