The effect of increased NaCl intake on rat brain endogenous μ-opioid receptor signalling

F. Dadam, F. Zádor, X. Caeiro, E. Szűcs, A. Erdei, R. Samavati, R. Gáspár, A. Borsodi, L. Vivas

Research output: Contribution to journalArticle

Abstract

Numerous studies demonstrate the significant role of central β-endorphin and its receptor, the μ-opioid receptor (MOR), in sodium intake regulation. The present study aimed to investigate the possible relationship between chronic high-NaCl intake and brain endogenous MOR functioning. We examined whether short-term (4 days) obligatory salt intake (2% NaCl solution) in rats induces changes in MOR mRNA expression, G-protein activity and MOR binding capacity in brain regions involved in salt intake regulation. Plasma osmolality and electrolyte concentrations after sodium overload and the initial and final body weight of the animals were also examined. After 4 days of obligatory hypertonic sodium chloride intake, there was clearly no difference in MOR mRNA expression and G-protein activity in the median preoptic nucleus (MnPO). In the brainstem, MOR binding capacity also remained unaltered, although the maximal efficacy of MOR G-protein significantly increased. Finally, no significant alterations were observed in plasma osmolality and electrolyte concentrations. Interestingly, animals that received sodium gained significantly less weight than control animals. In conclusion, we found no significant alterations in the MnPO and brainstem in the number of available cell surface MORs or de novo syntheses of MOR after hypertonic sodium intake. The increased MOR G-protein activity following acute sodium overconsumption may participate in the maintenance of normal blood pressure levels and/or in enhancing sodium taste aversion and sodium overload-induced anorexia.

Original languageEnglish
Article numbere12585
JournalJournal of Neuroendocrinology
Volume30
Issue number4
DOIs
Publication statusPublished - Apr 1 2018

Fingerprint

Opioid Receptors
Sodium
GTP-Binding Proteins
Brain
Preoptic Area
Osmolar Concentration
Electrolytes
Brain Stem
Salts
Messenger RNA
Anorexia
Sodium Chloride
Cell Count
Body Weight
Maintenance
Blood Pressure
Weights and Measures

Keywords

  • brainstem
  • G-protein activation
  • sodium ingestion
  • ß-endorphin
  • μ-opioid receptor signalling

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience

Cite this

The effect of increased NaCl intake on rat brain endogenous μ-opioid receptor signalling. / Dadam, F.; Zádor, F.; Caeiro, X.; Szűcs, E.; Erdei, A.; Samavati, R.; Gáspár, R.; Borsodi, A.; Vivas, L.

In: Journal of Neuroendocrinology, Vol. 30, No. 4, e12585, 01.04.2018.

Research output: Contribution to journalArticle

Dadam, F. ; Zádor, F. ; Caeiro, X. ; Szűcs, E. ; Erdei, A. ; Samavati, R. ; Gáspár, R. ; Borsodi, A. ; Vivas, L. / The effect of increased NaCl intake on rat brain endogenous μ-opioid receptor signalling. In: Journal of Neuroendocrinology. 2018 ; Vol. 30, No. 4.
@article{308a5b81273845c8bfe829d62e711f06,
title = "The effect of increased NaCl intake on rat brain endogenous μ-opioid receptor signalling",
abstract = "Numerous studies demonstrate the significant role of central β-endorphin and its receptor, the μ-opioid receptor (MOR), in sodium intake regulation. The present study aimed to investigate the possible relationship between chronic high-NaCl intake and brain endogenous MOR functioning. We examined whether short-term (4 days) obligatory salt intake (2{\%} NaCl solution) in rats induces changes in MOR mRNA expression, G-protein activity and MOR binding capacity in brain regions involved in salt intake regulation. Plasma osmolality and electrolyte concentrations after sodium overload and the initial and final body weight of the animals were also examined. After 4 days of obligatory hypertonic sodium chloride intake, there was clearly no difference in MOR mRNA expression and G-protein activity in the median preoptic nucleus (MnPO). In the brainstem, MOR binding capacity also remained unaltered, although the maximal efficacy of MOR G-protein significantly increased. Finally, no significant alterations were observed in plasma osmolality and electrolyte concentrations. Interestingly, animals that received sodium gained significantly less weight than control animals. In conclusion, we found no significant alterations in the MnPO and brainstem in the number of available cell surface MORs or de novo syntheses of MOR after hypertonic sodium intake. The increased MOR G-protein activity following acute sodium overconsumption may participate in the maintenance of normal blood pressure levels and/or in enhancing sodium taste aversion and sodium overload-induced anorexia.",
keywords = "brainstem, G-protein activation, sodium ingestion, {\ss}-endorphin, μ-opioid receptor signalling",
author = "F. Dadam and F. Z{\'a}dor and X. Caeiro and E. Szűcs and A. Erdei and R. Samavati and R. G{\'a}sp{\'a}r and A. Borsodi and L. Vivas",
year = "2018",
month = "4",
day = "1",
doi = "10.1111/jne.12585",
language = "English",
volume = "30",
journal = "Journal of Neuroendocrinology",
issn = "0953-8194",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - The effect of increased NaCl intake on rat brain endogenous μ-opioid receptor signalling

AU - Dadam, F.

AU - Zádor, F.

AU - Caeiro, X.

AU - Szűcs, E.

AU - Erdei, A.

AU - Samavati, R.

AU - Gáspár, R.

AU - Borsodi, A.

AU - Vivas, L.

PY - 2018/4/1

Y1 - 2018/4/1

N2 - Numerous studies demonstrate the significant role of central β-endorphin and its receptor, the μ-opioid receptor (MOR), in sodium intake regulation. The present study aimed to investigate the possible relationship between chronic high-NaCl intake and brain endogenous MOR functioning. We examined whether short-term (4 days) obligatory salt intake (2% NaCl solution) in rats induces changes in MOR mRNA expression, G-protein activity and MOR binding capacity in brain regions involved in salt intake regulation. Plasma osmolality and electrolyte concentrations after sodium overload and the initial and final body weight of the animals were also examined. After 4 days of obligatory hypertonic sodium chloride intake, there was clearly no difference in MOR mRNA expression and G-protein activity in the median preoptic nucleus (MnPO). In the brainstem, MOR binding capacity also remained unaltered, although the maximal efficacy of MOR G-protein significantly increased. Finally, no significant alterations were observed in plasma osmolality and electrolyte concentrations. Interestingly, animals that received sodium gained significantly less weight than control animals. In conclusion, we found no significant alterations in the MnPO and brainstem in the number of available cell surface MORs or de novo syntheses of MOR after hypertonic sodium intake. The increased MOR G-protein activity following acute sodium overconsumption may participate in the maintenance of normal blood pressure levels and/or in enhancing sodium taste aversion and sodium overload-induced anorexia.

AB - Numerous studies demonstrate the significant role of central β-endorphin and its receptor, the μ-opioid receptor (MOR), in sodium intake regulation. The present study aimed to investigate the possible relationship between chronic high-NaCl intake and brain endogenous MOR functioning. We examined whether short-term (4 days) obligatory salt intake (2% NaCl solution) in rats induces changes in MOR mRNA expression, G-protein activity and MOR binding capacity in brain regions involved in salt intake regulation. Plasma osmolality and electrolyte concentrations after sodium overload and the initial and final body weight of the animals were also examined. After 4 days of obligatory hypertonic sodium chloride intake, there was clearly no difference in MOR mRNA expression and G-protein activity in the median preoptic nucleus (MnPO). In the brainstem, MOR binding capacity also remained unaltered, although the maximal efficacy of MOR G-protein significantly increased. Finally, no significant alterations were observed in plasma osmolality and electrolyte concentrations. Interestingly, animals that received sodium gained significantly less weight than control animals. In conclusion, we found no significant alterations in the MnPO and brainstem in the number of available cell surface MORs or de novo syntheses of MOR after hypertonic sodium intake. The increased MOR G-protein activity following acute sodium overconsumption may participate in the maintenance of normal blood pressure levels and/or in enhancing sodium taste aversion and sodium overload-induced anorexia.

KW - brainstem

KW - G-protein activation

KW - sodium ingestion

KW - ß-endorphin

KW - μ-opioid receptor signalling

UR - http://www.scopus.com/inward/record.url?scp=85045892292&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85045892292&partnerID=8YFLogxK

U2 - 10.1111/jne.12585

DO - 10.1111/jne.12585

M3 - Article

VL - 30

JO - Journal of Neuroendocrinology

JF - Journal of Neuroendocrinology

SN - 0953-8194

IS - 4

M1 - e12585

ER -