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人α-突触核蛋白A30P转基因小鼠对MPTP的敏感性增加。

Increased sensitivity to MPTP in human alpha-synuclein A30P transgenic mice.

作者信息

Nieto María, Gil-Bea Francisco J, Dalfó Esther, Cuadrado Mar, Cabodevilla Felipe, Sánchez Belén, Catena Silvia, Sesma Teresa, Ribé Elena, Ferrer Isidro, Ramírez María J, Gómez-Isla Teresa

机构信息

Department of Neurology and Neurosurgery, Clinica Universitaria de Navarra, Universidad de Navarra, Pamplona, Navarre, Spain.

出版信息

Neurobiol Aging. 2006 Jun;27(6):848-56. doi: 10.1016/j.neurobiolaging.2005.04.010. Epub 2005 Jul 11.

Abstract

In addition to genetic factors, environmental factors have long been suspected to contribute to the pathogenesis of Parkinson's disease (PD). We investigated the possible interaction between genetic factors and neurotoxins by testing whether alpha-synuclein A30P Tg5093 transgenic mice show increased sensitivity to secondary toxic insults like 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or rotenone. While sensitivity to chronic treatment with rotenone was not enhanced in the Tg5093 line, chronic treatment with 80 or 150 mg/kg MPTP resulted in increased deterioration of the nigrostriatal dopaminergic system as assessed by quantitation of nigral tyrosine hydroxylase (TH) positive neurons and striatal dopamine (DA) levels in Tg5093 mice when compared to non-transgenic littermate controls. Thus, the results of this study demonstrate a role for the overexpression of mutant human alpha-synuclein A30P in increased vulnerability of DA neurons to MPTP.

摘要

除遗传因素外,环境因素长期以来一直被怀疑与帕金森病(PD)的发病机制有关。我们通过测试α-突触核蛋白A30P Tg5093转基因小鼠对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)或鱼藤酮等继发性毒性损伤的敏感性是否增加,来研究遗传因素与神经毒素之间可能的相互作用。虽然Tg5093品系对鱼藤酮慢性治疗的敏感性没有增强,但与非转基因同窝对照相比,通过定量Tg5093小鼠黑质酪氨酸羟化酶(TH)阳性神经元和纹状体多巴胺(DA)水平评估,80或150 mg/kg MPTP慢性治疗导致黑质纹状体多巴胺能系统的恶化加剧。因此,本研究结果表明突变型人α-突触核蛋白A30P的过表达在多巴胺能神经元对MPTP的易感性增加中起作用。

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