000151761 001__ 151761 000151761 005__ 20210129213544.0 000151761 020__ $$a978-3-642-42013-9 000151761 0247_ $$2doi$$a10.1007/978-3-642-42014-6_7 000151761 037__ $$aFZJ-2014-01650 000151761 1001_ $$0P:(DE-Juel1)131679$$aElmenhorst, David$$b0$$eCorresponding author$$ufzj 000151761 245__ $$aImaging of Adenosine Receptors 000151761 250__ $$aChapter 7 000151761 260__ $$aBerlin, Heidelberg$$bSpringer Berlin Heidelberg$$c2014 000151761 29510 $$aPET and SPECT of Neurobiological Systems 000151761 300__ $$a181-198 000151761 3367_ $$0PUB:(DE-HGF)7$$2PUB:(DE-HGF)$$aContribution to a book$$bcontb$$mcontb$$s1394461532_23332 000151761 3367_ $$2DRIVER$$abookPart 000151761 3367_ $$2ORCID$$aBOOK_CHAPTER 000151761 3367_ $$07$$2EndNote$$aBook Section 000151761 3367_ $$2BibTeX$$aINBOOK 000151761 3367_ $$2DataCite$$aOutput Types/Book chapter 000151761 500__ $$3POF3_Assignment on 2016-02-29 000151761 520__ $$aAdenosine is a fundamental molecule of life. It is a part of the DNA and the main degradation product of the central currency of energy metabolism in humans and animals – adenosine triphosphate (ATP). Under pathological conditions like hypoxia, the adenosine concentration can rise severalfold – up to micromolar concentrations. The net effect of adenosine on excitable tissue is inhibitory affecting the release of classical neurotransmitters like glutamate, GABA (gamma-aminobutyric acid), and dopamine. The widely used neurostimulant caffeine exerts its effects as an antagonist at adenosine receptors. Four different types of adenosine receptors have been described in mammals: A1, A2A, A2B, and A3 which are all G-protein-coupled receptors. Over the last 25 years, adenosine receptor ligands, agonists as well as antagonists, have emerged as a class of useful therapeutics. For the A1 and A2A subtypes several antagonist radioligands have been used successfully for PET imaging in humans and animals especially for the brain. 000151761 536__ $$0G:(DE-HGF)POF2-333$$a333 - Pathophysiological Mechanisms of Neurological and Psychiatric Diseases (POF2-333)$$cPOF2-333$$fPOF II$$x0 000151761 588__ $$aDataset connected to CrossRef Book 000151761 7001_ $$0P:(DE-Juel1)131810$$aBier, Dirk$$b1$$ufzj 000151761 7001_ $$0P:(DE-Juel1)131824$$aHolschbach, Marcus$$b2$$ufzj 000151761 7001_ $$0P:(DE-Juel1)131672$$aBauer, Andreas$$b3$$ufzj 000151761 773__ $$a10.1007/978-3-642-42014-6_7 000151761 8564_ $$uhttp://link.springer.com/chapter/10.1007%2F978-3-642-42014-6_7 000151761 8564_ $$uhttps://juser.fz-juelich.de/record/151761/files/FZJ-2014-01650.pdf$$yRestricted 000151761 909CO $$ooai:juser.fz-juelich.de:151761$$pVDB 000151761 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131679$$aForschungszentrum Jülich GmbH$$b0$$kFZJ 000151761 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131810$$aForschungszentrum Jülich GmbH$$b1$$kFZJ 000151761 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131824$$aForschungszentrum Jülich GmbH$$b2$$kFZJ 000151761 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131672$$aForschungszentrum Jülich GmbH$$b3$$kFZJ 000151761 9132_ $$0G:(DE-HGF)POF3-579H$$1G:(DE-HGF)POF3-570$$2G:(DE-HGF)POF3-500$$aDE-HGF$$bKey Technologies$$lDecoding the Human Brain$$vAddenda$$x0 000151761 9131_ $$0G:(DE-HGF)POF2-333$$1G:(DE-HGF)POF2-330$$2G:(DE-HGF)POF2-300$$3G:(DE-HGF)POF2$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lFunktion und Dysfunktion des Nervensystems$$vPathophysiological Mechanisms of Neurological and Psychiatric Diseases$$x0 000151761 9141_ $$y2014 000151761 9201_ $$0I:(DE-Juel1)INM-2-20090406$$kINM-2$$lMolekulare Organisation des Gehirns$$x0 000151761 9201_ $$0I:(DE-Juel1)INM-5-20090406$$kINM-5$$lNuklearchemie$$x1 000151761 980__ $$acontb 000151761 980__ $$aVDB 000151761 980__ $$aUNRESTRICTED 000151761 980__ $$aI:(DE-Juel1)INM-2-20090406 000151761 980__ $$aI:(DE-Juel1)INM-5-20090406 000151761 981__ $$aI:(DE-Juel1)INM-5-20090406