Journal
SLEEP MEDICINE CLINICS
Volume 2, Issue 2, Pages 161-169Publisher
ELSEVIER INC
DOI: 10.1016/j.jsmc.2007.03.003
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Funding
- National Institutes of Health [NS27250, NS25378, NS31453, HD36520, MH71830]
- Sleep Research Society Chris J. Gilin Young Investigators award
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IL1 and TNF are well-characterized SRSs, forming part of the sleep homeostat. Their release is enhanced by neuronal activity via ATP. IL1 and TNF activate nuclear factor kappa B, adenosine, and NO downstream mechanisms. The sleep homeostat is thus closely linked to cerebral metabolism and blood flow. Our knowledge of cytokine sleep mechanisms led to a view that sleep is a local property of neural networks being initiated, eg, within cortical columns. Cortical columns oscillate between functional states; the sleep-like state of cortical columns is promoted by TNF. Because TNF is involved in glutamanergic AMPA receptor expression and in synaptic scaling mechanisms, cytokine sleep mechanisms provide additional support for the hypothesis that sleep serves a synaptic-connectivity function.
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