Chronic 17β‐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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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 17β‐estradiol replacement on CA3 and CA1 dendritic morphology and spatial learning in ovariectomized (OVX) female Sprague–Dawley rats. OVX 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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