This title appears in the Scientific Report :
2008
Please use the identifier:
http://dx.doi.org/10.1007/s00259-007-0586-z in citations.
Cerebral A(1) adenosine receptors (A(1)AR) in liver cirrhosis
Cerebral A(1) adenosine receptors (A(1)AR) in liver cirrhosis
The cerebral mechanisms underlying hepatic encephalopathy (HE) are poorly understood. Adenosine, a neuromodulator that pre- and postsynaptically modulates neuronal excitability and release of classical neurotransmitters via A(1) adenosine receptors (A(1)AR), is likely to be involved. The present stu...
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Personal Name(s): | Boy, C. |
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Meyer, P. T. / Kircheis, G. / Holschbach, M. H. / Herzog, H. / Elmenhorst, D. / Kaiser, H. J. / Coenen, H. H. / Häussinger, D. / Zilles, K. / Bauer, A. | |
Contributing Institute: |
Institut für Neurowissenschaften und Biophysik - Medizin; INB-3 JARA-BRAIN; JARA-BRAIN Nuklearchemie; INB-4 |
Published in: | European Journal of Nuclear Medicine and Molecular Imaging, 35 (2008) S. 589 - 597 |
Imprint: |
Heidelberg [u.a.]
Springer-Verl.
2008
|
Physical Description: |
589 - 597 |
PubMed ID: |
18000666 |
DOI: |
10.1007/s00259-007-0586-z |
Document Type: |
Journal Article |
Research Program: |
Funktion und Dysfunktion des Nervensystems |
Series Title: |
European Journal of Nuclear Medicine and Molecular Imaging
35 |
Subject (ZB): | |
Publikationsportal JuSER |
The cerebral mechanisms underlying hepatic encephalopathy (HE) are poorly understood. Adenosine, a neuromodulator that pre- and postsynaptically modulates neuronal excitability and release of classical neurotransmitters via A(1) adenosine receptors (A(1)AR), is likely to be involved. The present study investigates changes of cerebral A(1)AR binding in cirrhotic patients by means of positron emission tomography (PET) and [(18)F]CPFPX, a novel selective A(1)AR antagonist.PET was performed in cirrhotic patients (n = 10) and healthy volunteers (n = 10). Quantification of in vivo receptor density was done by Logan's non-invasive graphical analysis (pons as reference region). The outcome parameter was the apparent binding potential (aBP, proportional to B (max)/K (D)).Cortical and subcortical regions showed lower A(1)AR binding in cirrhotic patients than in controls. The aBP changes reached statistical significance vs healthy controls (p < 0.05, U test with Bonferroni-Holm adjustment for multiple comparisons) in cingulate cortex (-50.0%), precentral gyrus (-40.9%), postcentral gyrus (-38.6%), insular cortex (-38.6%), thalamus (-32.9%), parietal cortex (-31.7%), frontal cortex (-28.6), lateral temporal cortex (-28.2%), orbitofrontal cortex (-27.9%), occipital cortex (-24.6), putamen (-22.7%) and mesial temporal lobe (-22.4%).Regional cerebral adenosinergic neuromodulation is heterogeneously altered in cirrhotic patients. The decrease of cerebral A(1)AR binding may further aggravate neurotransmitter imbalance at the synaptic cleft in cirrhosis and hepatic encephalopathy. Different pathomechanisms may account for these alterations including decrease of A(1)AR density or affinity, as well as blockade of the A(1)AR by endogenous adenosine or exogenous xanthines. |