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The Role of Oxidative Stress, Metabolic Compromise, and Inflammation in Neuronal Injury Produced by Amphetamine-Related Drugs of Abuse

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Abstract

Methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) are amphetamine derivatives with high abuse liability. These amphetamine-related drugs of abuse mediate their effects through the acute activation of both dopaminergic and serotonergic neurons. Long-term abuse of these amphetamine derivatives, however, results in damage to both dopaminergic and serotonergic terminals throughout the brain. This toxicity is mediated in part by oxidative stress, metabolic compromise, and inflammation. The overall objective of this review is to highlight experimental evidence that METH and MDMA increase oxidative stress, produce mitochondrial dysfunction, and increase inflammation that converge and culminate in the long-term toxicity to dopaminergic and serotonergic neurons.

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  1. Department of Pharmacology and Experimental Therapeutics, Laboratory of Neurochemistry, Boston University School of Medicine, L-613, 715 Albany St., Boston, MA, 02118, USA

    Bryan K. Yamamoto & Jamie Raudensky

  2. Department of Neurosciences, University of Toledo Health Science Campus, 3000 Arlington Avenue, Toledo, OH, 43614, USA

    Bryan K. Yamamoto

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Yamamoto, B.K., Raudensky, J. The Role of Oxidative Stress, Metabolic Compromise, and Inflammation in Neuronal Injury Produced by Amphetamine-Related Drugs of Abuse. J Neuroimmune Pharmacol 3, 203–217 (2008). https://doi.org/10.1007/s11481-008-9121-7

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