Journal article
Biochemical regulation of sleep and sleep biomarkers
Journal of clinical sleep medicine, Vol.7(5 Suppl), pp.S38-S42
10/15/2011
Handle:
https://hdl.handle.net/2376/110023
PMCID: PMC3190410
PMID: 22003330
Abstract
Symptoms commonly associated with sleep loss and chronic inflammation include sleepiness, fatigue, poor cognition, enhanced sensitivity to pain and kindling stimuli, excess sleep and increases in circulating levels of tumor necrosis factor α (TNF) in humans and brain levels of interleukin-1 β (IL1) and TNF in animals. Cytokines including IL1 and TNF partake in non-rapid eye movement sleep (NREMS) regulation under physiological and inflammatory conditions. Administration of exogenous IL1 or TNF mimics the accumulation of these cytokines occurring during sleep loss to the extent that it induces the aforementioned symptoms. Extracellular ATP associated with neuro- and glio-transmission, acting via purine type 2 receptors, e.g., the P2X7 receptor, has a role in glia release of IL1 and TNF. These substances in turn act on neurons to change their intrinsic membrane properties and sensitivities to neurotransmitters and neuromodulators such as adenosine, glutamate and GABA. These actions change the network input-output properties, i.e., a state shift for the network. State oscillations occur locally within cortical columns and are defined using evoked response potentials. One such state, so defined, shares properties with whole animal sleep in that it is dependent on prior cellular activity--it shows homeostasis. The cortical column sleep-like state is induced by TNF and is associated with experimental performance detriments. ATP released extracellularly as a consequence of cellular activity is posited to initiate a mechanism by which the brain tracks its prior sleep-state history to induce/prohibit sleep. Thus, sleep is an emergent property of populations of local neural networks undergoing state transitions. Specific neuronal groups participating in sleep depend upon prior network use driving local network state changes via the ATP-cytokine-adenosine mechanism. Such considerations add complexity to finding biochemical markers for sleepiness.
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Details
- Title
- Biochemical regulation of sleep and sleep biomarkers
- Creators
- James M Clinton - Sleep and Performance Research Center, WWAMI Medical Education Program, WA State University, Spokane, WA 99164, USA. jclinton@wsu.eduChristopher J DavisMark R ZielinskiKathryn A JewettJames M Krueger
- Publication Details
- Journal of clinical sleep medicine, Vol.7(5 Suppl), pp.S38-S42
- Academic Unit
- Biomedical Sciences, Department of; Integrative Physiology and Neuroscience, Department of
- Publisher
- United States
- Grant note
- NS 31453 / NINDS NIH HHS R01 NS025378 / NINDS NIH HHS HL104874 / NHLBI NIH HHS HD 36520 / NICHD NIH HHS R13 HL104874 / NHLBI NIH HHS NS 25378 / NINDS NIH HHS
- Identifiers
- 99900547037801842
- Language
- English
- Resource Type
- Journal article