Aug 19, 2008

The role of oxidative stress, metabolic compromise, and inflammation in neuronal injury produced by amphetamine-related drugs of abuse

Journal of Neuroimmune Pharmacology : the Official Journal of the Society on NeuroImmune Pharmacology
Bryan K Yamamoto, Jamie Raudensky

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.

Mentioned in this Paper

Metabolic Process, Cellular
Amphetamine
Derivatives
Neurons
Brain
Recreational Drugs
Nerve Degeneration
Methamphetamine Measurement
Oxidative Stress
Oxidative Stress Analysis

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