Long-term intermittent hypoxia in mice: Protracted hypersomnolence with oxidative injury to sleep-wake brain regions

Sigrid Carlen Veasey, Christine W. Davis, Polina Fenik, Guanxia Zhan, Yeou Jey Hsu, Domenico Pratico, Andrew Gow

Research output: Contribution to journalArticle

254 Citations (Scopus)

Abstract

Study Objectives: This study was designed to test the hypothesis that long-term intermittent hypoxia (LTIH), modeling the hypoxia-reoxygenation events of sleep apnea, results in oxidative neural injury, including wake-promoting neural groups, and that this injury contributes to residual impaired maintenance of wakefulness. Design: Sleep times and oxidative-injury parameters were compared for mice exposed to LTIH and mice exposed to sham LTIH. Subjects: Adult male C57BL/6J mice were studied. Interventions: Mice were exposed to LTIH or sham LTIH in the lights-on period daily for 8 weeks. Electrophysiologic sleep-wake recordings and oxidative-injury measures were performed either immediately or 2 weeks following LTIH exposures. Measurements and Results: At both intervals, total sleep time per 24 hours in LTIH-exposed mice was increased by more than 2 hours, (P2α-VI, 22%, P

Original languageEnglish
Pages (from-to)194-201
Number of pages8
JournalSleep
Volume27
Issue number2
Publication statusPublished - 2004
Externally publishedYes

Keywords

  • Apnea
  • Hypoxia
  • Oxidation
  • Oxidative stress
  • Wakefulness

ASJC Scopus subject areas

  • Physiology

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  • Cite this

    Veasey, S. C., Davis, C. W., Fenik, P., Zhan, G., Hsu, Y. J., Pratico, D., & Gow, A. (2004). Long-term intermittent hypoxia in mice: Protracted hypersomnolence with oxidative injury to sleep-wake brain regions. Sleep, 27(2), 194-201.