Prenatal alcohol exposure and prenatal stress differentially alter glucocorticoid signaling in the placenta and fetal brain

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• 作者：N. Lan^a ; ^b ; ^{lanni.lan@gmail.com} ; M.P.Y. Chiu^a ; L. Ellis^a ; J. Weinberg^a
• 关键词：11β-HSD1 ; 11β-hydroxysteroid dehydrogenase type 1 ; 11β-HSD2 ; 11β-hydroxysteroid dehydrogenase type 2 ; ANOVA ; analysis of variance ; C ; control ; CORT ; corticosterone ; CRH ; corticotropin-releasing hormone ; DOHaD ; developmental origins of health and disease ; GD ; gestation day ; GR ; glucocorticoid receptor ; h ; hour ; HPA ; hypothalamic&ndash ; pituitary&ndash ; adrenal ; mPFC ; medial prefrontal cortex ; MR ; mineralocorticoid receptor ; PAE ; prenatal alcohol exposure ; PF ; pair-fed ; PS ; prenatal stress ; RIA ; rad
• 刊名：Neuroscience
• 出版年：2017
• 出版时间：7 February 2017
• 年：2017
• 卷：342
• 期：Complete
• 页码：167-179
• 全文大小：838 K
• 卷排序：342

文摘

Both PAE and PS dams had higher corticosterone levels. 11β-HSD2 protein levels were increased in PAE and unchanged in PS placentae. PS female fetuses had higher MR protein levels in the hippocampus and amygdala compared to C female fetuses. PS female fetuses had lower GR protein levels in mPFC compared to C female fetuses. Both PAE and PS attenuated the sexually dimorphic expression of MR, GR and the MR/GR ratio seen in C fetuses.