Causes and consequences of methamphetamine and MDMA toxicity
Causes and consequences of methamphetamine and MDMA toxicity
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DOI：
10.1208/aapsj080238
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发表时间：
2006-01-01
期刊：
影响因子：
4.5
通讯作者：
Yamamoto, Bryan K.
中科院分区：
文献类型：
--
作者：
Quinton, Maria S.;Yamamoto, Bryan K.
甲基苯丙胺（METH）及其衍生物3，4-亚甲二氧基甲基苯丙胺（MDMA;摇头丸）是2种在美国滥用风险很高的取代苯丙胺。这些苯丙胺类兴奋剂与大脑中多巴胺能和多巴胺能末梢的多种标志物的丢失有关。除其他原因外，氧化应激、兴奋性毒性和线粒体功能障碍似乎在取代安非他明产生的神经毒性中起主要作用。本综述将重点关注这些事件以及它们如何相互作用和聚集以产生通常在METH或MDMA给药后观察到的单胺能消耗。此外，最近确定的METH或MDMA诱导的氧化应激，兴奋性毒性，和线粒体功能障碍的后果描述的经典标志物的METH诱导的多巴胺终端的损害。
Methamphetamine ( METH) and its derivative 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) are 2 substituted amphetamines with very high abuse liability in the United States. These amphetamine-like stimulants have been associated with loss of multiple markers for dopaminergic and serotonergic terminals in the brain. Among other causes, oxidative stress, excitotoxicity and mitochondrial dysfunction appear to play a major role in the neurotoxicity produced by the substituted amphetamines. The present review will focus on these events and how they interact and converge to produce the monoaminergic depletions that are typically observed after METH or MDMA administration. In addition, more recently identified consequences of METH or MDMA-induced oxidative stress, excitotoxicity, and mitochondrial dysfunction are described in relation to the classical markers of METH-induced damage to dopamine terminals.