Brain osmo-sodium sensitive channels and the onset of sodium appetite.

Autor: Porcari CY; Instituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba), Córdoba, Argentina., Debarba LK; Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Sao Paulo, Brazil., Amigone JL; Sección de Bioquímica Clínica, Hospital Privado, Córdoba, Argentina., Caeiro XE; Instituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba), Córdoba, Argentina., Reis LC; Department of Physiological Sciences, Institute of Biological and Health Sciences, Federal Rural University of Rio de Janeiro, Seropédica, Brazil., Cunha TM; Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Sao Paulo, Brazil., Mecawi AS; Laboratory of Molecular Neuroendocrinology, Department of Biophysics, Paulista Medical School, Federal University of São Paulo, São Paulo, Brazil., Elias LL; Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Sao Paulo, Brazil., Antunes-Rodrigues J; Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Sao Paulo, Brazil., Vivas L; Instituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba), Córdoba, Argentina; Facultad de Ciencias Exactas Físicas y Naturales, Universidad Nacional de Córdoba, Córdoba, Argentina., Godino A; Instituto de Investigación Médica Mercedes y Martín Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba), Córdoba, Argentina; Facultad de Psicología, Universidad Nacional de Córdoba, Córdoba, Argentina. Electronic address: agodino@immf.uncor.edu.
Jazyk: angličtina
Zdroj: Hormones and behavior [Horm Behav] 2020 Feb; Vol. 118, pp. 104658. Date of Electronic Publication: 2020 Jan 07.
DOI: 10.1016/j.yhbeh.2019.104658
Abstrakt: The aim of the present study was to determine whether the TRPV1 channel is involved in the onset of sodium appetite. For this purpose, we used TRPV1-knockout mice to investigate sodium depletion-induced drinking at different times (2/24 h) after furosemide administration combined with a low sodium diet (FURO-LSD). In sodium depleted wild type and TRPV1 KO (SD-WT/SD-TPRV1-KO) mice, we also evaluated the participation of other sodium sensors, such as TPRV4, Na X and angiotensin AT1-receptors (by RT-PCR), as well as investigating the pattern of neural activation shown by Fos immunoreactivity, in different nuclei involved in hydromineral regulation. TPRV1 SD-KO mice revealed an increased sodium preference, ingesting a higher hypertonic cocktail in comparison with SD-WT mice. Our results also showed in SD-WT animals that SFO-Trpv4 expression increased 2 h after FURO-LSD, compared to other groups, thus supporting a role of SFO-Trpv4 channels during the hyponatremic state. However, the SD-TPRV1-KO animals did not show this early increase, and maybe as a consequence drank more hypertonic cocktail. Regarding the SFO-Na X channel expression, in both genotypes our findings revealed a reduction 24 h after FURO-LSD. In addition, there was an increase in the OVLT-Na X expression of SD-WT 24 h after FURO-LSD, suggesting the participation of OVLT-Na X channels in the appearance of sodium appetite, possibly as an anticipatory response in order to limit sodium intake and to induce thirst. Our work demonstrates changes in the expression of different osmo‑sodium-sensitive channels at specific nuclei, related to the body sodium status in order to stimulate an adequate drinking.
(Copyright © 2019 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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