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Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia

Chronic hypernatremia activates the central osmoregulatory mechanisms and inhibits the function of the hypothalamic–pituitary–adrenal (HPA) axis. Noradrenaline (NE) release into the periventricular anteroventral third ventricle region (AV3V), the supraoptic (SON) and hypothalamic paraventricular nuc...

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Autores principales: Matuska, Rita, Zelena, Dóra, Könczöl, Katalin, Papp, Rege Sugárka, Durst, Máté, Guba, Dorina, Török, Bibiana, Varnai, Peter, Tóth, Zsuzsanna E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7166202/
https://www.ncbi.nlm.nih.gov/pubmed/32200401
http://dx.doi.org/10.1007/s00429-020-02049-y
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author Matuska, Rita
Zelena, Dóra
Könczöl, Katalin
Papp, Rege Sugárka
Durst, Máté
Guba, Dorina
Török, Bibiana
Varnai, Peter
Tóth, Zsuzsanna E.
author_facet Matuska, Rita
Zelena, Dóra
Könczöl, Katalin
Papp, Rege Sugárka
Durst, Máté
Guba, Dorina
Török, Bibiana
Varnai, Peter
Tóth, Zsuzsanna E.
author_sort Matuska, Rita
collection PubMed
description Chronic hypernatremia activates the central osmoregulatory mechanisms and inhibits the function of the hypothalamic–pituitary–adrenal (HPA) axis. Noradrenaline (NE) release into the periventricular anteroventral third ventricle region (AV3V), the supraoptic (SON) and hypothalamic paraventricular nuclei (PVN) from efferents of the caudal ventrolateral (cVLM) and dorsomedial (cDMM) medulla has been shown to be essential for the hypernatremia-evoked responses and for the HPA response to acute restraint. Notably, the medullary NE cell groups highly coexpress prolactin-releasing peptide (PrRP) and nesfatin-1/NUCB2 (nesfatin), therefore, we assumed they contributed to the reactions to chronic hypernatremia. To investigate this, we compared two models: homozygous Brattleboro rats with hereditary diabetes insipidus (DI) and Wistar rats subjected to chronic high salt solution (HS) intake. HS rats had higher plasma osmolality than DI rats. PrRP and nesfatin mRNA levels were higher in both models, in both medullary regions compared to controls. Elevated basal tyrosine hydroxylase (TH) expression and impaired restraint-induced TH, PrRP and nesfatin expression elevations in the cVLM were, however, detected only in HS, but not in DI rats. Simultaneously, only HS rats exhibited classical signs of chronic stress and severely blunted hormonal reactions to acute restraint. Data suggest that HPA axis responsiveness to restraint depends on the type of hypernatremia, and on NE capacity in the cVLM. Additionally, NE and PrRP signalization primarily of medullary origin is increased in the SON, PVN and AV3V in HS rats. This suggests a cooperative action in the adaptation responses and designates the AV3V as a new site for PrRP’s action in hypernatremia.
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spelling pubmed-71662022020-04-24 Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia Matuska, Rita Zelena, Dóra Könczöl, Katalin Papp, Rege Sugárka Durst, Máté Guba, Dorina Török, Bibiana Varnai, Peter Tóth, Zsuzsanna E. Brain Struct Funct Original Article Chronic hypernatremia activates the central osmoregulatory mechanisms and inhibits the function of the hypothalamic–pituitary–adrenal (HPA) axis. Noradrenaline (NE) release into the periventricular anteroventral third ventricle region (AV3V), the supraoptic (SON) and hypothalamic paraventricular nuclei (PVN) from efferents of the caudal ventrolateral (cVLM) and dorsomedial (cDMM) medulla has been shown to be essential for the hypernatremia-evoked responses and for the HPA response to acute restraint. Notably, the medullary NE cell groups highly coexpress prolactin-releasing peptide (PrRP) and nesfatin-1/NUCB2 (nesfatin), therefore, we assumed they contributed to the reactions to chronic hypernatremia. To investigate this, we compared two models: homozygous Brattleboro rats with hereditary diabetes insipidus (DI) and Wistar rats subjected to chronic high salt solution (HS) intake. HS rats had higher plasma osmolality than DI rats. PrRP and nesfatin mRNA levels were higher in both models, in both medullary regions compared to controls. Elevated basal tyrosine hydroxylase (TH) expression and impaired restraint-induced TH, PrRP and nesfatin expression elevations in the cVLM were, however, detected only in HS, but not in DI rats. Simultaneously, only HS rats exhibited classical signs of chronic stress and severely blunted hormonal reactions to acute restraint. Data suggest that HPA axis responsiveness to restraint depends on the type of hypernatremia, and on NE capacity in the cVLM. Additionally, NE and PrRP signalization primarily of medullary origin is increased in the SON, PVN and AV3V in HS rats. This suggests a cooperative action in the adaptation responses and designates the AV3V as a new site for PrRP’s action in hypernatremia. Springer Berlin Heidelberg 2020-03-21 2020 /pmc/articles/PMC7166202/ /pubmed/32200401 http://dx.doi.org/10.1007/s00429-020-02049-y Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Original Article
Matuska, Rita
Zelena, Dóra
Könczöl, Katalin
Papp, Rege Sugárka
Durst, Máté
Guba, Dorina
Török, Bibiana
Varnai, Peter
Tóth, Zsuzsanna E.
Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia
title Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia
title_full Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia
title_fullStr Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia
title_full_unstemmed Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia
title_short Colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia
title_sort colocalized neurotransmitters in the hindbrain cooperate in adaptation to chronic hypernatremia
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7166202/
https://www.ncbi.nlm.nih.gov/pubmed/32200401
http://dx.doi.org/10.1007/s00429-020-02049-y
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