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.

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.
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DOI:
10.1002/hipo.20678
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发表时间:
2010-06
期刊:
影响因子:
3.5
通讯作者:
Conrad, Cheryl D.
Conrad, Cheryl D.
中科院分区:
医学3区
文献类型:
--
作者:
McLaughin, Katie J.;Wilson, Jessica O.;Harman, James;Wright, Ryan L.;Wieczorek, Lindsay;Gomez, Juan;Korol, Donna L.;Conrad, Cheryl D.

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慢性应激可能对海马CA3和CA1神经元的形态和功能有不同的影响,这取决于激素的状态,但应激和性腺类固醇的操纵很少同时发生。实验1研究了慢性抑制和17β-雌二醇替代对雌性去卵巢大鼠CA3和CA1树突形态及空间学习的影响。将切除卵巢的大鼠分别植入25% 17β-雌二醇、100%胆固醇或空白硅胶胶囊,长期禁闭(6h/d/21d)或饲养于家庭笼中。17β-雌二醇或胆固醇可防止应激诱导的CA3树突内缩,增加CA1脊柱根尖密度,改变CA1脊柱形状。与慢性应激+空白植入和非应激对照组+ 17β-雌二醇相比,慢性应激和17β-雌二醇联合使用更容易获得水迷宫。为了进一步研究17β-雌二醇与应激对海马形态的相互作用,实验2以性腺完整的循环雌性大鼠为实验对象,分别在发情期(卵巢激素水平高)和发情期(卵巢激素水平低)进行长期抑制(6h/d/21d)和安乐死。循环雌性大鼠在任何发情期均未表现出慢性应激诱导的CA3树突缩回。实验1发现慢性应激可提高CA1型基底棘头与无头棘的比例。此外,无论应激史如何,发情大鼠均显示CA1脊柱密度增加。这些结果表明,17β-雌二醇或胆固醇可预防慢性应激诱导的雌性CA3树突缩回。这些应激和17β-雌二醇诱导的形态学变化可能有助于了解树突复杂性和脊柱特性如何影响空间能力。
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 17β-estradiol replacement on CA3 and CA1 dendritic morphology and spatial learning in ovariectomized female Sprague-Dawley rats. Ovariectomized rats were implanted with 25% 17β-estradiol, 100% cholesterol or blank silastic capsules, and then chronically restrained (6h/d/21d) or kept in home cages. 17β-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 17β-estradiol facilitated water maze acquisition compared to chronic stress + blank implants and nonstressed controls + 17β-estradiol. To further investigate the interaction between 17β-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 17β-estradiol or cholesterol protect against chronic stress-induced CA3 dendritic retraction in females. These stress- and 17β-estradiol-induced morphological changes may provide insight into how dendritic complexity and spine properties contribute to spatial ability.
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