A model of sleep-disordered breathing in the C57BL/6J mouse

Y. Tagaito, V. Y. Polotsky, M. J. Campen, J. A. Wilson, A. Balbir, P. L. Smith, A. R. Schwartz, C. P. O'Donnell

Research output: Contribution to journalArticlepeer-review

95 Scopus citations


To investigate the pathophysiological sequelae of sleep-disordered breathing (SDB), we have developed a mouse model in which hypoxia was induced during periods of sleep and was removed in response to arousal or wakefulness. An on-line sleep-wake detection system, based on the frequency and amplitude of electroencephalograph and electromyograph recordings, served to trigger intermittent hypoxia during periods of sleep. In adult male C57BL/6J mice (n = 5), the sleep-wake detection system accurately assessed wakefulness (97.2 ± 1.1%), non-rapid eye movement (NREM) sleep (96.0 ± 0.9%) and rapid eye movement (REM) sleep (85.6 e± 5.0%). After 5 consecutive days of SDB, 554 ± 29 (SE) hypoxic events were recorded over a 24-h period at a rate of 63.6 ± 2.6 events/h of sleep and with a duration of 28.2 ± 0.7 s. The mean nadir of fraction of inspired O2 (FIO2) on day 5 was 13.2 ± 0.1%, and 137.1 ± 13.2 of the events had a nadir FIO2 < 10% O2. Arterial blood gases confirmed that hypoxia of this magnitude lead to a significant degree of hypoxemia. Furthermore, 5 days of SDB were associated with decreases in both NREM and REM sleep during the light phase compared with the 24-h postintervention period. We conclude that our murine model of SDB mimics the rate and magnitude of sleep-induced hypoxia, sleep fragmentation, and reduction in total sleep time found in patients with moderate to severe SDB in the clinical setting.

Original languageEnglish (US)
Pages (from-to)2758-2766
Number of pages9
JournalJournal of applied physiology
Issue number6
StatePublished - 2001


  • Arousal
  • Intermittent hypoxia
  • Non-rapid eye movement sleep
  • Polysomnography
  • Rapid eye movement sleep

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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