Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-8-9
pubmed:abstractText
Sleep need is characterized by the level of slow-wave activity (SWA) and increases with time spent awake. The molecular nature of this sleep homeostatic process is practically unknown. Here, we show that intracerebroventricular administration of the neuropeptide, cortistatin (CST-14), enhances EEG synchronization by selectively promoting deep slow-wave sleep (SWS) during both the light and dark period in rats. CST-14 also increases the level of slow-wave activity (SWA) within deep SWS during the first two hours following CST-14 administration. Steady-state levels of preprocortistatin mRNA oscillate during the light:dark cycle and are four-fold higher upon total 24-h sleep deprivation, returning progressively to normal levels after eight hours of sleep recovery. Preprocortistatin mRNA is expressed upon sleep deprivation in a particular subset of cortical interneurons that colocalize with c-fos. In contrast, the number of CST-positive cells coexpressing pERK1/2 decreases under sleep deprivation. The capacity of CST-14 to increase SWA, together with preprocortistatin's inverse correlation with time spent in SWS, suggests a potential role in sleep homeostatic processes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
729-38
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Cortistatin promotes and negatively correlates with slow-wave sleep.
pubmed:affiliation
Department of Molecular Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural