Source:http://linkedlifedata.com/resource/pubmed/id/21062286
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001443,
umls-concept:C0006104,
umls-concept:C0028128,
umls-concept:C0035820,
umls-concept:C0037313,
umls-concept:C0040223,
umls-concept:C0132555,
umls-concept:C0205263,
umls-concept:C0234451,
umls-concept:C0392747,
umls-concept:C0443172,
umls-concept:C0750729,
umls-concept:C1298908,
umls-concept:C1517945,
umls-concept:C1707310
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pubmed:issue |
2
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pubmed:dateCreated |
2010-12-20
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pubmed:abstractText |
Both adenosine and nitric oxide (NO) are known for their role in sleep homeostasis, with the basal forebrain (BF) wakefulness center as an important site of action. Previously, we reported a cascade of homeostatic events, wherein sleep deprivation (SD) induces the production of inducible nitric oxide synthase (iNOS)-dependent NO in BF, leading to enhanced release of extracellular adenosine. In turn, increased BF adenosine leads to enhanced sleep intensity, as measured by increased non-rapid eye movement sleep EEG delta activity. However, the presence and time course of similar events in cortex has not been studied, although a frontal cortical role for the increase in non-rapid eye movement recovery sleep EEG delta power is known. Accordingly, we performed simultaneous hourly microdialysis sample collection from BF and frontal cortex (FC) during 11 h SD. We observed that both areas showed sequential increases in iNOS and NO, followed by increases in adenosine. BF increases began at 1 h SD, whereas FC increases began at 5 h SD. iNOS and Fos-double labeling indicated that iNOS induction occurred in BF and FC wake-active neurons. These data support the role of BF adenosine and NO in sleep homeostasis and indicate the temporal and spatial sequence of sleep homeostatic cascade for NO and adenosine.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1471-4159
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pubmed:author | |
pubmed:copyrightInfo |
© 2010 The Authors. Journal of Neurochemistry © 2010 International Society for Neurochemistry.
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pubmed:issnType |
Electronic
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pubmed:volume |
116
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
260-72
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pubmed:dateRevised |
2011-5-11
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pubmed:meshHeading |
pubmed-meshheading:21062286-Adenosine,
pubmed-meshheading:21062286-Animals,
pubmed-meshheading:21062286-Cerebral Cortex,
pubmed-meshheading:21062286-Electroencephalography,
pubmed-meshheading:21062286-Homeostasis,
pubmed-meshheading:21062286-Male,
pubmed-meshheading:21062286-Nitric Oxide,
pubmed-meshheading:21062286-Nitric Oxide Synthase Type II,
pubmed-meshheading:21062286-Prosencephalon,
pubmed-meshheading:21062286-Rats,
pubmed-meshheading:21062286-Rats, Wistar,
pubmed-meshheading:21062286-Sleep Deprivation,
pubmed-meshheading:21062286-Sleep Stages,
pubmed-meshheading:21062286-Time Factors
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pubmed:year |
2011
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pubmed:articleTitle |
The time course of adenosine, nitric oxide (NO) and inducible NO synthase changes in the brain with sleep loss and their role in the non-rapid eye movement sleep homeostatic cascade.
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pubmed:affiliation |
Laboratory of Neuroscience, Department of Psychiatry, VA Boston Healthcare System and Harvard Medical School, West Roxbury, Massachusetts, USA. anna_kalinchuk@hms.harvard.edu
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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