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| 001 | 150620 | ||
| 005 | 20210129213236.0 | ||
| 037 | _ | _ | |a FZJ-2014-00668 |
| 100 | 1 | _ | |a Elmenhorst, David |0 P:(DE-Juel1)131679 |b 0 |u fzj |e Corresponding author |
| 111 | 2 | _ | |a The XXVIth International Symposium on Cerebral Blood Flow, Metabolism and Function & XIth International Conference on Quantification of Brain Function with PET Xith International Conference on Quantification of Brain Function with PET |c Shanghai |d 2013-05-20 - 2013-05-23 |w China |
| 245 | _ | _ | |a Acute ethanol application increases A1 adenosine receptor availability in the human brain |
| 260 | _ | _ | |c 2013 |
| 336 | 7 | _ | |a Abstract |b abstract |m abstract |0 PUB:(DE-HGF)1 |s 1390469269_10461 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a Conference Paper |0 33 |2 EndNote |
| 336 | 7 | _ | |a Output Types/Conference Abstract |2 DataCite |
| 336 | 7 | _ | |a OTHER |2 ORCID |
| 336 | 7 | _ | |a conferenceObject |2 DRIVER |
| 336 | 7 | _ | |a INPROCEEDINGS |2 BibTeX |
| 520 | _ | _ | |a The fatiguing and sedating effects of alcohol in humans are supposed to be mediated partially by the inhibitory actions of cerebral adenosine, the main degradation product of ATP. Ethanol is known to increase extracellular adenosine several fold in the brain of rats by an increase in adenosine formation and a decrease of adenosine uptake. Interestingly, it has recently been reported that cerebral A1 adenosine receptor (A1AR) availability measured with [11C]MPDX was increased after ethanol exposure in rats. In the present pilot study we investigated the impact of acute ethanol exposure on A1AR availability in the human brain by the use of PET and the highly selective radioligand [18F]CPFPX. This method has been proved suitable for quantifying A1AR densities in the human brain. A bolus plus constant infusion for steady state quantification allows investigating acute drug interactions like the occupancy of A1AR by caffeine.
In this ongoing study we administered 40 g of ethanol (corresponding to 1 L of beer, n=3) or placebo (n=1) during the steady state period of the PET experiment in healthy volunteers. Ethanol was diluted in 1 L of isotonic NaCl solution and infused intravenously between 80 and 110 min of the 140 min PET scan. Blood alcohol concentration peaked individually between 0.65 and 0.98 mg/mL 30 min after start of the infusion. Arterialized venous blood samples were collected to determine the distribution volume (VT) of [18F]CPFPX by calculating the ratio of the concentrations between tissue and plasma during steady state. The timespan of this ratio represented either baseline (60 to 80 min) or ethanol condition (120 and 140 min). The distribution volumes of various cortical and subcortical regions remained basically constant before and after placebo exposure (relative difference 3%). In contrast, distribution volumes in the ethanol group increased quickly by on average 29%.
Our preliminary data exhibit for the first time a rapid increase in cerebral A1AR availability following acute intravenous ethanol application in humans. |
| 536 | _ | _ | |a 333 - Pathophysiological Mechanisms of Neurological and Psychiatric Diseases (POF2-333) |0 G:(DE-HGF)POF2-333 |c POF2-333 |x 0 |f POF II |
| 700 | 1 | _ | |a Matusch, Andreas |0 P:(DE-Juel1)138474 |b 1 |u fzj |
| 700 | 1 | _ | |a Kroll, Tina |0 P:(DE-Juel1)131691 |b 2 |u fzj |
| 700 | 1 | _ | |a Bauer, Andreas |0 P:(DE-Juel1)131672 |b 3 |u fzj |
| 909 | C | O | |o oai:juser.fz-juelich.de:150620 |p VDB |
| 910 | 1 | _ | |a Forschungszentrum Jülich GmbH |0 I:(DE-588b)5008462-8 |k FZJ |b 0 |6 P:(DE-Juel1)131679 |
| 910 | 1 | _ | |a Forschungszentrum Jülich GmbH |0 I:(DE-588b)5008462-8 |k FZJ |b 1 |6 P:(DE-Juel1)138474 |
| 910 | 1 | _ | |a Forschungszentrum Jülich GmbH |0 I:(DE-588b)5008462-8 |k FZJ |b 2 |6 P:(DE-Juel1)131691 |
| 910 | 1 | _ | |a Forschungszentrum Jülich GmbH |0 I:(DE-588b)5008462-8 |k FZJ |b 3 |6 P:(DE-Juel1)131672 |
| 913 | 1 | _ | |a DE-HGF |b Gesundheit |l Funktion und Dysfunktion des Nervensystems |1 G:(DE-HGF)POF2-330 |0 G:(DE-HGF)POF2-333 |2 G:(DE-HGF)POF2-300 |v Pathophysiological Mechanisms of Neurological and Psychiatric Diseases |x 0 |4 G:(DE-HGF)POF |3 G:(DE-HGF)POF2 |
| 914 | 1 | _ | |y 2013 |
| 920 | 1 | _ | |0 I:(DE-Juel1)INM-2-20090406 |k INM-2 |l Molekulare Organisation des Gehirns |x 0 |
| 980 | _ | _ | |a abstract |
| 980 | _ | _ | |a VDB |
| 980 | _ | _ | |a UNRESTRICTED |
| 980 | _ | _ | |a I:(DE-Juel1)INM-2-20090406 |
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