The methamphetarnine experience: a NIDA partnership
The methamphetarnine experience: a NIDA partnership
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DOI：
10.1016/j.neuropharm.2004.06.004
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发表时间：
2004-01-01
影响因子：
4.7
通讯作者：
Fleckenstein, AE
中科院分区：
文献类型：
--
作者：
Hanson, GR;Rau, KS;Fleckenstein, AE
甲基苯丙胺（冰毒）等安非他明的神经毒性最初是在20世纪70年代初由美国国家药物滥用研究所的组织描述的。人们花了20多年的时间来证实这些对人类的神经毒性。就像帕金森病一样，多次大剂量服用甲基苯丙胺在一定程度上选择性地损害了大脑的黑质纹状体多巴胺（DA）投射。这种效应似乎与胞质内DA的积累及其氧化成活性氧的能力有关。多巴胺质乳转运蛋白和水疱单胺转运蛋白-2似乎在这种神经毒性中起关键作用。甲基苯丙胺和相关的类似物，如亚甲基二氧基甲基苯丙胺（MDMA）也可以损害选择性中枢神经系统血清素神经元。5 -羟色胺能神经毒性的机制尚不清楚，但似乎与活性氧和单胺转运体的形成有关。研究安非他明的药理学和神经毒理学特性有助于阐明单胺调节的一些关键特征，并有助于提高我们对与退行性疾病（如帕金森病）相关的过程的理解。(C) 2004 Elsevier Ltd.版权所有。
The neurotoxic properties of the amphetamines such as methamphetamine (METH) were originally described about the time of the National Institute on Drug Abuse's organization, in the early 1970s. It required more than 20 years to confirm these neurotoxic properties in humans. Much like Parkinson's disease, multiple high-dose administration of METH somewhat selectively damages the nigrostriatal dopamine (DA) projection of the brain. This effect appears to be related to the intracellular accumulation of cytosolic DA and its ability to oxidize into reactive oxygen species. Both the dopamine plasmalemmal transporter and the vesicular monoamine transporter-2 seem to play critical roles in this neurotoxicity. METH and related analogs such as methylenedioxymethamphetamine (MDMA) can also damage selective CNS serotonin neurons. The mechanism of the serotonergic neurotoxicity is not as well characterized, but also appears to be related to the formation of reactive oxygen species and monoamine transporters. Studies examining the pharmacological and neurotoxicological properties of the amphetamines have helped to elucidate some critical features of monoamine regulations as well as helped to improve our understanding of the processes associated with degenerative disorders such as Parkinson's disease. (C) 2004 Elsevier Ltd. All rights reserved.