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This Article Full Text Full Text (PDF) All Versions of this Article: 292/4/E1173    most recent 00102.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Figueiredo, H. F. Articles by Herman, J. P. Search for Related Content PubMed PubMed Citation Articles by Figueiredo, H. F. Articles by Herman, J. P.

Estrogen potentiates adrenocortical responses to stress in female rats

¹Departments of Psychiatry and ²Cell Biology, Neurobiology and Anatomy, and ³Neuroscience Graduate Program, University of Cincinnati, Reading, Ohio

Submitted 6 March 2006 ; accepted in final form 4 December 2006

It is well established that estrogens markedly enhance the glucocorticoid response to acute stress in females. However, the precise mechanism responsible for this regulation is poorly understood. Here, we tested whether estrogens enhance the activation of the paraventricular nucleus (PVN) of the hypothalamus by measuring stress-induced c-fos mRNA expression in the PVN of restraint-stressed ovariectomized (OVX) rats treated with physiologically relevant doses of estradiol (E₂), the major female estrogen. As expected, E₂ enhanced plasma corticosterone responses to restraint in OVX females. However, E₂ markedly attenuated the stress-induced c-fos gene expression in the PVN and inhibited plasma ACTH responses in these animals. Furthermore, E₂-inhibitory effects were mimicked by progesterone (P) alone or in combination with E₂. Interestingly, the suppressive central effects of both E₂ and P were apparently independent of basal paraventricular corticotropin-releasing hormone (CRH) transcription, since these ovarian steroids did not significantly affect PVN CRH mRNA expression in unstressed rats. These unexpected findings suggested that E₂ promotes glucocorticoid hypersecretion in females by additional peripheral (i.e., adrenal) mechanisms. Indeed, E₂ markedly enhanced plasma corticosterone responses and adrenal corticosterone content in dexamethasone-blocked OVX rats challenged with varying doses of exogenous ACTH. These results suggest that enhanced adrenal sensitive to ACTH is an important physiological mechanism mediating E₂-related glucocorticoid hypersecretion in stressed females.

corticosterone; progesterone; c-fos; adrenal; paraventricular nucleus

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