Methamphetamine and methylenedioxymethamphetamine neurotoxicity: possible mechanisms of cell destruction.
Methamphetamine and methylenedioxymethamphetamine neurotoxicity: possible mechanisms of cell destruction.
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甲基苯丙胺和亚甲二氧基甲基苯丙胺神经毒性：细胞破坏的可能机制。
DOI：
10.1037/e495672006-014
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
K. E. Sabol
中科院分区：
文献类型：
--
作者：
L. Seiden;K. E. Sabol
甲基苯丙胺和MDMA以及类似的取代苯乙胺对DA和/或5-羟色胺神经元有毒性作用。这些影响的持续时间和大小与剂量有关，并伴随着不同程度的恢复。MDMA诱导的5-羟色胺损伤在大鼠中持续长达52周，甲基苯丙胺诱导的DA损伤在恒河猴中持续长达3年。对苯丙胺类似物毒性的几种可能机制进行了综述。兴奋性前馈环路理论得到了文献的最好支持。然而，这一理论涉及面很广，很难证明或反驳。羟基自由基理论和DA调节理论都得到了综述数据的很好支持。应该指出的是，这两个假设是密切相关的。DA中介理论是基于甲基苯丙胺和MDMA神经毒性发生的完整DA系统的要求。羟基自由基理论也是基于DA和5-HT的存在；此外，它还提出了苯丙胺类似物神经毒性的具体机制是DA或5-HT生成有毒的羟基自由基。羟基自由基理论还解释了苯丙胺类神经毒性对大脑的DA和/或5-羟色胺系统选择性毒性的事实，即毒素要么在突触中形成，要么由于苯丙胺类似物处理而在释放DA和/或5-羟色胺的神经元内形成。毒性药物代谢物理论虽然没有得到详尽的研究，但目前几乎没有得到文献的支持。同样，NMDA受体中介理论，以其最直接的形式，也几乎没有得到文献的支持。NMDA受体拮抗剂MK-801的保护作用可能是温度调节变化引起的调制作用，而不是直接拮抗毒性机制本身的一个环节。应该指出的是，保护剂加上苯丙胺类似物对体温的影响，在彻底调查后，可以用来将通过冷却机制保护的药剂与通过干扰毒性过程本身保护的药剂分开。
Methamphetamine and MDMA as well as similar substituted phenethylamines are toxic to DA and/or 5-HT neurons. The duration and magnitude of these effects are dose dependent and are accompanied by different degrees of recovery. MDMA-induced 5-HT damage persists for up to 52 weeks in the rat, and methamphetamine-induced DA damage persists for up to 3 years in the rhesus monkey. Several possible mechanisms of amphetamine-analog toxicity have been reviewed. The excitatory feed-forward loop theory is best supported by the literature. This theory, however, is very wide ranging and difficult to prove or disprove. The hydroxy radical and DA mediation theories are both well supported by the data reviewed. It should be noted that these two hypotheses are closely related to each other. The DA mediation theory is based on the requirement of an intact DA system for methamphetamine and MDMA neurotoxicity to occur. The hydroxy radical theory is also based on the presence of DA and 5-HT; in addition, it suggests the formation of toxic hydroxy radicals from DA or 5-HT as the specific mechanism for the amphetamine-analog neurotoxicity. The hydroxy radical theory also accounts for the fact that amphetamine-analog neurotoxicity is selectively toxic to the DA and/or 5-HT systems of the brain; that is, the toxin is formed either in the synapse or within the neurons that release DA and/or 5-HT as a result of amphetamine analog treatment. The toxic drug metabolite theory, while not exhaustively studied, has little support from the literature at present. Similarly, the NMDA receptor mediation theory, in its most straightforward form, also has little support from the literature. The protective effects of the NMDA receptor antagonist MK-801 may be a modulatory effect resulting from changes in temperature regulation, rather than a direct effect of antagonizing a link in the toxic mechanism itself. It should be noted that the effects of the protective agent plus amphetamine-analog combinations on body temperature, when thoroughly investigated, may serve to separate agents which protect through a cooling mechanism from agents that protect by interfering with the toxic process itself.
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DOI：
--
发表时间：
1986-09
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
P. Sonsalla;J. Gibb;G. Hanson
通讯作者：
P. Sonsalla;J. Gibb;G. Hanson
DOI：
--
发表时间：
1991-02
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
P. Sonsalla;D. E. Riordan;R. Heikkila
通讯作者：
P. Sonsalla;D. E. Riordan;R. Heikkila
通过体内微透析测量，酮色林预处理可减弱纹状体中 MDMA 诱导的多巴胺释放。
影响因子：
6.1
作者：
Nash,JF
通讯作者：
Nash,JF
半胱氨酸对苯丙胺、对氯苯丙胺和 MPTP 持续消耗脑单胺的影响。
影响因子：
5
作者：
Steranka,LR;Rhind,AW
通讯作者：
Rhind,AW
影响因子：
--
作者：
Na, Wonho;Lee, Jee Youn;Ju, Bong-Gun
通讯作者：
Ju, Bong-Gun