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四氧嘧啶诱导的糖尿病大鼠薄束核的超微结构变化

Ultrastructural changes in the gracile nucleus of alloxan-induced diabetic rats.

作者信息

Tay S S, Wong W C

机构信息

Department of Anatomy, Faculty of Medicine, National University of Singapore.

出版信息

Acta Anat (Basel). 1990;139(4):367-73. doi: 10.1159/000147025.

Abstract

The present study reports ultrastructural changes in the gracile nucleus of male Wistar rats after alloxan-induced diabetes. During the acute phase (3-7 days) degenerating electron-dense dendrites and axon terminals were dispersed in the neuropil. Degenerating dendrites were characterized by an electron-dense cytoplasm, swollen mitochondria, dilated endoplasmic reticulum and randomized ribosomes. Degenerating axon terminals were characterized by an electron-dense cytoplasm and clustering of small spherical agranular vesicles. Degenerating axon terminals may form the central element or part of a synaptic glomerulus. Macrophages were present in the neuropil and in the process of engulfing neuronal elements. During the medium phase (1-6 months), most of the degenerating dendrites and axon terminals had been engulfed or removed by macrophages. During the late phase (9-12 months), a second wave of degeneration occurred in the gracile nucleus, similar to the acute phase.

摘要

本研究报告了四氧嘧啶诱导糖尿病后雄性Wistar大鼠薄束核的超微结构变化。在急性期(3 - 7天),退化的电子致密树突和轴突终末散在于神经毡中。退化的树突特征为电子致密的细胞质、肿胀的线粒体、扩张的内质网和随机分布的核糖体。退化的轴突终末特征为电子致密的细胞质和小的球形无颗粒小泡聚集。退化的轴突终末可能形成突触小球的中心成分或一部分。巨噬细胞存在于神经毡中并在吞噬神经元成分的过程中。在中期(1 - 6个月),大多数退化的树突和轴突终末已被巨噬细胞吞噬或清除。在后期(9 - 12个月),薄束核中出现了第二波退化,类似于急性期。

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