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@ARTICLE{Elmenhorst:3639,
author = {Elmenhorst, D. and Basheer, R. and McCarley, R.W. and
Bauer, A.},
title = {{S}leep deprivation increases {A}1 adenosine receptor
density in the rat brain.},
journal = {Brain research},
volume = {1258},
issn = {0006-8993},
address = {Amsterdam},
publisher = {Elsevier},
reportid = {PreJuSER-3639},
pages = {53 - 58},
year = {2009},
note = {Sabine Wilms, Markus Cremer and Ramkumar Karthikeyan are
gratefully acknowledged for excellent technical assistance
and Marcus Holschbach for providing Tritium labeled
CPFPX.This work was supported by the Department of Veterans
Affairs Medical Research Service Award to RB, the National
Institute of Mental Health (NIMH39683) to RWM, the Heinrich
Hertz Foundation of the Ministry of Science and Technology,
North-Rhine Westfalia, Germany to DE and the German Federal
Ministry of Education and Research (Brain Imaging Center
West, to DE and AB; and Biopharma Initiative-NeuroAllianz,
to AB).},
abstract = {Adenosine, increasing after sleep deprivation and acting
via the A(1) adenosine receptor (A(1)AR), is likely a key
factor in the homeostatic control of sleep. This study
examines the impact of sleep deprivation on A(1)AR density
in different parts of the rat brain with [(3)H]CPFPX
autoradiography. Binding of [(3)H]CPFPX was significantly
increased in parietal cortex (PAR) $(7\%),$ thalamus
$(11\%)$ and caudate-putamen $(9\%)$ after 24 h of sleep
deprivation compared to a control group with an undisturbed
circadian sleep-wake rhythm. Sleep deprivation of 12 h
changed receptor density regionally between $-5\%$ and
$+9\%$ (motor cortex (M1), statistically significant)
compared to the circadian control group. These results
suggest cerebral A(1)ARs are involved in effects of sleep
deprivation and the regulation of sleep. The increase of
A(1)AR density could serve the purpose of not only
maintaining the responsiveness to increased adenosine levels
but also amplifying the effect of sleep deprivation and is
in line with a sleep-induced homoeostatic reorganization at
the synaptic level.},
keywords = {Adenosine A1 Receptor Antagonists / Analysis of Variance /
Animals / Autoradiography / Brain: metabolism / Circadian
Rhythm / Male / Rats / Rats, Sprague-Dawley / Receptor,
Adenosine A1: metabolism / Sleep: physiology / Sleep
Deprivation: metabolism / Tritium / Xanthines: metabolism /
8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine (NLM
Chemicals) / Adenosine A1 Receptor Antagonists (NLM
Chemicals) / Receptor, Adenosine A1 (NLM Chemicals) /
Xanthines (NLM Chemicals) / Tritium (NLM Chemicals) / J
(WoSType)},
cin = {INM-2},
ddc = {150},
cid = {I:(DE-Juel1)INM-2-20090406},
pnm = {Funktion und Dysfunktion des Nervensystems},
pid = {G:(DE-Juel1)FUEK409},
shelfmark = {Neurosciences},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:19146833},
UT = {WOS:000264536100006},
doi = {10.1016/j.brainres.2008.12.056},
url = {https://juser.fz-juelich.de/record/3639},
}