Format

Send to

Choose Destination
See comment in PubMed Commons below
Metabolism. 2006 Oct;55(10 Suppl 2):S24-9.

Metabolic mechanism of wakefulness (and hunger) and sleep (and satiety): Role of adenosine triphosphate and hypocretin and other peptides.

Author information

1
Centre National de Recherche Scientifique (CNRS) of the Coll├Ęge de France, Paris 5, France. snicolaidis@laposte.net

Abstract

The concurrent background level of metabolic activity may control state of vigilance, promoting wakefulness (and hunger) when it is low, or sleep (and satiety) when it is high. In a series of experiments, we have shown that sleep is dependent on feeding, but only because of the metabolic consequences of food ingestion. These consequences are sensed by glioneuronal populations (at least in the rostromedial hypothalamus), which probably respond to channel-bound adenosine triphosphate/diphosphate turnover (ischymetric monitoring) rather than to the binding of such downstream molecules as adenosine and cytochrome c oxidase. This basic signal is communicated to the vigilance-controlling centers by a cascade of peptidic and nonpeptidic messengers-messengers that promote wakefulness and hunger, possibly via a hypometabolic action (as in the case of neuropeptide Y or hypocretins), or somnolence and satiety, possibly via a hypermetabolic action (as in the case of leptin or certain serotonergic agents).

PMID:
16979423
DOI:
10.1016/j.metabol.2006.07.009
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center