Is there a role for nitric oxide in methamphetamine-induced dopamine terminal degeneration?
Is there a role for nitric oxide in methamphetamine-induced dopamine terminal degeneration?
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DOI：
10.1007/s12640-013-9415-2
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发表时间：
2014-02
影响因子：
3.7
通讯作者：
Keefe KA
中科院分区：
文献类型：
--
作者：
Friend DM;Fricks-Gleason AN;Keefe KA
滥用甲基苯丙胺会导致多巴胺能系统的长期损害，表现为多巴胺(DA)组织含量减少，DA转运体(DAT)结合，以及酪氨酸羟化酶(TH)和囊泡单胺转运体(VMAT)免疫染色。然而，最终导致这种损害的一连串事件的确切原因尚不清楚。与冰毒诱导的多巴胺终末变性密切相关的一个因素是一氧化氮(NO)的产生。不幸的是，许多试图阐明NO在冰毒诱导的神经毒性中的作用的研究都被诸如中断冰毒诱导的体温过高、阻止形成强有力的结论等问题所混淆。因此，有大量工作表明，NO足以引起冰毒诱导的神经毒性，而其他研究表明，NO在冰毒诱导的DA神经末梢变性中不起作用。本文综述了NO在冰毒神经毒性中作用的现有研究，认为虽然NO在冰毒神经毒性中可能是必需的，但它是不够的。最后，对未来研究的重点领域进行了展望和讨论。
Methamphetamine (METH) abuse results in long-term damage to the dopaminergic system, manifesting as decreases in dopamine (DA) tissue content, DA transporter (DAT) binding, as well as tyrosine hydroxylase (TH) and vesicular monoamine transporter (VMAT) immunostaining. However, the exact cascade of events that ultimately results in this damage has not been clearly elucidated. One factor that has been heavily implicated in METH-induced DA terminal degeneration is the production of nitric oxide (NO). Unfortunately, many of the studies attempting to clarify the role of NO in METH-induced neurotoxicity have been confounded by issues such as the disruption of METH-induced hyperthermia, preventing the formation of strong conclusions. As a result, there is a body of work suggesting that NO is sufficient for METH-induced neurotoxicity, while other studies suggest that NO does not play a role in METH-induced degeneration of DA nerve terminals. This review summarizes the existing studies investigating the role of NO in METH-induced neurotoxicity, and argues that while NO may be necessary for METH-induced neurotoxicity, it is not sufficient. Finally, important areas of future investigation are highlighted and discussed.