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慢性 17β-雌二醇或胆固醇可预防去卵巢雌性大鼠应激诱导的海马 CA3 树突回缩:CA1 棘突特性与空间获取之间的可能对应关系。

Chronic 17beta-estradiol or cholesterol prevents stress-induced hippocampal CA3 dendritic retraction in ovariectomized female rats: possible correspondence between CA1 spine properties and spatial acquisition.

机构信息

Department of Psychology, Arizona State University, Tempe, Arizona 85287-1104, USA.

出版信息

Hippocampus. 2010 Jun;20(6):768-86. doi: 10.1002/hipo.20678.

DOI:10.1002/hipo.20678
PMID:19650122
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2878912/
Abstract

Chronic stress may have different effects on hippocampal CA3 and CA1 neuronal morphology and function depending upon hormonal status, but rarely are manipulations of stress and gonadal steroids combined. Experiment 1 investigated the effects of chronic restraint and 17beta-estradiol replacement on CA3 and CA1 dendritic morphology and spatial learning in ovariectomized (OVX) female Sprague-Dawley rats. OVX rats were implanted with 25% 17beta-estradiol, 100% cholesterol, or blank silastic capsules and then chronically restrained (6h/d/21d) or kept in home cages. 17beta-Estradiol or cholesterol prevented stress-induced CA3 dendritic retraction, increased CA1 apical spine density, and altered CA1 spine shape. The combination of chronic stress and 17beta-estradiol facilitated water maze acquisition compared to chronic stress + blank implants and nonstressed controls + 17beta-estradiol. To further investigate the interaction between 17beta-estradiol and stress on hippocampal morphology, experiment 2 was conducted on gonadally intact, cycling female rats that were chronically restrained (6h/d/21d), and then euthanized at proestrus (high ovarian hormones) or estrus (low ovarian hormones). Cycling female rats failed to show chronic stress-induced CA3 dendritic retraction at either estrous phase. Chronic stress enhanced the ratio of CA1 basal spine heads to headless spines as found in experiment 1. In addition, proestrous rats displayed increased CA1 spine density regardless of stress history. These results show that 17beta-estradiol or cholesterol protect against chronic stress-induced CA3 dendritic retraction in females. These stress- and 17beta-estradiol-induced morphological changes may provide insight into how dendritic complexity and spine properties contribute to spatial ability.

摘要

慢性应激可能会对海马 CA3 和 CA1 神经元的形态和功能产生不同的影响,这取决于激素状态,但很少有应激和性腺类固醇的联合处理。实验 1 研究了慢性束缚和 17β-雌二醇替代对去卵巢(OVX)雌性 Sprague-Dawley 大鼠 CA3 和 CA1 树突形态和空间学习的影响。OVX 大鼠植入 25%的 17β-雌二醇、100%的胆固醇或空白硅酮胶囊,然后进行慢性束缚(6h/d/21d)或放在家笼中。17β-雌二醇或胆固醇可防止应激引起的 CA3 树突回缩,增加 CA1 顶树突密度,并改变 CA1 树突棘形状。与慢性应激+空白植入物和非应激对照+17β-雌二醇相比,慢性应激和 17β-雌二醇的组合促进了水迷宫的获得。为了进一步研究 17β-雌二醇和应激对海马形态的相互作用,实验 2在性成熟、发情周期的雌性大鼠中进行,这些大鼠进行了慢性束缚(6h/d/21d),然后在发情前期(高卵巢激素)或发情期(低卵巢激素)时安乐死。在发情期的任何阶段,发情周期的雌性大鼠都没有表现出慢性应激引起的 CA3 树突回缩。正如实验 1 所发现的,慢性应激增强了 CA1 基底棘突与无头棘突的比例。此外,发情前期的大鼠无论应激史如何,CA1 棘突密度都增加。这些结果表明,17β-雌二醇或胆固醇可防止雌性慢性应激引起的 CA3 树突回缩。这些应激和 17β-雌二醇诱导的形态变化可能为树突复杂性和棘突特性如何有助于空间能力提供了一些见解。

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