Quinton Maria S, Yamamoto Bryan K
Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Room L -613, 715 Albany Street, Boston, MA 02118, USA.
AAPS J. 2006 May 12;8(2):E337-47. doi: 10.1007/BF02854904.
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.
甲基苯丙胺（METH）及其衍生物3,4-亚甲基二氧基甲基苯丙胺（MDMA；摇头丸）是两种在美国具有极高滥用倾向的苯丙胺类兴奋剂。这些类苯丙胺兴奋剂与大脑中多巴胺能和5-羟色胺能神经末梢多种标志物的丧失有关。在其他原因中，氧化应激、兴奋性毒性和线粒体功能障碍似乎在这些苯丙胺类兴奋剂产生的神经毒性中起主要作用。本综述将聚焦于这些事件，以及它们如何相互作用和共同作用，从而导致在给予METH或MDMA后通常观察到的单胺能耗竭。此外，还描述了METH或MDMA诱导的氧化应激、兴奋性毒性和线粒体功能障碍的最新发现的后果，这些后果与METH诱导的多巴胺能末梢损伤的经典标志物有关。
