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强迫跑步应激对大鼠弓状核的超微结构变化

Fine structural changes in the rat arcuate nucleus by forced running stress.

作者信息

Otani M

机构信息

Department of Psychiatry, Mie University School of Medicine, Tsu, Japan.

出版信息

Jpn J Psychiatry Neurol. 1990 Mar;44(1):99-110. doi: 10.1111/j.1440-1819.1990.tb00447.x.

Abstract

The forced running stress in male rats induced some fine structural changes in the arcuate nucleus. By inducing stress for 2 days, the number of multilamellar astrocytic wrappings and endoplasmic reticular (ER) whorls increased significantly. After a stress of 12 days, half of the rats remained inactive for several weeks, and the other half regained their normal activity. In the inactive group, the ER whorls were partially degenerated at 2 weeks after the stress. These degenerative changes remained for 14 weeks after the stress with the increased lysosomes and the disorganization of r-ER. These findings may suggest that long-term stress induces degenerative changes in the arcuate nucleus neurons and that some of these changes persist with some aging-like morphological changes.

摘要

雄性大鼠的强迫跑步应激在弓状核诱导了一些细微的结构变化。通过诱导应激2天,多层星形胶质细胞包裹和内质网(ER)涡旋的数量显著增加。在应激12天后,一半的大鼠数周内保持不活动状态,另一半恢复了正常活动。在不活动组中,应激后2周内质网涡旋部分退化。这些退行性变化在应激后14周持续存在,伴有溶酶体增加和粗面内质网紊乱。这些发现可能表明长期应激会诱导弓状核神经元的退行性变化,并且其中一些变化会随着一些类似衰老的形态变化持续存在。

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