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@INPROCEEDINGS{Elmenhorst:186610,
      author       = {Elmenhorst, David and Elmenhorst, E. M. and Kroll, Tina and
                      Matusch, Andreas and Aeschbach, D. and Bauer, Andreas},
      title        = {{I}mpact of recovery sleep after sleep deprivation on
                      cerebral {A}1 adenosine receptor density},
      reportid     = {FZJ-2015-00683},
      year         = {2014},
      abstract     = {Impact of recovery sleep after sleep deprivation on
                      cerebral A1 adenosine receptor densityElmenhorst D1,
                      Elmenhorst EM2, Kroll T1, Matusch A1 Aeschbach D2 and Bauer
                      A1,3 1 Forschungszentrum Jülich, Institute of Neuroscience
                      and Medicine 2, Jülich, Germany, 2 German Aerospace Center,
                      Institute of aerospace medicine, Cologne Germany, 3 Heinrich
                      Heine University Düsseldorf, Medical Faculty, Neurological
                      Department, Düsseldorf, Germany Objectives: Sleep loss
                      triggers a reaction of the homeostatic sleep regulatory
                      system in which adenosine is believed to play a key role.
                      The brain adenosine concentration increases during
                      wakefulness thereby inducing sleepiness [1]. If wakefulness
                      is extended by sleep deprivation, this increase is
                      accompanied by an up-regulation of adenosine receptor
                      density [2].Previously, we found in subjects deprived of
                      sleep for 28 hours, an increase of the distribution volume
                      (VT) of the highly selective A1 adenosine receptor (A1AR)
                      radioligand 18F CPFPX in a region-specific pattern in
                      several brain regions (maximum: orbitofrontal cortex
                      $15.3\%,$ p=0.014, n=12). Whereas there were no significant
                      changes $(1.5\%)$ in a control group (n=10) with regular
                      sleep between both scans [2].The objective of the current
                      study was to investigate if an extension of the wake period
                      to 58 hours leads to a further increase of A1AR densities
                      and if subsequent recovery sleep restores baseline levels of
                      receptor densities.Methods: 15 healthy male volunteers
                      participated in a dynamic 18F CPFPX bolus/infusions-PET
                      study with blood sampling and metabolite correction.
                      Subjects were scanned after 58 hours of sustained
                      wakefulness and after 14 hours of recovery sleep at the same
                      time of day on consecutive days under identical
                      conditions.Regional VT were determined by calculating the
                      tissue to plasma ratio during the steady state
                      phase.Results: The distribution volumes after sleep
                      deprivation (e.g. VT=0.83, orbitofrontal cortex) were found
                      to be significantly higher than after the recovery sleep
                      condition in all (sub)cortical regions investigated
                      $(10-14\%,$ p=0.001-0.008). Compared to the baseline group
                      of the preceding experiment (VT=0.73, n=22) the receptor
                      density after recovery sleep (VT=0.72) was not significantly
                      different. Conclusions: This study demonstrates that a
                      single night of recovery sleep returns the increased A1AR
                      availability in the human brain after prolonged sleep
                      deprivation back to the level of normal sleeping controls.
                      These findings support the general hypothesis of an increase
                      in synaptic strength during wakefulness and downscaling
                      during normal sleep as a maintenance mechanism of synaptic
                      functionality. Research support: References: [1]
                      Porkka-Heiskanen et al. 1997 Science
                      276:1265–1268[2]Elmenhorst D et al. J Neuroscience 2007;
                      27(9):2410 –2415},
      month         = {May},
      date          = {2014-05-21},
      organization  = {10th International Symposium on
                       Functional NeuroReceptor Mapping of the
                       Living Brain, Amsterdam (The
                       Netherlands), 21 May 2014 - 24 May
                       2014},
      cin          = {INM-2},
      cid          = {I:(DE-Juel1)INM-2-20090406},
      pnm          = {333 - Pathophysiological Mechanisms of Neurological and
                      Psychiatric Diseases (POF2-333) / 89571 - Connectivity and
                      Activity (POF2-89571)},
      pid          = {G:(DE-HGF)POF2-333 / G:(DE-HGF)POF2-89571},
      typ          = {PUB:(DE-HGF)1},
      url          = {https://juser.fz-juelich.de/record/186610},
}