Literature DB >> 15124711

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

Sigrid C Veasey1, Christine W Davis, Polina Fenik, Guanxia Zhan, Yeou-Jey Hsu, Domenico Pratico, Andrew Gow.   

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, (P<.01). Mean sleep latency was reduced in LTIH-exposed mice relative to sham LTIH mice (8.9 +/- 1.0 minutes vs 12.7 +/- 0.5 minutes, respectively, P<.01). Oxidative injury was present 2 weeks following LTIH in wake-promoting regions of the basal forebrain and brainstem: elevated isoprostane 8,12-iso-IPF2alpha-VI, 22%, P<.05; increased protein carbonylation, 50%, P<.05, increased nitration, 200%, P<.05, and induction of antioxidant enzymes glutathione reductase and methionine sulfoxide reductase A, P<.01.
CONCLUSIONS: Exposure to LTIH results in an array of significant oxidative injuries in sleep-wake regions of the brain, and these biochemical changes are associated with marked hypersomnolence and increased susceptibility to short-term sleep loss. The residual forebrain redox alterations in wake-promoting brain regions may contribute to persistent sleepiness in a prevalent disorder, obstructive sleep apnea.

Entities:  

Mesh:

Year:  2004        PMID: 15124711     DOI: 10.1093/sleep/27.2.194

Source DB:  PubMed          Journal:  Sleep        ISSN: 0161-8105            Impact factor:   5.849


  127 in total

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