High-sucrose diet changes sleep architecture and memory function in mice

  • Datum: 12.12.2019
  • Uhrzeit: 12:00 - 13:00
  • Vortragende(r): Yvonne Ritze
  • Department of Medical Psychology and Behavioral Neurobiology, University of Tübingen
  • Ort: Max-Planck-Ring 8
  • Raum: room 203
  • Gastgeber: Peter Dayan
High-sucrose diet changes sleep architecture and memory function in mice

Background: Sleep and metabolism have been shown to be interrelated, but the effect of specific nutrients on sleep and, in particular, their sleep-related contribution to cognitive function has not been assessed. In this regard, the memory-promoting effect of sleep is of foremost interest considering that metabolic and memory impairments, especially in older age, are often associated. Here, we are investigating the effect of a sugar-rich diet on electrophysiological sleep parameters and sleep-mediated memory function in mice.

Methods: Male C57BL6/J mice are fed a diet containing either 30% of liquid sucrose or water and standard chow for eight weeks (n=10 per group). Sleep is electrocorticographically (ECoG) assessed during 24-hour periods at the beginning after four and eight weeks. Animals perform two memory tasks at the end of the dietary intervention, the novel-object and the object-place recognition task. In each task, encoding is followed by a 180-min retention interval of sleep. Exploration of novel vs. versus familiar and object-place combinations is assessed as a measure of memory consolidation.

Results: Analyses of the 24-hour sleep/wake assessment periods indicate that liquid sucrose seems to reduce sleep during the first hour of the inactive (light) phase for total sleep (p<0.01), slow wave sleep (SWS, p<0.01) and rapid eye-movement (REM) sleep (p=0.05) after the eight week feeding period. In addition, the discrimination index during the first minute of the novel- object recognition (NOR) task is reduced in sucrose compared to control mice (p<0.05). Similarly, REM sleep was reduced during the first 120 min of the retention interval (p<0.05). Other sleep phases as well as spindle density and frequency during retention time seem not to be influenced by the high-sucrose diet.

Conclusion: Our data indicate that sucrose-rich in comparison to control diet exerts a change in 24h sleep architecture showing reduced sleep during the first hour of the inactive phase. Learning behavior seems to be impaired during the first minute of the NOR task compared to the control group. Interestingly, also REM sleep is reduced during retention time leading us to the conclusion that the transition from an active to an inactive phase might be changed due to the high-sucrose diet in mice. The reduction of REM sleep might lead to the delay of learning behavior implicating the impaired memory. Further analysis are needed to unravel underlying mechanisms.

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