Investigations on methamphetamine-neurotoxicity by using an animal model

本研究提示，考虑到甲基苯丙胺对氧化应激所致的神经毒性作用，对一氧化氮合酶的药物干预可能有助于减轻甲基苯丙胺的单胺消耗和诱导细胞凋亡的作用，小剂量甲基苯丙胺对中脑的甲基苯丙胺神经毒性有保护作用，部分通过内质网应激相关途径抑制氧化应激和细胞凋亡机制。从法医病理学的观点来看，在神经毒性剂量管理之前增加药物摄取和低剂量冰毒预处理的动物模型可能有助于研究人类冰毒滥用者神经毒性的机制。

This study suggests that, in consideration of the neurotoxic effects of methamphetamine(METH) due to oxidative stress, pharmacological intervention on NO synthase may help reduce the monoamine-depleting and apoptosis-inducing effects of methamphetamine and that pretreatment with low-dose METH may be protective against METH neurotoxicity in the midbrain, leading to the suppression of oxidative stress and apoptotic mechanisms, in part via ER stress-related pathways. In the point of view of forensic pathology, an animal model of escalation drug intake and pretraetment of low-dose METH prior to neurotoxic-dose admistration could be useful to investigate the mechanisms involved in neurotoxicity of human METH abusers.