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(The FASEB Journal. 2003;17:1775-1788.)
© 2003 FASEB

Speed kills: cellular and molecular bases of methamphetamine-induced nerve terminal degeneration and neuronal apoptosis

JEAN LUD CADET1, SUBRAMANIAM JAYANTHI and XIAOLIN DENG

Molecular Neuropsychiatry Branch, NIH/NIDA, Intramural Research Program, Department of Health and Human Services, Baltimore, Maryland, USA

1Correspondence: Molecular Neuropsychiatry Branch, NIH, NIDA, Intramural Research Program, DHHS, 5500 Nathan Shock Dr., Baltimore, MD 21224, USA. E-mail: jcadet{at}intra.nida.nih.gov

Methamphetamine (METH) is a drug of abuse that has long been known to damage monoaminergic systems in the mammalian brain. Recent reports have provided conclusive evidence that METH can cause neuropathological changes in the rodent brain via apoptotic mechanisms akin to those reported in various models of neuronal death. The purpose of this review is to provide an interim account for a role of oxygen-based radicals and the participation of transcription factors and the involvement of cell death genes in METH-induced neurodegeneration. We discuss data suggesting the participation of endoplasmic reticulum and mitochondria-mediated activation of caspase-dependent and -independent cascades in the manifestation of METH-induced apoptosis. Studies that use more comprehensive approaches to gene expression profiling should allow us to draw more instructive molecular portraits of the complex plastic and degenerative effects of this drug.—Cadet, J. L., Jayanthi, S., Deng, X. Speed kills: cellular and molecular bases of methamphetamine-induced nerve terminal degeneration and neuronal apoptosis.


Key Words: Bcl-2 family proteins • cDNA array • IEGs • mitochondria • endoplasmic reticulum • neurodegeneration • terminal apoptosis




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