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

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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).

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  1. Intramural Research Program, Department of Health and Human Services, Molecular Neuropsychiatry Branch, NIH/NIDA, 5500 Nathan Shock Drive, 21224, Baltimore, MD, USA

    Jean Lud Cadet, Subramaniam Jayanthi & Xiaolin Deng

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  1. Jean Lud Cadet
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Cadet, J.L., Jayanthi, S. & Deng, X. Methamphetamine-induced neuronal apoptosis involves the activation of multiple death pathways. Review. neurotox res 8, 199–206 (2005). https://doi.org/10.1007/BF03033973

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