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短暂性脑缺血后沙鼠海马体的选择性易损性

Selective vulnerability in the gerbil hippocampus following transient ischemia.

作者信息

Kirino T, Sano K

出版信息

Acta Neuropathol. 1984;62(3):201-8. doi: 10.1007/BF00691853.

Abstract

Following brief ischemia, the Mongolian gerbil is reported to develop unusual hippocampal cell injury (Brain Res 239:57--69, 1982). To further clarify this hippocampal vulnerability, gerbils were subjected to ischemia for 3, 5, 10, 20, and 30 min by bilateral occlusion of the common carotid arteries. They were perfusion-fixed after varying intervals of survival time ranging from 3 h up to 7 days. Following brief ischemia (5--10 min), about 90% of the animals developed typical hippocampal damage. The lesion was present throughout the extent of the dorsal hippocampus, whereas damage outside the hippocampus was not observed. Each sector of the hippocampus showed different types of cell reaction to ischemia. Ischemia cell change was seen in scattered CA4 neurons , and reactive change was found in CA2, whereas CA1 pyramidal cells developed a strikingly slow cell death process. Ischemia for 3 min did not produce hippocampal lesion in most cases. Following prolonged ischemia (20--30 min), brain injury had a wide variety in its extent and distribution. These results revealed that the gerbil brief ischemia model can serve as an excellent, reliable model to study the long-known hippocampal selective vulnerability to ischemia. Delayed neuronal death in CA1 pyramidal cells was confirmed after varying degrees of ischemic insult. These findings demonstrated that the pathology of neuronal injury following brief ischemia was by no means uniform nor simple.

摘要

据报道,短暂缺血后,蒙古沙鼠会出现异常的海马细胞损伤(《脑研究》239:57 - 69,1982年)。为了进一步阐明这种海马易损性,通过双侧颈总动脉闭塞使沙鼠缺血3、5、10、20和30分钟。在从3小时到7天不等的不同存活时间间隔后,对它们进行灌注固定。短暂缺血(5 - 10分钟)后,约90%的动物出现典型的海马损伤。损伤存在于整个背侧海马区域,而海马以外未观察到损伤。海马的每个区域对缺血表现出不同类型的细胞反应。在散在的CA4神经元中可见缺血细胞变化,CA2区发现反应性变化,而CA1锥体细胞则出现显著缓慢的细胞死亡过程。在大多数情况下,3分钟的缺血未产生海马损伤。长时间缺血(20 - 30分钟)后,脑损伤的范围和分布具有广泛的多样性。这些结果表明,沙鼠短暂缺血模型可作为研究长期以来已知的海马对缺血的选择性易损性的优秀、可靠模型。在不同程度的缺血损伤后,证实了CA1锥体细胞中的延迟性神经元死亡。这些发现表明,短暂缺血后神经元损伤的病理情况绝非一致或简单。

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