Total sleep deprivation inhibits the neuronal nitric oxide synthase and cytochrome oxidase reactivities in the nodose ganglion of adult rats

Hung Ming Chang, Un In Wu, Tzer Bin Lin, Chyn Tair Lan, Wei Ching Chien, Wei Ling Huang, Jeng Yung Shieh

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Sleep disorders are a form of stress associated with increased sympathetic activity, and they are a risk factor for the occurrence of cardiovascular disease. Given that nitric oxide (NO) may play an inhibitory role in the regulation of sympathetic tone, this study set out to determine the NO synthase (NOS) reactivity in the primary cardiovascular afferent neurons (i.e. nodose neurons) following total sleep deprivation (TSD). TSD was performed by the disc-on-water method. Following 5.days of TSD, all experimental animals were investigated for quantitative nicotinamine adenine dinucleotide phosphate-diaphorase (NADPH-d, a co-factor of NOS) histochemistry, neuronal NOS immunohistochemistry and neuronal NOS activity assay. In order to evaluate the endogenous metabolic activity of nodose neurons, cytochrome oxidase (COX) reactivity was further tested. All the above-mentioned reactivities were objectively assessed by computerized image analysis. The clinical significance of the reported changes was demonstrated by alterations of mean arterial blood pressure (MAP). The results indicated that in normal untreated rats, numerous NADPH-d/NOS- and COX-reactive neurons were found in the nodose ganglion (NG). Following TSD, however, both the labelling and staining intensity of NADPH-d/NOS as well as COX reactivity were drastically reduced in the NG compared with normal untreated ganglions. MAP was significantly higher in TSD rats (136 ± 4 mmHg) than in normal untreated rats (123 ± 2mmHg). NO may serve as an important sympathoinhibition messenger released by the NG neurons, and decrease of NOS immunoexpression following TSD may account for the decrease in NOS content. In association with the reduction of NOS activity, a defect in NOS expression in the primary cardiovascular afferent neurons would enhance clinical hypertension, which might serve as a potential risk factor in the development of TSD-relevant cardiovascular disturbances.

Original languageEnglish
Pages (from-to)239-250
Number of pages12
JournalJournal of Anatomy
Volume209
Issue number2
DOIs
Publication statusPublished - Aug 2006
Externally publishedYes

Fingerprint

Nodose Ganglion
Nitric Oxide Synthase Type I
Sleep Deprivation
sleep
Electron Transport Complex IV
nitric oxide
Nitric Oxide Synthase
cytochrome-c oxidase
cytochrome
rats
neurons
Arterial Pressure
sensory neurons
nitric oxide synthase
NADP (coenzyme)
Neurons
Afferent Neurons
blood pressure
risk factor
risk factors

Keywords

  • Cytochrome oxidase
  • Immunohistochemistry
  • Nitric oxide synthase
  • Quantitative image analysis
  • Sympathetic activity
  • Total sleep deprivation

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Anatomy

Cite this

Total sleep deprivation inhibits the neuronal nitric oxide synthase and cytochrome oxidase reactivities in the nodose ganglion of adult rats. / Chang, Hung Ming; Wu, Un In; Lin, Tzer Bin; Lan, Chyn Tair; Chien, Wei Ching; Huang, Wei Ling; Shieh, Jeng Yung.

In: Journal of Anatomy, Vol. 209, No. 2, 08.2006, p. 239-250.

Research output: Contribution to journalArticle

Chang, Hung Ming ; Wu, Un In ; Lin, Tzer Bin ; Lan, Chyn Tair ; Chien, Wei Ching ; Huang, Wei Ling ; Shieh, Jeng Yung. / Total sleep deprivation inhibits the neuronal nitric oxide synthase and cytochrome oxidase reactivities in the nodose ganglion of adult rats. In: Journal of Anatomy. 2006 ; Vol. 209, No. 2. pp. 239-250.
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AU - Wu, Un In

AU - Lin, Tzer Bin

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AU - Chien, Wei Ching

AU - Huang, Wei Ling

AU - Shieh, Jeng Yung

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