Hauptseite > Publikationsdatenbank > Effects of Long-Term Caffeine Consumption on the Adenosine A1 Receptor in the Rat Brain: an In Vivo PET Study with [18F]CPFPX > print

001     848313
005     20210129234053.0
024 7 _ |a 10.1007/s11307-017-1116-4
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024 7 _ |a 1536-1632
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024 7 _ |a 1860-2002
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037 _ _ |a FZJ-2018-03558
082 _ _ |a 610
100 1 _ |a Nabbi, Danje
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245 _ _ |a Effects of Long-Term Caffeine Consumption on the Adenosine A1 Receptor in the Rat Brain: an In Vivo PET Study with [18F]CPFPX
260 _ _ |a Amsterdam [u.a.]
|c 2018
|b Elsevier Science
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520 _ _ |a Purpose- Caffeine, a nonselective antagonist of adenosine receptors, is the most popular psychostimulant worldwide. Recently, a protective role of moderate chronic caffeine consumption against neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease has been discussed. Thus, aim of the present study was an in vivo investigation of effects of long-term caffeine consumption on the adenosine A1 receptor (A1AR) in the rat brain.ProceduresSixteen adult, male rats underwent five positron emission tomography (PET) scans with the highly selective A1AR radioligand [18F]CPFPX in order to determine A1AR availability. After the first baseline PET scan, the animals were assigned to two groups: Caffeine treatment and control group. The caffeine-treated animals received caffeinated tap water (30 mg/kg bodyweight/day, corresponding to 4–5 cups of coffee per day in humans) for 12 weeks. Subsequently, caffeine was withdrawn and repeated PET measurements were performed on day 1, 2, 4, and 7 of caffeine withdrawal. The control animals were measured according to the same time schedule.ResultsAt day 1, after 4.4 h of caffeine withdrawal, a significant decrease (− 34.5%, p < 0.001) of whole brain A1AR availability was observed. Unlike all other investigated brain regions in caffeine-treated rats, the hypothalamus and nucleus accumbens showed no significant intraindividual differences between baseline and first withdrawal PET scan. After approximately 27 h of caffeine withdrawal, the region- and group-specific effects disappeared and A1AR availability settled around baseline.ConclusionsThe present study provides evidence that chronic caffeine consumption does not lead to persistent changes in functional availability of cerebral A1ARs which have previously been associated with neuroprotective effects of caffeine. The acute and region-specific decrease in cerebral A1AR availability directly after caffeine withdrawal is most likely caused by residual amounts of caffeine metabolites disguising an unchanged A1AR expression at this early time-point.
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700 1 _ |a Elmenhorst, David
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700 1 _ |a Oskamp, Angela
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700 1 _ |a Laskowski, Stefanie
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700 1 _ |a Bauer, Andreas
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700 1 _ |a Kroll, Tina
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773 _ _ |a 10.1007/s11307-017-1116-4
|g Vol. 20, no. 2, p. 284 - 291
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|t Molecular imaging & biology
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