人水肿性大脑皮层树突的形态学变化。透射电镜研究。

O J Castejón, G J Arismendi
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引用次数: 0

摘要

对38例临床诊断为脑外伤、脑肿瘤和先天性畸形的患者进行了树突突结构病理检查。额叶、顶叶、颞叶和枕叶皮层的皮层活组织检查通常用于透射电子显微镜。用分离的超薄切片和电子显微图蒙太奇追踪皮层内树突的发育过程。在所有检查的病例中都观察到肿胀和珠状树突,这表明限制质膜和细胞骨架结构的断裂。肿胀的树突表现为空泡化,残体致密,内质网粗大光滑,线粒体水肿,清暗,轴突触突触密度降低,脊柱器官水肿,营养不良,部分树突棘缺失。树突状脊柱形态多样:蘑菇型、粗短型、宝石状丝状脊柱和巨棘,在先天性畸形中被认为是脊柱发育不良,在脑外伤和脑肿瘤中被认为是脊柱可塑性强。与脑水肿和脑缺血相关的多因素过程,如钙超载、钙依赖性蛋白水解酶的激活、蛋白质聚集、谷氨酸诱导的神经毒性、溶酶体酶的释放、ATP的缺陷、应激氧化和脂质过氧化被认为与病理性树突状改变有关。脑水肿和脑缺血引起的树突毒性似乎是其基本的发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Morphological changes of dendrites in the human edematous cerebral cortex. A transmission electron microscopic study.

The structural pathology of dendritic processes has been examined in 38 patients with clinical diagnosis of brain trauma, brain tumours and congenital malformations. Cortical biopsies of frontal, parietal, temporal and occipital cortex were conventionally processed for transmission electron microscopy. Isolated ultrathin sections and montages of electron micrographs were used to trace the intracortical dendritic course. Swollen and beaded dendrites were observed in all cases examined, which exhibited fragmentation of limiting plasma membrane and cytoskeletal structures. The swollen dendrites showed vacuolization, dense residual bodies, enlarged rough and smooth endoplasmic reticulum, edematous clear and dark mitochondria, a decreased synaptic density of shaft synapses, edematous and dystrophic changes of spine apparatus and a partial loss of dendritic spines. A wide variety of dendritic spine shapes were observed: mushroom-type, stubby, gem-like filiform spine, and megaspine, considered as spine dysgenesis in the congenital malformations and spine pathology and spine plasticity in brain traumatic injuries and brain tumours. The multifactorial processes associated with brain edema and brain ischemia, such as calcium overload, activation of calcium-dependent proteolytic enzymes, protein aggregation, glutamate-induced neurotoxicity, release of lysosomal enzymes, deficit of ATP, stress oxidative and lipid peroxidation have been considered in relation with the pathological dendritic changes. Dendrotoxicity due to brain edema and brain ischemia seems to be the fundamental pathogenetic mechanism.

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