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慢性酒精摄入和脱水诱导大鼠下丘脑视上核超微结构变化的体视学研究

Stereological study of the ultrastructural changes induced by chronic alcohol consumption and dehydration in the supraoptic nucleus of the rat hypothalamus.

作者信息

Ruela C, Sousa N, Madeira M D, Paula-Barbosa M M

机构信息

Department of Anatomy, Porto Medical School, Portugal.

出版信息

J Neurocytol. 1994 Jul;23(7):410-21. doi: 10.1007/BF01207113.

Abstract

We have previously shown that prolonged alcohol ingestion leads to neuronal loss in the supraoptic nucleus of the rat and that the surviving neurons, mainly the vasopressinergic ones, display marked increase in volume. In an attempt to establish correlates for the volumetric alterations we have studied the organelles of supraoptic nucleus neurons in three groups of rats--ethanol-fed, pair-fed, and dehydrated, in all cases treated from 2 to 12 months of age. The volume and surface area of the rough endoplasmic reticulum and Golgi apparatus, and the volume of nucleoli and neurosecretory granules were estimated on the basis of the respective volume and surface densities. The volumes and surface areas of all quantified organelles were increased in both alcohol-fed and dehydrated animals, although the increases were greater in the former group. Changes in the organelles studied are commonly regarded as reliable indicators of the neurosecretory activity of magnocellular neurons. Thus, our results suggest that under conditions of chronic alcohol exposure, the synthesizing activity of the surviving supra-optic neurons is augmented to compensate for the alcohol-induced neuronal loss and/or as a consequence of the alcohol-induced hyperosmolality. Changes in the transport and release of the neurosecretory material cannot, however, be ruled out as an additional cause of neuronal enlargement.

摘要

我们之前已经表明,长期摄入酒精会导致大鼠视上核神经元丢失,而存活的神经元,主要是血管加压素能神经元,体积会显著增大。为了确定体积变化的相关因素,我们研究了三组大鼠视上核神经元的细胞器——乙醇喂养组、配对喂养组和脱水组,所有大鼠均在2至12月龄时接受处理。根据各自的体积和表面密度估算粗面内质网、高尔基体的体积和表面积,以及核仁、神经分泌颗粒的体积。在酒精喂养组和脱水组动物中,所有定量细胞器的体积和表面积均增加,尽管前一组的增加幅度更大。所研究细胞器的变化通常被视为大细胞神经元神经分泌活动的可靠指标。因此,我们的结果表明,在慢性酒精暴露条件下,存活的视上神经元的合成活性增强,以补偿酒精诱导的神经元丢失和/或酒精诱导的高渗血症的结果。然而,神经分泌物质的运输和释放变化不能排除为神经元增大的另一个原因。

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