Elmenhorst, David
[VerfasserIn];
Elmenhorst, Eva-Maria
[VerfasserIn];
Hennecke, Eva
[VerfasserIn];
Kroll, Tina
[VerfasserIn];
Matusch, Andreas
[VerfasserIn];
Aeschbach, Daniel
[VerfasserIn];
Bauer, Andreas
[VerfasserIn]
Recovery sleep after extended wakefulness restores elevated A 1 adenosine receptor availability in the human brain
Sie können Bookmarks mittels Listen verwalten, loggen Sie sich dafür bitte in Ihr SLUB Benutzerkonto ein.
Medientyp:
E-Artikel
Titel:
Recovery sleep after extended wakefulness restores elevated A 1 adenosine receptor availability in the human brain
Beteiligte:
Elmenhorst, David
[VerfasserIn];
Elmenhorst, Eva-Maria
[VerfasserIn];
Hennecke, Eva
[VerfasserIn];
Kroll, Tina
[VerfasserIn];
Matusch, Andreas
[VerfasserIn];
Aeschbach, Daniel
[VerfasserIn];
Bauer, Andreas
[VerfasserIn]
Erschienen:
National Acad. of Sciences, 2017
Erschienen in:Proceedings of the National Academy of Sciences of the United States of America 114(16), 4243-4248/201614677 (2017). doi:10.1073/pnas.1614677114
Sprache:
Englisch
DOI:
https://doi.org/10.1073/pnas.1614677114
ISSN:
0027-8424;
1091-6490
Entstehung:
Anmerkungen:
Diese Datenquelle enthält auch Bestandsnachweise, die nicht zu einem Volltext führen.
Beschreibung:
Adenosine and functional A1 adenosine receptor (A1AR) availability are supposed to mediate sleep–wake regulation and cognitive performance. We hypothesized that cerebral A1AR availability after an extended wake period decreases to a well-rested state after recovery sleep. [18F]CPFPX positron emission tomography was used to quantify A1AR availability in 15 healthy male adults after 52 h of sleep deprivation and following 14 h of recovery sleep. Data were additionally compared with A1AR values after 8 h of baseline sleep from an earlier dataset. Polysomnography, cognitive performance, and sleepiness were monitored. Recovery from sleep deprivation was associated with a decrease in A1AR availability in several brain regions, ranging from 11% (insula) to 14% (striatum). A1AR availabilities after recovery did not differ from baseline sleep in the control group. The degree of performance impairment, sleepiness, and homeostatic sleep-pressure response to sleep deprivation correlated negatively with the decrease in A1AR availability. Sleep deprivation resulted in a higher A1AR availability in the human brain. The increase that was observed after 52 h of wakefulness was restored to control levels during a 14-h recovery sleep episode. Individuals with a large increase in A1AR availability were more resilient to sleep-loss effects than those with a subtle increase. This pattern implies that differences in endogenous adenosine and A1AR availability might be causal for individual responses to sleep loss.