2008, Number S2
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Rev Med UV 2008; 8 (S2)
Humoral Regulation of Sleep; Implications for Sleep as an Emergent Use-Dependent Local Process
Krueger JM
Language: English
References: 37
Page: 46-52
PDF size: 465.27 Kb.
ABSTRACT
Sleep is regulated in part by substances that are produced in response to wakefulness cellular activity. These substances in turn induce state changes in neural networks. Several of these sleep regulatory substances are well-characterized and include tumor necrosis factor (TNF), interleukin-1, adenosine, prostaglandin D2, and growth hormone releasing hormone. This review is focused on TNF -sleep mechanisms. ATP co-released during neurotransmission induces the release of TNF from glia via purine P2 receptors. TNF acts directly on neurons to alter membrane potentials and gene expression of adenosine and glutamate receptors. Changes in the number of these receptors on neurons alter the sensitivities of the neurons. Thus the input-output relationships of the networks within which the neurons are located are changed. We posit that these events lead to state oscillations and these changes are thus use-dependent and local. The concept that cortical assemblies such as cortical columns oscillate between states has broad implications for sleep regulation, pathologies and function.
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