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链脲佐菌素诱导的糖尿病对大鼠迷走神经背核的短期和长期影响。

Short- and long-term effects of streptozotocin-induced diabetes on the dorsal motor nucleus of the vagus nerve in the rat.

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). 1994;150(4):274-81. doi: 10.1159/000147630.

Abstract

The present study describes ultrastructural changes in the dorsal motor nucleus of the vagus nerve of male Wistar rats after induction of diabetes by streptozotocin. 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 containing short segments of dilated rough endoplasmic reticulum, swollen mitochondria and scattered ribosomes, while degenerating axon terminals were characterized by an electron-defense cytoplasm, clustering of small spherical agranular vesicles and swollen mitochondria. Some of these degenerating axon terminals formed axodendritic synapses with seemingly normal as well as degenerating dendrites. During the mid phase (1-6 months), most of the degenerating neuronal profiles had been engulfed or removed by macrophages that infiltrated the neuropil. During the late phase (9-12 months), a second wave of degeneration occurred in the dorsal motor nucleus of the vagus nerve, similar to that of the acute phase. In addition to the degenerating dendrites and axon terminals, several neuronal cell bodies with electron-dense cytoplasm were observed. Numerous macrophages containing degenerating debris were also present in the neuropil. It is concluded that the ultrastructural changes in the dorsal motor nucleus of the vagus nerve are the result of streptozotocin-induced diabetes.

摘要

本研究描述了用链脲佐菌素诱导雄性Wistar大鼠患糖尿病后,其迷走神经背运动核的超微结构变化。在急性期(3 - 7天),变性的电子致密树突和轴突终末散在于神经毡中。变性树突的特征是电子致密的细胞质,含有短段扩张的粗面内质网、肿胀的线粒体和散在的核糖体,而变性轴突终末的特征是电子透亮的细胞质、小的球形无颗粒小泡聚集和肿胀的线粒体。其中一些变性轴突终末与看似正常以及变性的树突形成轴 - 树突触。在中期(1 - 6个月),大多数变性的神经元轮廓已被浸润到神经毡中的巨噬细胞吞噬或清除。在后期(9 - 12个月),迷走神经背运动核出现了第二波变性,类似于急性期。除了变性的树突和轴突终末外,还观察到几个细胞质电子致密的神经元胞体。神经毡中也存在大量含有变性碎片的巨噬细胞。结论是,迷走神经背运动核的超微结构变化是链脲佐菌素诱导的糖尿病的结果。

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