Journal article

cGMP-dependent protein kinase type I is implicated in the regulation of the timing and quality of sleep and wakefulness

  • Langmesser, Sonja Division of Biochemistry, Department of Medicine, University of Fribourg, Switzerland
  • Franken, Paul Center for Integrative Genomics, University of Lausanne, Switzerland
  • Feil, Susanne Interfakultäres Institut für Biochemie, Universität Tübingen, Tübingen, Germany
  • Emmenegger, Yann Center for Integrative Genomics, University of Lausanne, Switzerland
  • Albrecht, Urs Division of Biochemistry, Department of Medicine, University of Fribourg, Switzerland
  • Feil, Robert Interfakultäres Institut für Biochemie, Universität Tübingen, Tübingen, Germany
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    21.01.2009
Published in:
  • PLoS ONE. - 2009, vol. 4, no. 1, p. e4238
English Many effects of nitric oxide (NO) are mediated by the activation of guanylyl cyclases and subsequent production of the second messenger cyclic guanosine-3′,5′-monophosphate (cGMP). cGMP activates cGMP-dependent protein kinases (PRKGs), which can therefore be considered downstream effectors of NO signaling. Since NO is thought to be involved in the regulation of both sleep and circadian rhythms, we analyzed these two processes in mice deficient for cGMP-dependent protein kinase type I (PRKG1) in the brain. Prkg1 mutant mice showed a strikingly altered distribution of sleep and wakefulness over the 24 hours of a day as well as reductions in rapid-eye-movement sleep (REMS) duration and in non-REM sleep (NREMS) consolidation, and their ability to sustain waking episodes was compromised. Furthermore, they displayed a drastic decrease in electroencephalogram (EEG) power in the delta frequency range (1–4 Hz) under baseline conditions, which could be normalized after sleep deprivation. In line with the re-distribution of sleep and wakefulness, the analysis of wheel-running and drinking activity revealed more rest bouts during the activity phase and a higher percentage of daytime activity in mutant animals. No changes were observed in internal period length and phase-shifting properties of the circadian clock while chi-squared periodogram amplitude was significantly reduced, hinting at a less robust oscillator. These results indicate that PRKG1 might be involved in the stabilization and output strength of the circadian oscillator in mice. Moreover, PRKG1 deficiency results in an aberrant pattern, and consequently a reduced quality, of sleep and wakefulness, possibly due to a decreased wake-promoting output of the circadian system impinging upon sleep.
Faculty
Faculté des sciences et de médecine
Department
Département de Biologie
Language
  • English
Classification
Biology, life sciences
License
License undefined
Identifiers
Persistent URL
https://folia.unifr.ch/unifr/documents/301281
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