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Development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess

The blood–brain barrier (BBB) is a critical contributor to brain function. To understand its development and potential function in different brain regions, the postnatal (P) BBB was investigated in the mouse cortex (CTX), lateral hypothalamus, and paraventricular nucleus of the hypothalamus (PVN). B...

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Autores principales: Frahm, Krystle A., Tobet, Stuart A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4481307/
https://www.ncbi.nlm.nih.gov/pubmed/24817635
http://dx.doi.org/10.1007/s00429-014-0787-8
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author Frahm, Krystle A.
Tobet, Stuart A.
author_facet Frahm, Krystle A.
Tobet, Stuart A.
author_sort Frahm, Krystle A.
collection PubMed
description The blood–brain barrier (BBB) is a critical contributor to brain function. To understand its development and potential function in different brain regions, the postnatal (P) BBB was investigated in the mouse cortex (CTX), lateral hypothalamus, and paraventricular nucleus of the hypothalamus (PVN). Brains were examined on postnatal days (P)12, P22 and P52 for BBB competency and for pericytes as key cellular components of the BBB demarcated by immunoreactive desmin. Glucocorticoid influences (excess dexamethasone; dex) during prenatal development were also assessed for their impact on the blood vessels within these regions postnatally. At P12, there was significantly more extravascular leakage of a low molecular weight dye (fluorescein isothiocyanate) in the CTX than within hypothalamic regions. For pericytes, there were low levels of desmin immunoreactivity at P12 that increased with age for all regions. There was more desmin immunoreactivity present in the PVN at each age examined. Fetal dex exposure resulted in decreased blood vessel density within the PVN at P20. In the CTX, dex exposure increased BBB competency, in contrast to the PVN where there was a decrease in BBB competency and increased pericyte presence. Overall, unique alterations in the functioning of the BBB within the PVN may provide a novel mechanism for fetal antecedent programming that may influence adult disorders. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00429-014-0787-8) contains supplementary material, which is available to authorized users.
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spelling pubmed-44813072015-07-02 Development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess Frahm, Krystle A. Tobet, Stuart A. Brain Struct Funct Original Article The blood–brain barrier (BBB) is a critical contributor to brain function. To understand its development and potential function in different brain regions, the postnatal (P) BBB was investigated in the mouse cortex (CTX), lateral hypothalamus, and paraventricular nucleus of the hypothalamus (PVN). Brains were examined on postnatal days (P)12, P22 and P52 for BBB competency and for pericytes as key cellular components of the BBB demarcated by immunoreactive desmin. Glucocorticoid influences (excess dexamethasone; dex) during prenatal development were also assessed for their impact on the blood vessels within these regions postnatally. At P12, there was significantly more extravascular leakage of a low molecular weight dye (fluorescein isothiocyanate) in the CTX than within hypothalamic regions. For pericytes, there were low levels of desmin immunoreactivity at P12 that increased with age for all regions. There was more desmin immunoreactivity present in the PVN at each age examined. Fetal dex exposure resulted in decreased blood vessel density within the PVN at P20. In the CTX, dex exposure increased BBB competency, in contrast to the PVN where there was a decrease in BBB competency and increased pericyte presence. Overall, unique alterations in the functioning of the BBB within the PVN may provide a novel mechanism for fetal antecedent programming that may influence adult disorders. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00429-014-0787-8) contains supplementary material, which is available to authorized users. Springer Berlin Heidelberg 2014-05-11 2015 /pmc/articles/PMC4481307/ /pubmed/24817635 http://dx.doi.org/10.1007/s00429-014-0787-8 Text en © The Author(s) 2014 https://creativecommons.org/licenses/by/4.0/ Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Original Article
Frahm, Krystle A.
Tobet, Stuart A.
Development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess
title Development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess
title_full Development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess
title_fullStr Development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess
title_full_unstemmed Development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess
title_short Development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess
title_sort development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4481307/
https://www.ncbi.nlm.nih.gov/pubmed/24817635
http://dx.doi.org/10.1007/s00429-014-0787-8
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