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@ARTICLE{Elmenhorst:12002,
      author       = {Elmenhorst, D. and Garibotto, V. and Prescher, A. and
                      Bauer, A.},
      title        = {{A}denosine {A}(1) receptors in human brain and transfected
                      {CHO} cells: inhibition of [(3){H}]{CPFPX} binding by
                      adenosine and caffeine},
      journal      = {Neuroscience letters},
      volume       = {487},
      issn         = {0304-3940},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {PreJuSER-12002},
      pages        = {415 - 420},
      year         = {2011},
      note         = {This work was supported by 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).},
      abstract     = {In vivo imaging of adenosine function has become feasible
                      with the specific A(1) adenosine receptor ligand
                      [(18)F]CPFPX and positron emission tomography (PET). It is,
                      however, still an open question whether [(18)F]CPFPX is
                      displaceable by endogenous adenosine, which would allow to
                      detect activity-dependent adenosine release in vivo. We used
                      the tritiated analog of [(18)F]CPFPX, [(3)H]CPFPX, to
                      quantify A(1) adenosine receptors (A(1)AR) in grey matter
                      tissue homogenates of four human brains and A(1)AR
                      transfected Chinese hamster ovary cells, respectively.
                      Saturation binding experiments in the presence of a stable
                      GTP analog revealed a dissociation constant (K(D)) of
                      2.4±0.5nM. The unselective endogenous A(1)AR agonist
                      adenosine and the antagonist caffeine displaced specific
                      [(3)H]CPFPX binding completely at high doses. Concentrations
                      sufficient to inhibit $50\%$ of binding (IC(50)) were
                      6.9±2.7μM for adenosine and 148±15.4μM for caffeine.
                      Respective inhibition constants (K(i)) were 2.8±0.9μM and
                      61.4±11.2μM.The present report supports the possibility of
                      studying acute effects of adenosine and caffeine in vivo
                      with [(18)F]CPFPX and PET. Pathophysiological conditions
                      like hypoxia which increase endogenous adenosine
                      concentrations several folds might interfere with in vivo
                      [(18)F]CPFPX binding. Caffeine intake previous to the
                      investigation should be considered as a confounding factor
                      regarding the determination of receptor densities with
                      [(18)F]CPFPX and PET.},
      keywords     = {Adenosine: pharmacokinetics / Animals / Binding,
                      Competitive / Brain: radionuclide imaging / CHO Cells /
                      Caffeine: pharmacokinetics / Cricetinae / Cricetulus /
                      Humans / Positron-Emission Tomography: methods /
                      Radiopharmaceuticals: pharmacokinetics / Receptor, Adenosine
                      A1: metabolism / Transfection / Tritium: diagnostic use /
                      Xanthines: pharmacokinetics /
                      8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine (NLM
                      Chemicals) / Radiopharmaceuticals (NLM Chemicals) /
                      Receptor, Adenosine A1 (NLM Chemicals) / Xanthines (NLM
                      Chemicals) / Tritium (NLM Chemicals) / Caffeine (NLM
                      Chemicals) / Adenosine (NLM Chemicals) / J (WoSType)},
      cin          = {INM-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406},
      pnm          = {Funktion und Dysfunktion des Nervensystems (FUEK409) /
                      89571 - Connectivity and Activity (POF2-89571)},
      pid          = {G:(DE-Juel1)FUEK409 / G:(DE-HGF)POF2-89571},
      shelfmark    = {Neurosciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21056087},
      UT           = {WOS:000286697400035},
      doi          = {10.1016/j.neulet.2010.10.068},
      url          = {https://juser.fz-juelich.de/record/12002},
}