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Adverse maternal environment alters Oprl1 variant expression in mouse hippocampus

An adverse maternal environment (AME) and Western diet (WD) in early life predispose offspring toward cognitive impairment in humans and mice. Cognitive impairment associates with hippocampal dysfunction. An important regulator of hippocampal function is the hippocampal Nociceptin/Orphanin FQ (N/OFQ...

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Autores principales: Ke, Xingrao, Huang, Yingliu, Fu, Qi, Majnik, Amber, Sampath, Venkatesh, Lane, Robert H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Inc. 2022
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10087895/
https://www.ncbi.nlm.nih.gov/pubmed/35983908
http://dx.doi.org/10.1002/ar.25056
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author Ke, Xingrao
Huang, Yingliu
Fu, Qi
Majnik, Amber
Sampath, Venkatesh
Lane, Robert H.
author_facet Ke, Xingrao
Huang, Yingliu
Fu, Qi
Majnik, Amber
Sampath, Venkatesh
Lane, Robert H.
author_sort Ke, Xingrao
collection PubMed
description An adverse maternal environment (AME) and Western diet (WD) in early life predispose offspring toward cognitive impairment in humans and mice. Cognitive impairment associates with hippocampal dysfunction. An important regulator of hippocampal function is the hippocampal Nociceptin/Orphanin FQ (N/OFQ) system. Previous studies find links between dysregulation of hippocampal N/OFQ receptor (NOP) expression and impaired cognitive function. NOP is encoded by the opioid receptor‐like 1 (Oprl1) gene that contains multiple mRNA variants and isoforms. Regulation of Oprl1 expression includes histone modifications within the promoter. We tested the hypothesis that an AME and a postweaning WD increase the expression of hippocampal Oprl1 and select variants concurrent with altered histone code in the promoter. We created an AME‐WD model combining maternal WD and prenatal environmental stress plus postweaning WD in the mouse. We analyzed the hippocampal expression of Oprl1, Oprl1 variants, and histone modifications in the Oprl1 promoter in offspring at postnatal day (P) 21 and P100. An AME and an AME‐WD significantly increased the total hippocampal expression of Oprl1 and variant V4 concurrently with an increased accumulation of active histone marks in the promoter of male offspring. We concluded that an AME and an AME‐WD alter hippocampal Oprl1 expression in offspring through an epigenetic mechanism in a variant‐specific and sex‐specific manner. Altered hippocampal Oprl1 expression may contribute to cognitive impairment seen in adult males in this model. Epigenetic regulation of Oprl1 is a potential mechanism by which an AME and a WD may contribute to neurocognitive impairment in male offspring.
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spelling pubmed-100878952023-04-12 Adverse maternal environment alters Oprl1 variant expression in mouse hippocampus Ke, Xingrao Huang, Yingliu Fu, Qi Majnik, Amber Sampath, Venkatesh Lane, Robert H. Anat Rec (Hoboken) FULL LENGTH ARTICLES An adverse maternal environment (AME) and Western diet (WD) in early life predispose offspring toward cognitive impairment in humans and mice. Cognitive impairment associates with hippocampal dysfunction. An important regulator of hippocampal function is the hippocampal Nociceptin/Orphanin FQ (N/OFQ) system. Previous studies find links between dysregulation of hippocampal N/OFQ receptor (NOP) expression and impaired cognitive function. NOP is encoded by the opioid receptor‐like 1 (Oprl1) gene that contains multiple mRNA variants and isoforms. Regulation of Oprl1 expression includes histone modifications within the promoter. We tested the hypothesis that an AME and a postweaning WD increase the expression of hippocampal Oprl1 and select variants concurrent with altered histone code in the promoter. We created an AME‐WD model combining maternal WD and prenatal environmental stress plus postweaning WD in the mouse. We analyzed the hippocampal expression of Oprl1, Oprl1 variants, and histone modifications in the Oprl1 promoter in offspring at postnatal day (P) 21 and P100. An AME and an AME‐WD significantly increased the total hippocampal expression of Oprl1 and variant V4 concurrently with an increased accumulation of active histone marks in the promoter of male offspring. We concluded that an AME and an AME‐WD alter hippocampal Oprl1 expression in offspring through an epigenetic mechanism in a variant‐specific and sex‐specific manner. Altered hippocampal Oprl1 expression may contribute to cognitive impairment seen in adult males in this model. Epigenetic regulation of Oprl1 is a potential mechanism by which an AME and a WD may contribute to neurocognitive impairment in male offspring. John Wiley & Sons, Inc. 2022-08-19 2023-01 /pmc/articles/PMC10087895/ /pubmed/35983908 http://dx.doi.org/10.1002/ar.25056 Text en © 2022 The Authors. The Anatomical Record published by Wiley Periodicals LLC on behalf of American Association for Anatomy. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle FULL LENGTH ARTICLES
Ke, Xingrao
Huang, Yingliu
Fu, Qi
Majnik, Amber
Sampath, Venkatesh
Lane, Robert H.
Adverse maternal environment alters Oprl1 variant expression in mouse hippocampus
title Adverse maternal environment alters Oprl1 variant expression in mouse hippocampus
title_full Adverse maternal environment alters Oprl1 variant expression in mouse hippocampus
title_fullStr Adverse maternal environment alters Oprl1 variant expression in mouse hippocampus
title_full_unstemmed Adverse maternal environment alters Oprl1 variant expression in mouse hippocampus
title_short Adverse maternal environment alters Oprl1 variant expression in mouse hippocampus
title_sort adverse maternal environment alters oprl1 variant expression in mouse hippocampus
topic FULL LENGTH ARTICLES
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10087895/
https://www.ncbi.nlm.nih.gov/pubmed/35983908
http://dx.doi.org/10.1002/ar.25056
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