前脑缺血2、4、10 d后大鼠海马CA1区细胞死亡的超微结构分析

Anatomy and Embryology Pub Date : 2006-10-01 Epub Date: 2006-05-04 DOI:10.1007/s00429-006-0095-z
Eliane Roseli Winkelmann, Alexandre Charcansky, M Cristina Faccioni-Heuser, Carlos Alexandre Netto, Matilde Achaval
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引用次数: 19

摘要

通过超微结构研究,观察雄性成年Wistar大鼠在短暂性脑缺血10、20 min后,再灌注2、4、10 d后海马CA1区锥体神经元的细胞死亡类型。采用四血管闭塞法诱导缺血损伤10或20 min,然后分别给予2、4或10 d的再灌注。然后,这些动物被麻醉,它们的大脑被移除、脱水、植入、切片,并在透射电子显微镜下进行检查。缺血损伤后,CA1区神经元呈现相应于退行性过程的初始、中期和最终阶段的改变。10分钟和20分钟缺血组之间观察到的唯一差异是损伤程度;20分钟组的反应强于10分钟组。虽然在各组肿瘤坏死的不同阶段均发现神经元,但在流行阶段发现各组之间存在差异。缺血组和缺血组在再灌注2 d后,肿瘤性坏死的初始阶段普遍存在,大量神经元出现正常。在两组中,再灌注4天后,大多数神经元表现出更高级的改变,典型的中间阶段。两组再灌注10 d后,与中晚期肿瘤坏死相对应的改变也占主导地位。然而,很少有完整的神经元被鉴定出来,神经堆看起来更有组织,有许多胶质细胞。综上所述,CA1区锥体神经元表现出选择性易损性,并表现出与肿瘤坏死通路完全对应的形态学死亡模式。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
An ultrastructural analysis of cellular death in the CA1 field in the rat hippocampus after transient forebrain ischemia followed by 2, 4 and 10 days of reperfusion.

An ultrastructural study was performed to investigate the type of cellular death that occurs in hippocampal CA1 field pyramidal neurons after 10 and 20 min of transient cerebral ischemia in the male adult Wistar rats, followed by 2, 4 and 10 days of reperfusion. The four-vessel occlusion method was used to induce ischemic insult for either 10 or 20 min, following which the animals were submitted to either 2, 4 or 10 days of reperfusion. The animals were then anaesthetised, and their brains removed, dehydrated, embedded, sectioned and examined under a transmission electron microscope. After ischemic insult, neurons from the CA1 field presented alterations, corresponding to the initial, intermediate and final stages of the degenerative process. The only difference observed between the 10 and 20 min ischemic groups was the degree of damage; the reaction was stronger in 20 min groups than in the 10 min groups. While neurons were found in the different stages of oncotic necrosis in all groups, differences were found between the groups in relation to prevalent stages. In both ischemic groups, after 2 days of reperfusion, the initial stage of oncotic necrosis was prevalent and large numbers of neurons appeared normal. In both groups, after 4 days of reperfusion, most of the neurons showed more advanced alterations, typical of an intermediate stage. In both groups, after 10 days of reperfusion, alterations corresponding to the intermediate and final stages of oncotic necrosis were also predominant. However, few intact neurons were identified and the neuropile appeared more organised, with numerous glial cells. In summary, the pyramidal neurons of the CA1 field displayed selective vulnerability and exhibited a morphological death pattern corresponding exclusively to an oncotic necrotic pathway.

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