NDLI: Prenatal ethanol exposure induces an intrauterine programming of enhanced sensitivity of the hypothalamic–pituitary–adrenal axis in female offspring rats fed with post-weaning high-fat diet

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Toxicology Research Vol - 4 Issue - 4

Toxicology Research Vol - 4 Issue - 3

Toxicology Research Vol - 4 Issue - 2

Toxicology Research Vol - 4 Issue - 1

Toxicology Research Vol -3

Toxicology Research Vol -2

Toxicology Research Vol -1

Prenatal ethanol exposure induces an intrauterine programming of enhanced sensitivity of the hypothalamic–pituitary–adrenal axis in female offspring rats fed with post-weaning high-fat diet

Content Provider	Royal Society of Chemistry (RSC)
Author	Chen, Liaobin Zhang, Lu Wang, Hui Wen, Yinxian Zhang, Li Xu, Dan Lu, Juan Zhong, Weihua Yu, Ying Zhang, Chong
Copyright Year	2015
Abstract	Our previous study demonstrated that prenatal ethanol exposure (PEE) enhances the sensitivity of the hypothalamic–pituitary–adrenal (HPA) axis in adult offspring rats. This study aims to investigate the underlying mechanism. PEE treated female offspring rats were fed with high-fat diet and subjected to the unpredictable chronic stresses (UCS) in adulthood. For adult offspring, the PEE group exhibited increased expression of hypothalamic corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) as well as elevated gain rates of serum adrenocorticotropic hormone (ACTH) and corticosterone after UCS. Meanwhile, PEE significantly decreased the expression of glutamic acid decarboxylase 65 (GAD65) and Reelin (Reln), and the expression ratio of hypothalamic vesicular glutamate transporter 2 (VGluT2)/GAD65 was enhanced in the adult PEE offspring. These changes were also accompanied by the enhanced expression of glucocorticoid receptor (GR), N-methyl-D-aspartate-subtype glutamate receptor 2B and the decreased expression ratio of mineralocorticoid receptor (MR)/GR in the hippocampus. Furthermore, the abnormal hippocampus neurons were observed especially in the cornu ammonis 3 (CA3) and dentate gyrus subfields. For fetuses, PEE significantly decreased the expression of mammalian achaete-scute homolog-1 (Mash1) as well as GAD65 and Reln. Both VGluT2/GAD65 expression ratio and GR expression were increased while the MR/GR expression ratio was decreased in the PEE group. PEE also caused ultrastructural injury in CA3. Our findings suggest that PEE causes the persistent remodeling alterations of impaired morphology and decreased MR/GR expression ratio in the hippocampus, as well as the imbalanced glutamatergic/GABAergic afferent inputs in the hypothalamus. All of these would contribute to the enhanced sensitivity of the HPA axis in adult offspring.
Starting Page	1238
Ending Page	1249
Page Count	12
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	4
Issue Number	5
Journal	Toxicology Research
DOI	10.1039/c5tx00012b
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Hormone Glutamic acid UCS Ethanol Corticosterone Cell surface receptor Hypothalamus Vasopressin Vesicular glutamate transporter 1 Dentate gyrus Adrenocorticotropic hormone Magnetic resonance imaging Mineralocorticoid receptor Glucocorticoid receptor HPA Hippocampus anatomy Gamma-Aminobutyric acid Hippocampus
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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