Impaired sodium levels in the suprachiasmatic nucleus are associated with the formation of cardiovascular deficiency in sleep-deprived rats

Hung Ming Chang, Fu Der Mai, Shiou Ling Lei, Yong Chien Ling

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Biological rhythms are a ubiquitous feature of all higher organisms. The rhythmic center of mammals is located in the suprachiasmatic nucleus (SCN), which projects to a number of brainstem centers to exert diurnal control over many physiological processes, including cardiovascular regulation. Total sleep deprivation (TSD) is a harmful condition known to impair cardiovascular activity, but the molecular mechanisms are unknown. As the inward sodium current has long been suggested as playing an important role in driving the spontaneous firing of the SCN, the present study aimed to determine if changes in sodium expression, together with its molecular machinery (Na-K ATPase) and rhythmic activity within the SCN, would occur during TSD. Adult rats subjected to different periods of TSD were processed for time-of-flight secondary ion mass spectrometry, Na-K ATPase assay, and cytochrome oxidase (COX) (an endogenous bioenergetic marker for neuronal activity) histochemistry. Cardiovascular dysfunction was determined through analysis of heart rate and changes in mean arterial pressure. Results indicated that, in normal rats, strong sodium signals were expressed throughout the entire SCN. Enzymatic data corresponded well with spectrometric findings in which high levels of Na-K ATPase and COX were observed in this nucleus. However, following TSD, all parameters including sodium imaging, sodium intensity as well as COX activities were drastically decreased. Na-K ATPase showed an increase in responsiveness following TSD. Both heart rate and mean arterial pressure measurements indicated an exaggerated pressor effect following TSD treatment. As proper sodium levels are essential for SCN activation, reduced SCN sodium levels may interrupt the oscillatory control, which could serve as the underlying mechanism for the initiation or development of TSD-related cardiovascular deficiency.

Original languageEnglish
Pages (from-to)694-704
Number of pages11
JournalJournal of Anatomy
Volume217
Issue number6
DOIs
Publication statusPublished - Dec 2010
Externally publishedYes

Fingerprint

Suprachiasmatic Nucleus
Sleep Deprivation
sleep
Sleep
Sodium
sodium
sodium-potassium-exchanging ATPase
rats
Electron Transport Complex IV
cytochrome-c oxidase
cytochrome
heart rate
Arterial Pressure
Heart Rate
biological rhythm
Cardiovascular Physiological Phenomena
Secondary Ion Mass Spectrometry
biological rhythms
bioenergetics
histochemistry

Keywords

  • Cardiovascular rhythm
  • Cytochrome oxidase
  • Quantitative molecular image analysis
  • Sleep deprivation
  • Suprachiasmatic nucleus
  • Time-of-flight secondary ion mass spectrometry

ASJC Scopus subject areas

  • Anatomy
  • Histology
  • Developmental Biology
  • Ecology, Evolution, Behavior and Systematics
  • Molecular Biology
  • Cell Biology

Cite this

Impaired sodium levels in the suprachiasmatic nucleus are associated with the formation of cardiovascular deficiency in sleep-deprived rats. / Chang, Hung Ming; Mai, Fu Der; Lei, Shiou Ling; Ling, Yong Chien.

In: Journal of Anatomy, Vol. 217, No. 6, 12.2010, p. 694-704.

Research output: Contribution to journalArticle

@article{a219dc0f1ccf4dedaa6e21064e982e64,
title = "Impaired sodium levels in the suprachiasmatic nucleus are associated with the formation of cardiovascular deficiency in sleep-deprived rats",
abstract = "Biological rhythms are a ubiquitous feature of all higher organisms. The rhythmic center of mammals is located in the suprachiasmatic nucleus (SCN), which projects to a number of brainstem centers to exert diurnal control over many physiological processes, including cardiovascular regulation. Total sleep deprivation (TSD) is a harmful condition known to impair cardiovascular activity, but the molecular mechanisms are unknown. As the inward sodium current has long been suggested as playing an important role in driving the spontaneous firing of the SCN, the present study aimed to determine if changes in sodium expression, together with its molecular machinery (Na-K ATPase) and rhythmic activity within the SCN, would occur during TSD. Adult rats subjected to different periods of TSD were processed for time-of-flight secondary ion mass spectrometry, Na-K ATPase assay, and cytochrome oxidase (COX) (an endogenous bioenergetic marker for neuronal activity) histochemistry. Cardiovascular dysfunction was determined through analysis of heart rate and changes in mean arterial pressure. Results indicated that, in normal rats, strong sodium signals were expressed throughout the entire SCN. Enzymatic data corresponded well with spectrometric findings in which high levels of Na-K ATPase and COX were observed in this nucleus. However, following TSD, all parameters including sodium imaging, sodium intensity as well as COX activities were drastically decreased. Na-K ATPase showed an increase in responsiveness following TSD. Both heart rate and mean arterial pressure measurements indicated an exaggerated pressor effect following TSD treatment. As proper sodium levels are essential for SCN activation, reduced SCN sodium levels may interrupt the oscillatory control, which could serve as the underlying mechanism for the initiation or development of TSD-related cardiovascular deficiency.",
keywords = "Cardiovascular rhythm, Cytochrome oxidase, Quantitative molecular image analysis, Sleep deprivation, Suprachiasmatic nucleus, Time-of-flight secondary ion mass spectrometry",
author = "Chang, {Hung Ming} and Mai, {Fu Der} and Lei, {Shiou Ling} and Ling, {Yong Chien}",
year = "2010",
month = "12",
doi = "10.1111/j.1469-7580.2010.01312.x",
language = "English",
volume = "217",
pages = "694--704",
journal = "Journal of Anatomy",
issn = "0021-8782",
publisher = "Wiley-Blackwell",
number = "6",

}

TY - JOUR

T1 - Impaired sodium levels in the suprachiasmatic nucleus are associated with the formation of cardiovascular deficiency in sleep-deprived rats

AU - Chang, Hung Ming

AU - Mai, Fu Der

AU - Lei, Shiou Ling

AU - Ling, Yong Chien

PY - 2010/12

Y1 - 2010/12

N2 - Biological rhythms are a ubiquitous feature of all higher organisms. The rhythmic center of mammals is located in the suprachiasmatic nucleus (SCN), which projects to a number of brainstem centers to exert diurnal control over many physiological processes, including cardiovascular regulation. Total sleep deprivation (TSD) is a harmful condition known to impair cardiovascular activity, but the molecular mechanisms are unknown. As the inward sodium current has long been suggested as playing an important role in driving the spontaneous firing of the SCN, the present study aimed to determine if changes in sodium expression, together with its molecular machinery (Na-K ATPase) and rhythmic activity within the SCN, would occur during TSD. Adult rats subjected to different periods of TSD were processed for time-of-flight secondary ion mass spectrometry, Na-K ATPase assay, and cytochrome oxidase (COX) (an endogenous bioenergetic marker for neuronal activity) histochemistry. Cardiovascular dysfunction was determined through analysis of heart rate and changes in mean arterial pressure. Results indicated that, in normal rats, strong sodium signals were expressed throughout the entire SCN. Enzymatic data corresponded well with spectrometric findings in which high levels of Na-K ATPase and COX were observed in this nucleus. However, following TSD, all parameters including sodium imaging, sodium intensity as well as COX activities were drastically decreased. Na-K ATPase showed an increase in responsiveness following TSD. Both heart rate and mean arterial pressure measurements indicated an exaggerated pressor effect following TSD treatment. As proper sodium levels are essential for SCN activation, reduced SCN sodium levels may interrupt the oscillatory control, which could serve as the underlying mechanism for the initiation or development of TSD-related cardiovascular deficiency.

AB - Biological rhythms are a ubiquitous feature of all higher organisms. The rhythmic center of mammals is located in the suprachiasmatic nucleus (SCN), which projects to a number of brainstem centers to exert diurnal control over many physiological processes, including cardiovascular regulation. Total sleep deprivation (TSD) is a harmful condition known to impair cardiovascular activity, but the molecular mechanisms are unknown. As the inward sodium current has long been suggested as playing an important role in driving the spontaneous firing of the SCN, the present study aimed to determine if changes in sodium expression, together with its molecular machinery (Na-K ATPase) and rhythmic activity within the SCN, would occur during TSD. Adult rats subjected to different periods of TSD were processed for time-of-flight secondary ion mass spectrometry, Na-K ATPase assay, and cytochrome oxidase (COX) (an endogenous bioenergetic marker for neuronal activity) histochemistry. Cardiovascular dysfunction was determined through analysis of heart rate and changes in mean arterial pressure. Results indicated that, in normal rats, strong sodium signals were expressed throughout the entire SCN. Enzymatic data corresponded well with spectrometric findings in which high levels of Na-K ATPase and COX were observed in this nucleus. However, following TSD, all parameters including sodium imaging, sodium intensity as well as COX activities were drastically decreased. Na-K ATPase showed an increase in responsiveness following TSD. Both heart rate and mean arterial pressure measurements indicated an exaggerated pressor effect following TSD treatment. As proper sodium levels are essential for SCN activation, reduced SCN sodium levels may interrupt the oscillatory control, which could serve as the underlying mechanism for the initiation or development of TSD-related cardiovascular deficiency.

KW - Cardiovascular rhythm

KW - Cytochrome oxidase

KW - Quantitative molecular image analysis

KW - Sleep deprivation

KW - Suprachiasmatic nucleus

KW - Time-of-flight secondary ion mass spectrometry

UR - http://www.scopus.com/inward/record.url?scp=78349251336&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78349251336&partnerID=8YFLogxK

U2 - 10.1111/j.1469-7580.2010.01312.x

DO - 10.1111/j.1469-7580.2010.01312.x

M3 - Article

C2 - 20946541

AN - SCOPUS:78349251336

VL - 217

SP - 694

EP - 704

JO - Journal of Anatomy

JF - Journal of Anatomy

SN - 0021-8782

IS - 6

ER -