The effects of dietary iron deprivation on murine circadian sleep architecture

Iron deficiency is considered a putative cause for restless legs syndrome (RLS), a human sensorimotor disorder characterized by a circadian presentation of symptoms during the evening hours that disrupts one’s ability to sleep. We sought to evaluate the sleep–wake effects of diet-induced iron defici...

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Bibliographic Details
Published in:Sleep medicine 2006-12, Vol.7 (8), p.634-640
Main Authors: Dean, Terry, Allen, Richard P., O’Donnell, Christopher P., Earley, Christopher J.
Format: Article
Language:English
Subjects:
Animals
C57
Circadian rhythm
Circadian Rhythm - physiology
Deficiency Diseases - complications
Deficiency Diseases - physiopathology
Disease Models, Animal
Iron - deficiency
Iron deprivation
Male
Mice
Mice, Inbred C57BL
Polysomnography
Restless legs
Restless Legs Syndrome - etiology
Restless Legs Syndrome - physiopathology
RLS
Sleep
Sleep - physiology
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Summary:Iron deficiency is considered a putative cause for restless legs syndrome (RLS), a human sensorimotor disorder characterized by a circadian presentation of symptoms during the evening hours that disrupts one’s ability to sleep. We sought to evaluate the sleep–wake effects of diet-induced iron deficiency in mice as an animal model of RLS. To this end, we hypothesized that the iron-deprived mice would exhibit a sleep–wake circadian pattern characteristic of the human syndrome: increased wakefulness during the hours immediately preceding the sleep-predominant period. Following weaning at post-natal day (PND) 21, C57BL/6J mice were assigned to one of two dietary treatments: iron-deficient (ID, n=7) or iron-adequate (i.e., control, CTL, n=6). At PND 44, the mice were surgically instrumented for polysomnographic (PSG) recording, and data were collected at young adulthood: PNDs 59 and 60. Sleep–wake architecture was characterized for the 12-h light and dark periods and also for six consecutive 4-h blocks comprising a 24-h day. The ID mice showed marked increases in wake time in the 4-h period prior to lights-on; both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep were reduced. In contrast, sleep–wake activity did not differ across the 12-h light period. Dietary iron deficiency in mice elicited increases in wakefulness during a particular circadian time point that corresponds to the period during which RLS symptoms would maximally disturb sleep onset and progression in humans. These data indicate that iron-deficient mice may provide a potentially useful animal model for RLS.
ISSN:1389-9457
1878-5506
DOI:10.1016/j.sleep.2006.07.002