Mechanisms of methamphetamine-induced dopaminergic neurotoxicity
Mechanisms of methamphetamine-induced dopaminergic neurotoxicity
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DOI：
10.1007/bf02854914
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发表时间：
2006-01-01
期刊：
影响因子：
4.5
通讯作者：
Hanson, Glen R.
中科院分区：
文献类型：
--
作者：
Riddle, Evan L.;Fleckenstein, Annette E.;Hanson, Glen R.
甲基苯丙胺（METH）是一种具有强烈成瘾性和神经毒性的强效兴奋剂。超过2.5年前，描述了对多巴胺能神经元的甲基苯丙胺诱导的损伤。从那时起，在寻找METH导致这些持续性多巴胺能缺陷的潜在机制方面取得了许多进展。虽然我们对这些机制的理解仍然不完整，但围绕涉及活性物质（如活性氧和/或氮物质（分别为ROS和RNS））的中心主题，已经描述了各种复杂过程的组合。例如，MET诱导的体温过高、异常多巴胺（DA）或谷氨酸传递;或线粒体破坏导致产生具有神经毒性后果的反应性物质。这篇综述将描述目前的理解如何高剂量的甲基管理导致这些有毒的反应性物种的生产和随之而来的永久性多巴胺能缺陷。
Methamphetamine ( METH) is a powerful stimulant of abuse with potent addictive and neurotoxic properties. More than 2.5 decades ago, METH-induced damage to dopaminergic neurons was described. Since then, numerous advancements have been made in the search for the underlying mechanisms whereby METH causes these persistent dopaminergic deficits. Although our understanding of these mechanisms remains incomplete, combinations of various complex processes have been described around a central theme involving reactive species, such as reactive oxygen and/or nitrogen species (ROS and RNS, respectively). For example, METH-induced hyperthermia, aberrant dopamine (DA), or glutamate transmission; or mitochondrial disruption leads to the generation of reactive species with neurotoxic consequences. This review will describe the current understanding of how high-dose METH administration leads to the production of these toxic reactive species and consequent permanent dopaminergic deficits.