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产前和产后酒精暴露后的小脑组织发生和突触成熟:大鼠小脑皮质的电子显微镜研究

Cerebellar histogenesis and synaptic maturation following pre- and postnatal alcohol administration. An electron-microscopic investigation of the rat cerebellar cortex.

作者信息

Volk B

出版信息

Acta Neuropathol. 1984;63(1):57-65. doi: 10.1007/BF00688471.

Abstract

Fetal alcohol syndrome was produced in rats by feeding an ethanol-enriched, vitamine -supplemented liquid diet over a period of 4 weeks before mating and throughout pregnancy. The amount of ethanol was equivalent to 38-40% of the daily calories; control animals were fed an isocaloric amount of sucrose. The offspring of experimental animals displayed a diminished birth weight. In contrast to previous experiments, the ethanol diet was also administered during the lactating period. On postnatal day 7, experimental animals and controls were killed by perfusion and the cerebella prepared for electron microscopy. Morphometric analysis showed a reduced number of Purkinje cells. On day 12, Purkinje cells of experimental animals displayed ultrastructurally fewer organelles. Furthermore, a delayed synaptogenesis in the molecular layer was demonstrated with osmium-zinc iodide and ethanolic phosphotungstic acid showing an immature appearance of the presynaptic grid and weaker stained synaptic cleft material. The following discussion deals with possible mechanisms underlying these alcohol-induced alterations of cerebellar synaptogenesis.

摘要

在交配前4周及整个孕期,通过给大鼠喂食富含乙醇且补充了维生素的流质饮食来诱发胎儿酒精综合征。乙醇含量相当于每日热量的38 - 40%;对照动物喂食等热量的蔗糖。实验动物的后代出生体重减轻。与之前的实验不同,乙醇饮食在哺乳期也持续投喂。在出生后第7天,通过灌注处死实验动物和对照动物,并制备小脑用于电子显微镜检查。形态计量分析显示浦肯野细胞数量减少。在第12天,实验动物的浦肯野细胞在超微结构上细胞器较少。此外,用碘化锇锌和乙醇磷钨酸证明分子层突触发生延迟,显示突触前网格外观不成熟且突触间隙物质染色较弱。以下讨论涉及这些酒精诱导的小脑突触发生改变的潜在机制。

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