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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >REMODELING OF SYNAPSES IN THE CA1 AREA OF THE HIPPOCAMPUS AFTER TRANSIENT GLOBAL ISCHEMIA
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REMODELING OF SYNAPSES IN THE CA1 AREA OF THE HIPPOCAMPUS AFTER TRANSIENT GLOBAL ISCHEMIA

机译:短暂性全脑缺血后海马CA1区的突触重塑

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摘要

Synapses are essential to neuronal functions. Synaptic changes occur under physiological and pathological conditions. Here we report the remodeling of synapses in the CA1 area of the hippocampus after transient global ischemia using electron microscopy. Much electron-dense material appeared in the cytoplasm of dendrites at 24 h after ischemia. Many dark axons or terminals were found in the CA1 neuropil; some of which were phagocytized by dendrites. Interestingly autophagosomes appeared in many axons or dendrites at 48 h after ischemia. In addition, post-synaptic density (PSD) - like structures or synaptic - like structures were found inside spines and dendrites. Statistical analysis demonstrated that the thickness of PSDs in the CA1 neuropil increased from 12 to 48 h after ischemia. The frequency of autophagosomes appeared to escalate from 12 to 48 h after ischemia. The frequency of asymmetric synapses was significantly increased at 12 h and 24 h after ischemia in stratum oriens, proximal and distal stratum rad-iatum. Among asymmetric synapses, the number of perforated synapses consistently increased and reached a peak (approximately 10-fold increase) at 48 h after ischemia. On the other hand, the number of multiple synaptic boutons decreased after ischemia reaching a two to fourfold decrease at 48 h after ischemia. These results have shown that ischemia induces an increase of asymmetric synapses as well as synaptic autophagy, which may contribute to the neuronal death in the CA1 area after transient global ischemia.
机译:突触对神经元功能至关重要。突触变化发生在生理和病理条件下。在这里我们报告瞬态全局缺血后使用电子显微镜在海马CA1区突触的重塑。缺血后24 h,树突状细胞质中出现大量电子密集物质。在CA1神经纤维中发现了许多深色的轴突或末端。其中一些被树突吞噬。有趣的是,自噬在缺血后48小时出现在许多轴突或树突中。此外,在棘和树突内部发现了类似突触后密度(PSD)的结构或类似突触的结构。统计分析表明,缺血后CA1神经纤维中PSD的厚度从12小时增加到48小时。自噬的频率似乎从缺血后的12小时增加到48小时。缺血后12 h和24 h,层间,近端和远端层状不对称突触的频率显着增加。在不对称突触中,穿孔突触的数目持续增加,并在缺血后48小时达到峰值(约增加10倍)。另一方面,缺血后多个突触钮扣的数量减少,在缺血后48小时达到减少2到4倍。这些结果表明,局部缺血会引起不对称突触和突触自噬的增加,这可能会导致短暂性整体缺血后CA1区的神经元死亡。

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