Journal Article PreJuSER-3639

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Sleep deprivation increases A1 adenosine receptor density in the rat brain.

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2009
Elsevier Amsterdam

Brain research 1258, 53 - 58 () [10.1016/j.brainres.2008.12.056]

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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.

Keyword(s): Adenosine A1 Receptor Antagonists (MeSH) ; Analysis of Variance (MeSH) ; Animals (MeSH) ; Autoradiography (MeSH) ; Brain: metabolism (MeSH) ; Circadian Rhythm (MeSH) ; Male (MeSH) ; Rats (MeSH) ; Rats, Sprague-Dawley (MeSH) ; Receptor, Adenosine A1: metabolism (MeSH) ; Sleep: physiology (MeSH) ; Sleep Deprivation: metabolism (MeSH) ; Tritium (MeSH) ; Xanthines: metabolism (MeSH) ; 8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine ; Adenosine A1 Receptor Antagonists ; Receptor, Adenosine A1 ; Xanthines ; Tritium ; J ; Adenosine A(1) receptor (auto) ; Receptor autoradiography (auto) ; [3H]CPFPX (auto) ; Sleep deprivation (auto) ; Sleep homeostasis (auto) ; Rat (auto)

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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).

Contributing Institute(s):
  1. Molekulare Organisation des Gehirns (INM-2)
Research Program(s):
  1. Funktion und Dysfunktion des Nervensystems (P33)

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 Record created 2012-11-13, last modified 2018-02-08



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