Effects of global ischemia duration on neuronal, astroglial, oligodendroglial, and microglial reactions in the vulnerable hippocampal CA1 subregion in rats
Effects of global ischemia duration on neuronal, astroglial, oligodendroglial, and microglial reactions in the vulnerable hippocampal CA1 subregion in rats
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DOI：
10.1089/089771502753460268
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发表时间：
2002-01-01
影响因子：
4.2
通讯作者：
Chan, PH
中科院分区：
文献类型：
--
作者：
Sugawara, T;Lewén, A;Chan, PH
海马CA 1区神经元选择性地易受全脑缺血的影响，神经元死亡以延迟的方式发生。诱导神经元死亡的全脑缺血持续时间的阈值已被研究，但缺血持续时间和海马CA 1区胶质细胞死亡之间的关系尚未得到充分研究。我们研究了不同持续时间的全脑缺血后CA 1亚区神经元/胶质细胞的活力和形态学变化。在Sprague-Dawley大鼠中通过双侧颈总动脉闭塞和低血压10、5和3分钟诱导全脑缺血。在缺血后1-56天，免疫组化评价神经元、星形胶质细胞、少突胶质细胞和小胶质细胞的形态学反应。海马CA 1区锥体神经元在缺血10/5 min后第3天出现迟发性死亡，而缺血3 min后未见迟发性死亡。缺血10/5 min后星形胶质细胞数量逐渐减少，存活的星形胶质细胞表现出特征性的阶段性形态学反应。缺血10/5 min后，少突胶质细胞的突起也发生了形态学变化。小胶质细胞仅在缺血10/5破坏后5天转化为反应性形式。这些数据表明，胶质细胞的一些形态学变化并不依赖于神经元细胞死亡，但它们自己的反应，不同程度的缺血。
The hippocampal CA1 neurons are selectively vulnerable to global ischemia, and neuronal death occurs in a delayed manner. The threshold of global ischemia duration that induces neuronal death has been studied, but the relationship between ischemia duration and glial death in the hippocampal CA1 area has not been fully studied. We examined neuronal/glial viability and morphological changes in the CA1 subregion after different durations of global ischemia. Global ischemia was induced in Sprague-Dawley rats by 10, 5, and 3 min of bilateral common carotid artery occlusion and hypotension. At 1-56 days after ischemia, the morphological reactions of neurons, astrocytes, oligo-dendrocytes, and microglia were immunohistochemically evaluated. Most of the hippocampal CA1 pyramidal neurons underwent delayed death at 3 days after 10/5 min of ischemia, but not after 3 min of ischemia. The number of astrocytes gradually declined after 10/5 min of ischemia, and viable astrocytes showed characteristic staged morphological reactions. Oligodendrocytes also showed morphological changes in their processes after 10/5 min of ischemia. Microglia transformed into a reactive form at 5 days only after 10/5 ruin of ischemia. These data suggest that some morphological changes in glial cells were not dependent on neuronal cell death, but their own reactions to the different severity of isehemia.