Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.

It has been well established that maternal inflammation during pregnancy alters neurological function in the offspring, but its impact on cortical development and long-term consequences on the cytoarchitecture is largely unstudied. Here we report that lipopolysaccharide-induced systemic maternal inf...

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Autors principals: Stolp, H, Turnquist, C, Dziegielewska, K, Saunders, N, Anthony, D, Molnár, Z
Format: Journal article
Idioma:English
Publicat: 2011
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author Stolp, H
Turnquist, C
Dziegielewska, K
Saunders, N
Anthony, D
Molnár, Z
author_facet Stolp, H
Turnquist, C
Dziegielewska, K
Saunders, N
Anthony, D
Molnár, Z
author_sort Stolp, H
collection OXFORD
description It has been well established that maternal inflammation during pregnancy alters neurological function in the offspring, but its impact on cortical development and long-term consequences on the cytoarchitecture is largely unstudied. Here we report that lipopolysaccharide-induced systemic maternal inflammation in C57Bl/6 mice at embryonic Day 13.5 of pregnancy, as early as 8 h after challenge, caused a significant reduction in cell proliferation in the ventricular zone of the developing cerebral cortex, as revealed by quantification of anti-phospho-Histone H3 immunoreactivity and bromodeoxyuridine pulse labelling. The angle of mitotic cleavage, determined from analysis of haematoxylin and eosin staining, cyclin E1 gene expression and the pattern of β-catenin immunoreactivity were also altered by the challenge, which suggests a change from symmetric to asymmetric division in the radial progenitor cells. Modifications of cortical lamination and gene expression patterns were detected at post-natal Day 8 suggesting prolonged consequences of these alterations during embryonic development. Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour.
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spelling oxford-uuid:1c30d45b-2837-4793-8a3d-60a602855b402022-03-26T11:04:23ZReduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:1c30d45b-2837-4793-8a3d-60a602855b40EnglishSymplectic Elements at Oxford2011Stolp, HTurnquist, CDziegielewska, KSaunders, NAnthony, DMolnár, ZIt has been well established that maternal inflammation during pregnancy alters neurological function in the offspring, but its impact on cortical development and long-term consequences on the cytoarchitecture is largely unstudied. Here we report that lipopolysaccharide-induced systemic maternal inflammation in C57Bl/6 mice at embryonic Day 13.5 of pregnancy, as early as 8 h after challenge, caused a significant reduction in cell proliferation in the ventricular zone of the developing cerebral cortex, as revealed by quantification of anti-phospho-Histone H3 immunoreactivity and bromodeoxyuridine pulse labelling. The angle of mitotic cleavage, determined from analysis of haematoxylin and eosin staining, cyclin E1 gene expression and the pattern of β-catenin immunoreactivity were also altered by the challenge, which suggests a change from symmetric to asymmetric division in the radial progenitor cells. Modifications of cortical lamination and gene expression patterns were detected at post-natal Day 8 suggesting prolonged consequences of these alterations during embryonic development. Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour.
spellingShingle Stolp, H
Turnquist, C
Dziegielewska, K
Saunders, N
Anthony, D
Molnár, Z
Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.
title Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.
title_full Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.
title_fullStr Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.
title_full_unstemmed Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.
title_short Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.
title_sort reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse
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AT turnquistc reducedventricularproliferationinthefoetalcortexfollowingmaternalinflammationinthemouse
AT dziegielewskak reducedventricularproliferationinthefoetalcortexfollowingmaternalinflammationinthemouse
AT saundersn reducedventricularproliferationinthefoetalcortexfollowingmaternalinflammationinthemouse
AT anthonyd reducedventricularproliferationinthefoetalcortexfollowingmaternalinflammationinthemouse
AT molnarz reducedventricularproliferationinthefoetalcortexfollowingmaternalinflammationinthemouse