Molecular neurobiological markers in the onset of sodium appetite

Abstract Sodium appetite is a motivational state involving homeostatic behavior, seeking the ingest of salty substances after sodium loss. There is a temporal dissociation between sodium depletion (SD) and the appearance of sodium appetite. However, the responsible mechanisms for this delay remain p...

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Main Authors: Cintia Y. Porcari, María J. Cambiasso, André S. Mecawi, Ximena E. Caeiro, José Antunes-Rodrigues, Laura M. Vivas, Andrea Godino
Format: Article
Language:English
Published: Nature Portfolio 2022-08-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-022-18220-w
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author Cintia Y. Porcari
María J. Cambiasso
André S. Mecawi
Ximena E. Caeiro
José Antunes-Rodrigues
Laura M. Vivas
Andrea Godino
author_facet Cintia Y. Porcari
María J. Cambiasso
André S. Mecawi
Ximena E. Caeiro
José Antunes-Rodrigues
Laura M. Vivas
Andrea Godino
author_sort Cintia Y. Porcari
collection DOAJ
description Abstract Sodium appetite is a motivational state involving homeostatic behavior, seeking the ingest of salty substances after sodium loss. There is a temporal dissociation between sodium depletion (SD) and the appearance of sodium appetite. However, the responsible mechanisms for this delay remain poorly elucidated. In the present study, we measured the temporal changes at two and 24 h after SD in the gene expression of key elements within excitatory, inhibitory, and sensory areas implicated in the signaling pathways involved in the onset of sodium appetite. In SD rats, we observed that the expression of critical components within the brain control circuit of sodium appetite, including Angiotensin-type-1 receptor (Agtr1a), Oxytocin-(OXT-NP)-neurophysin-I, and serotonergic-(5HT)-type-2c receptor (Htr2c) were modulated by SD, regardless of time. However, we observed reduced phosphorylation of mitogen-activated protein kinases (MAPK) at the paraventricular nucleus (PVN) and increased oxytocin receptor (Oxtr) mRNA expression at the anteroventral of the third ventricle area (AV3V), at two hours after SD, when sodium appetite is inapparent. At twenty-four hours after SD, when sodium appetite is released, we observed a reduction in the mRNA expression of the transient receptor potential channel 1gene (Trpv1) and Oxtr in the AV3V and the dorsal raphe nucleus, respectively. The results indicate that SD exerts a coordinated timing effect, promoting the appearance of sodium appetite through changes in MAPK activity and lower Trpv1 channel and Oxtr expression that trigger sodium consumption to reestablish the hydroelectrolytic homeostasis.
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spelling doaj.art-d5f144ea7eac4bb591136112d57ede882022-12-22T02:15:14ZengNature PortfolioScientific Reports2045-23222022-08-0112111410.1038/s41598-022-18220-wMolecular neurobiological markers in the onset of sodium appetiteCintia Y. Porcari0María J. Cambiasso1André S. Mecawi2Ximena E. Caeiro3José Antunes-Rodrigues4Laura M. Vivas5Andrea Godino6Instituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba)Instituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba)Laboratory of Molecular Neuroendocrinology, Department of Biophysics, Paulista Medical School, Federal University of São PauloInstituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba)Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao PauloInstituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba)Instituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba)Abstract Sodium appetite is a motivational state involving homeostatic behavior, seeking the ingest of salty substances after sodium loss. There is a temporal dissociation between sodium depletion (SD) and the appearance of sodium appetite. However, the responsible mechanisms for this delay remain poorly elucidated. In the present study, we measured the temporal changes at two and 24 h after SD in the gene expression of key elements within excitatory, inhibitory, and sensory areas implicated in the signaling pathways involved in the onset of sodium appetite. In SD rats, we observed that the expression of critical components within the brain control circuit of sodium appetite, including Angiotensin-type-1 receptor (Agtr1a), Oxytocin-(OXT-NP)-neurophysin-I, and serotonergic-(5HT)-type-2c receptor (Htr2c) were modulated by SD, regardless of time. However, we observed reduced phosphorylation of mitogen-activated protein kinases (MAPK) at the paraventricular nucleus (PVN) and increased oxytocin receptor (Oxtr) mRNA expression at the anteroventral of the third ventricle area (AV3V), at two hours after SD, when sodium appetite is inapparent. At twenty-four hours after SD, when sodium appetite is released, we observed a reduction in the mRNA expression of the transient receptor potential channel 1gene (Trpv1) and Oxtr in the AV3V and the dorsal raphe nucleus, respectively. The results indicate that SD exerts a coordinated timing effect, promoting the appearance of sodium appetite through changes in MAPK activity and lower Trpv1 channel and Oxtr expression that trigger sodium consumption to reestablish the hydroelectrolytic homeostasis.https://doi.org/10.1038/s41598-022-18220-w
spellingShingle Cintia Y. Porcari
María J. Cambiasso
André S. Mecawi
Ximena E. Caeiro
José Antunes-Rodrigues
Laura M. Vivas
Andrea Godino
Molecular neurobiological markers in the onset of sodium appetite
Scientific Reports
title Molecular neurobiological markers in the onset of sodium appetite
title_full Molecular neurobiological markers in the onset of sodium appetite
title_fullStr Molecular neurobiological markers in the onset of sodium appetite
title_full_unstemmed Molecular neurobiological markers in the onset of sodium appetite
title_short Molecular neurobiological markers in the onset of sodium appetite
title_sort molecular neurobiological markers in the onset of sodium appetite
url https://doi.org/10.1038/s41598-022-18220-w
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