Ekström von Lubitz D K, Diemer N H
Neuropathol Appl Neurobiol. 1982 May-Jun;8(3):197-215. doi: 10.1111/j.1365-2990.1982.tb00275.x.
An ultrastructural study and a stereological analysis of the distal stratum radiatum in the hippocampal CA-1 region of the rat were performed after 10 min of complete cerebral ischaemia followed by 10, 20 and 60 min of blood reflow periods. Post-ischaemic changes were mainly limited to the region of synaptic terminals which showed either clumping or dispersion of the synaptic vesicle pools and damage to synaptic membranes. Presynaptic terminals and astrocytes were swollen after 10 and 20 min of reflow, but this abated after 60 min. Mitochondria in neurons showed varying degrees of swelling, but in astrocytes their structure was normal. There were no changes in capillaries. After 20 and 60 min of blood reflow, disruption of cell membranes was observed, mainly in the vicinity of the synaptic terminals. The size of the extracellular space diminished by approximately 30% in all three ischaemic groups. The data show that synaptic terminals are a primary and early target in the development of postischaemic nerve cell damage.
在大鼠海马CA-1区远端辐射层进行超微结构研究和体视学分析，方法是先进行10分钟的全脑缺血，然后分别进行10、20和60分钟的血流再灌注期。缺血后变化主要局限于突触终末区域，表现为突触小泡池的聚集或分散以及突触膜的损伤。再灌注10和20分钟后，突触前终末和星形胶质细胞肿胀，但60分钟后减轻。神经元中的线粒体呈现不同程度的肿胀，但星形胶质细胞中线粒体结构正常。毛细血管无变化。血流再灌注20和60分钟后，观察到细胞膜破坏，主要在突触终末附近。在所有三个缺血组中，细胞外间隙大小减少了约30%。数据表明，突触终末是缺血后神经细胞损伤发展过程中的主要早期靶点。
