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大鼠大脑中动脉闭塞 15 分钟和 30 分钟后纹状体的神经元丢失和神经胶质增生。

Neuronal loss and gliosis in the rat striatum subjected to 15 and 30 minutes of middle cerebral artery occlusion.

机构信息

Department of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University, 1 Hallymdaehak-gil, Chuncheon, Gangwon, 24252, Republic of Korea.

Department of Neurobiology, School of Medicine, Kangwon National University, 1 Kangwondaehak-gil, Chuncheon, Gangwon, 24341, Republic of Korea.

出版信息

Metab Brain Dis. 2018 Jun;33(3):775-784. doi: 10.1007/s11011-018-0192-8. Epub 2018 Jan 21.

DOI:10.1007/s11011-018-0192-8
PMID:29354885
Abstract

Selective neuronal death or loss in certain brain regions has been well characterized in animal models of transient global cerebral ischemia. However, selective neuronal death in transient focal cerebral ischemia needs more investigation. Therefore, in this study, we studied selective neuronal death in the striatum (caudate putamen) of rats subjected to 15 or 30 min middle cerebral artery occlusion (MCAO). Neuronal death occurred in the dorsolateral field, not in the medial field in 30 min, not 15 min, MCAO-operated rats 5 days after MCAO using neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining. In this group, immunoreactivity of glial fibrillary acidic protein in astrocytes was hardly shown in the dorsolateral field, although the immunoreactivity increased in the medial field. In addition, immunoreactivity of ionized calcium binding adapter molecule 1 in microglia was dramatically increased in the dorsolateral, not in the medial, field only in 30 min MCAO-operated rats. Briefly, these results show that at least 30 min of MCAO can evoke selective neuronal death, astrocytic dysfunction and microglial activation in the dorsolateral field of the rat striatum and suggest that a rat model of 30 min MCAO can be used to investigate mechanisms of neuronal death and gliosis following brief transient focal cerebral ischemic events for acute transient ischemic attack.

摘要

在短暂性全脑缺血的动物模型中,已经很好地描述了某些脑区的选择性神经元死亡或缺失。然而,短暂性局灶性脑缺血中的选择性神经元死亡需要更多的研究。因此,在这项研究中,我们研究了经历 15 或 30 分钟大脑中动脉闭塞(MCAO)的大鼠纹状体(尾状核壳核)中的选择性神经元死亡。使用神经元核抗原免疫组织化学和氟硼二吡咯Histofluorescence 染色,在 MCAO 后 5 天,在 30 分钟而不是 15 分钟 MCAO 操作的大鼠中,在背外侧场而非内侧场发生神经元死亡。在该组中,星形胶质细胞中胶质纤维酸性蛋白的免疫反应性在背外侧场几乎没有显示,尽管在内侧场中免疫反应性增加。此外,在 30 分钟 MCAO 操作的大鼠中,小胶质细胞中离子钙结合接头分子 1 的免疫反应性仅在背外侧场而不在内侧场显著增加。简而言之,这些结果表明,至少 30 分钟的 MCAO 可以引起大鼠纹状体背外侧场的选择性神经元死亡、星形胶质细胞功能障碍和小胶质细胞激活,并提示 30 分钟 MCAO 的大鼠模型可用于研究短暂性局灶性脑缺血后神经元死亡和神经胶质增生的机制对于急性短暂性缺血发作。

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