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@ARTICLE{Elmenhorst:829311,
author = {Elmenhorst, David and Elmenhorst, Eva-Maria and Hennecke,
Eva and Kroll, Tina and Matusch, Andreas and Aeschbach,
Daniel and Bauer, Andreas},
title = {{R}ecovery sleep after extended wakefulness restores
elevated {A} 1 adenosine receptor availability in the human
brain},
journal = {Proceedings of the National Academy of Sciences of the
United States of America},
volume = {114},
number = {16},
issn = {1091-6490},
address = {Washington, DC},
publisher = {National Acad. of Sciences},
reportid = {FZJ-2017-03031},
pages = {4243-4248/201614677},
year = {2017},
abstract = {Adenosine and functional A1 adenosine receptor (A1AR)
availability are supposed to mediate sleep–wake regulation
and cognitive performance. We hypothesized that cerebral
A1AR availability after an extended wake period decreases to
a well-rested state after recovery sleep. [18F]CPFPX
positron emission tomography was used to quantify A1AR
availability in 15 healthy male adults after 52 h of sleep
deprivation and following 14 h of recovery sleep. Data were
additionally compared with A1AR values after 8 h of baseline
sleep from an earlier dataset. Polysomnography, cognitive
performance, and sleepiness were monitored. Recovery from
sleep deprivation was associated with a decrease in A1AR
availability in several brain regions, ranging from $11\%$
(insula) to $14\%$ (striatum). A1AR availabilities after
recovery did not differ from baseline sleep in the control
group. The degree of performance impairment, sleepiness, and
homeostatic sleep-pressure response to sleep deprivation
correlated negatively with the decrease in A1AR
availability. Sleep deprivation resulted in a higher A1AR
availability in the human brain. The increase that was
observed after 52 h of wakefulness was restored to control
levels during a 14-h recovery sleep episode. Individuals
with a large increase in A1AR availability were more
resilient to sleep-loss effects than those with a subtle
increase. This pattern implies that differences in
endogenous adenosine and A1AR availability might be causal
for individual responses to sleep loss.},
cin = {INM-2},
ddc = {000},
cid = {I:(DE-Juel1)INM-2-20090406},
pnm = {571 - Connectivity and Activity (POF3-571)},
pid = {G:(DE-HGF)POF3-571},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000399387400069},
pubmed = {pmid:28373571},
doi = {10.1073/pnas.1614677114},
url = {https://juser.fz-juelich.de/record/829311},
}