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A mechanism for sickness sleep: lessons from invertebrates
Kristen C Davis1, David M Raizen1
1Department of Neurology, Centre for Sleep and Neurobiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
The Journal of Physiology
|December 29, 2016
Summary
Sickness triggers distinct sleep mechanisms involving neuroendocrine cells and RFamide peptides, differing from healthy sleep regulation. These pathways may offer insights into fatigue in human diseases.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Animal sleep is normally regulated by circadian rhythms and prior wakefulness.
- During sickness, cytokines from peripheral or central sources induce sleep by acting on the nervous system.
Purpose of the Study:
- To review key findings on the central neuroendocrine mechanisms of sickness-induced sleep.
- To explore the distinct pathways regulating sickness sleep compared to healthy sleep.
Main Methods:
- Research in invertebrates like Caenorhabditis elegans and Drosophila melanogaster.
- Analysis of cellular stress responses, epidermal growth factor signaling, and neuropeptide release.
Main Results:
- Sickness, triggered by stressors like infection or UV light, causes cellular stress and epidermal growth factor release.
- Stressed cells activate neuroendocrine cells that release RFamide peptides, inducing sickness sleep.
- Mechanisms for sickness sleep are partially distinct from those for healthy sleep.
Conclusions:
- Sickness sleep involves a central neuroendocrine pathway distinct from healthy sleep regulation.
- Adaptive mechanisms in sickness sleep may restore cellular homeostasis.
- These pathways could be maladaptive in human conditions like autoimmune diseases and depression.
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