Journal
JOURNAL OF NEUROCHEMISTRY
Volume 116, Issue 2, Pages 260-272Publisher
WILEY
DOI: 10.1111/j.1471-4159.2010.07100.x
Keywords
adenosine; cholinergic basal forebrain; nitric oxide; frontal cortex; inducible nitric oxide synthase; sleep homeostasis
Categories
Funding
- Department of Veterans Affairs
- SRSF
- National Institute of Mental Health [NIMH39683]
- Academy of Finland
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH039683] Funding Source: NIH RePORTER
- Veterans Affairs [I01BX001404] Funding Source: NIH RePORTER
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P>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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