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

BK Yamamoto, J Raudensky - Journal of Neuroimmune Pharmacology, 2008 - Springer
BK Yamamoto, J Raudensky
Journal of Neuroimmune Pharmacology, 2008Springer
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 …
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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