Ito U, Hanyu S, Hakamata Y, Nakamura M, Arima K
Department of Neurosurgery, Musashino Red Cross Hospital, Tokyo, Japan.
Acta Neurochir Suppl. 1997;70:46-9. doi: 10.1007/978-3-7091-6837-0_14.
Astrocytic swelling after ischemic insult has been considered a sign of parturbed cell viability. Investigations using cultured astrocytes and C6 glioma cells have revealed that viable astrocytes swell, spatially buffering various metabolites which are increased by the metabolic turmoil following ischemic insults. In the present study, we have studied the temporal profile of ultrastructural changes of astrocytes in the cerebral cortex associated with progressive selective neuronal, death where infarction is not induced. We occluded the left carotid artery of the Mongolian gerbil twice for 10 minutes at a 5 hr interval. In this model, following reperfusion, selective neuronal death progresses in the coronal section cut at the infundibular level. The whole brains of the sham operated control and postischemic animals were fixed by transcardiac perfusion of glutaraldehyde fixatives, at 15 min, 5 and 12 hr after the 2nd 10 min ischemia. Ultrathin sections including the 3rd and 5th cortical layers were prepared from the cut surface at the level of infundibulum. Mild swelling of astrocytic processes and perivascular end-feet was observed in the 15 min group. Glycogen granules were not prominent. In the 5 hr group, we found a few necrotic neurons disseminated in the cortex. All astrocytic cell processes were swollen with increased number of glycogen granules, especially marked in the perivascular end-feet. In the 12 hr group, necrotic neurons increased in number, astrocytic swelling was more extensive, and glycogen granules were evident in astrocytes. No cellular destruction was observed. We conclude: 1. Swelling progresses in astrocytes which however still remain viable and this process is associated with selective progression of neuronal death. 2. Glycogen granules increase in the swollen yet viable astrocytic cell processes.
缺血性损伤后星形胶质细胞肿胀一直被视为细胞活力紊乱的标志。使用培养的星形胶质细胞和C6胶质瘤细胞进行的研究表明，存活的星形胶质细胞会肿胀，在空间上缓冲各种代谢产物，这些代谢产物会因缺血性损伤后的代谢紊乱而增加。在本研究中，我们研究了与渐进性选择性神经元死亡相关的大脑皮质星形胶质细胞超微结构变化的时间特征，其中未诱发梗死。我们以5小时的间隔两次阻断蒙古沙鼠的左颈动脉，每次10分钟。在这个模型中，再灌注后，在漏斗水平处切割的冠状切片中选择性神经元死亡会进展。假手术对照组和缺血后动物的全脑在第二次10分钟缺血后的15分钟、5小时和12小时通过经心脏灌注戊二醛固定剂进行固定。从漏斗水平的切割表面制备包括第三和第五皮质层的超薄切片。在15分钟组中观察到星形胶质细胞突起和血管周围终足轻度肿胀。糖原颗粒不明显。在5小时组中，我们在皮质中发现了一些散在的坏死神经元。所有星形胶质细胞突起均肿胀，糖原颗粒数量增加，在血管周围终足中尤为明显。在12小时组中，坏死神经元数量增加，星形胶质细胞肿胀更广泛，并且在星形胶质细胞中糖原颗粒明显可见。未观察到细胞破坏。我们得出结论：1. 星形胶质细胞肿胀在进展，但仍保持存活，并且这个过程与神经元死亡的选择性进展相关。2. 在肿胀但仍存活的星形胶质细胞突起中糖原颗粒增加。
