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长时间暴露于亚微摩尔浓度的喹啉酸会在大鼠皮质纹状体系统的器官型培养物中引起兴奋性毒性损伤。

Prolonged exposure to submicromolar concentrations of quinolinic acid causes excitotoxic damage in organotypic cultures of rat corticostriatal system.

作者信息

Whetsell W O, Schwarcz R

机构信息

Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN 37232.

出版信息

Neurosci Lett. 1989 Feb 27;97(3):271-5. doi: 10.1016/0304-3940(89)90609-5.

DOI:10.1016/0304-3940(89)90609-5
PMID:2524015
Abstract

Mature organotypic cultures of rat corticostriatal system (CXCA cultures) or caudate nucleus (CA cultures) were chronically exposed to 100 nM quinolinic acid (QUIN) for up to 7 weeks. Light and electron microscopic analysis showed no pathological changes in QUIN-exposed CA cultures or in control cultures incubated in regular feeding medium for this time period. In contrast, in CXCA cultures exposed to QUIN, there was focal degeneration characterized by the presence of vacuoles in neuropil, swollen dendrites, occasional swollen post-synaptic elements and degenerated neurons. Prolonged exposure to only slightly hyper-physiological concentrations of QUIN may cause neuronal death in slowly progressive neurodegenerative disorders such as Huntington's disease (HD).

摘要

大鼠皮质纹状体系统的成熟器官型培养物(CXCA培养物)或尾状核(CA培养物)被长期暴露于100 nM喹啉酸(QUIN)中长达7周。光学和电子显微镜分析显示,在此时间段内,暴露于QUIN的CA培养物或在常规培养基中培养的对照培养物均未出现病理变化。相反,在暴露于QUIN的CXCA培养物中,存在局灶性变性,其特征为神经毡中有空泡、树突肿胀、偶尔出现突触后元件肿胀以及神经元变性。长期暴露于仅略高于生理浓度的QUIN可能会在诸如亨廷顿舞蹈病(HD)等缓慢进展的神经退行性疾病中导致神经元死亡。

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