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@INBOOK{Elmenhorst:151761,
      author       = {Elmenhorst, David and Bier, Dirk and Holschbach, Marcus and
                      Bauer, Andreas},
      title        = {{I}maging of {A}denosine {R}eceptors; {C}hapter 7},
      address      = {Berlin, Heidelberg},
      publisher    = {Springer Berlin Heidelberg},
      reportid     = {FZJ-2014-01650},
      isbn         = {978-3-642-42013-9},
      pages        = {181-198},
      year         = {2014},
      comment      = {PET and SPECT of Neurobiological Systems},
      booktitle     = {PET and SPECT of Neurobiological
                       Systems},
      abstract     = {Adenosine is a fundamental molecule of life. It is a part
                      of the DNA and the main degradation product of the central
                      currency of energy metabolism in humans and animals –
                      adenosine triphosphate (ATP). Under pathological conditions
                      like hypoxia, the adenosine concentration can rise
                      severalfold – up to micromolar concentrations. The net
                      effect of adenosine on excitable tissue is inhibitory
                      affecting the release of classical neurotransmitters like
                      glutamate, GABA (gamma-aminobutyric acid), and dopamine. The
                      widely used neurostimulant caffeine exerts its effects as an
                      antagonist at adenosine receptors. Four different types of
                      adenosine receptors have been described in mammals: A1, A2A,
                      A2B, and A3 which are all G-protein-coupled receptors. Over
                      the last 25 years, adenosine receptor ligands, agonists as
                      well as antagonists, have emerged as a class of useful
                      therapeutics. For the A1 and A2A subtypes several antagonist
                      radioligands have been used successfully for PET imaging in
                      humans and animals especially for the brain.},
      cin          = {INM-2 / INM-5},
      cid          = {I:(DE-Juel1)INM-2-20090406 / I:(DE-Juel1)INM-5-20090406},
      pnm          = {333 - Pathophysiological Mechanisms of Neurological and
                      Psychiatric Diseases (POF2-333)},
      pid          = {G:(DE-HGF)POF2-333},
      typ          = {PUB:(DE-HGF)7},
      doi          = {10.1007/978-3-642-42014-6_7},
      url          = {https://juser.fz-juelich.de/record/151761},
}