Sleep fragmentation has differential effects on obese and lean mice
Junyun He1, Abba J Kastin, Yuping Wang
1Blood Brain Barrier Group, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA, 70808, USA.
Journal of Molecular Neuroscience : MN
|August 26, 2014
Summary
Chronic sleep fragmentation (SF) impacts neurobehavior differently in lean and obese mice. Obesity may blunt the behavioral effects of sleep fragmentation, suggesting a complex interaction.
Area of Science:
- Neuroscience
- Sleep Science
- Obesity Research
Background:
- Chronic sleep fragmentation (SF) is linked to obesity development.
- Sleep apnea patients commonly experience SF.
- The neurobehavioral impact of SF in obesity is not fully understood.
Purpose of the Study:
- To investigate the differential effects of SF on neurobehavior in lean wild-type (WT) and obese pan-leptin receptor knockout (POKO) mice.
- To understand how obesity modulates responses to sleep fragmentation.
Main Methods:
- Established an SF paradigm by sleep interruption every 2 minutes during the light phase.
- Assessed changes in sleep architecture (NREM, REM, sleep latency, delta power).
- Evaluated neurobehavioral outcomes including thermal pain threshold, locomotor activity, and anxiety.
Main Results:
- SF reduced sleep duration and bout length, increasing state transitions and waking.
- SF altered sleep architecture, decreasing NREM and REM sleep, and increasing delta power.
- SF increased pain threshold in WT mice but not POKO mice; both SF and POKO mutation reduced activity and increased anxiety without additive effects.
Conclusions:
- SF and the POKO mutation differentially regulate mouse behavior.
- Obesity may blunt neurobehavioral responses to SF.
- Findings highlight the complex interplay between sleep fragmentation, obesity, and neurobehavioral regulation.
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