Altered circadian activity rhythms and sleep in mice devoid of prion protein

I Tobler, S E Gaus, T Deboer, P Achermann, M Fischer, T Rülicke, M Moser, B Oesch, P A McBride, Jean Manson

Research output: Contribution to journalArticlepeer-review

Abstract

There is a wealth of data supporting a central role for the prion protein (PrP) in the neurodegenerative prion diseases of both humans and other species, yet the normal function of PrP, which is expressed at the cell surface of neurons and glial cells, is unknown. It has been speculated that neuropathology may be due to loss of normal function of PrP. Here we show that in mice devoid of PrP there is an alteration in both circadian activity rhythms and patterns. To our knowledge, this is the first null mutation that has been shown to affect sleep regulation and our results indicate that at least one of the inherited prion diseases, fatal familial insomnia, where there is a profound alteration in sleep and the daily rhythms of many hormones, may be related to the normal function of the prion protein.
Original languageEnglish
Pages (from-to)639-42
Number of pages4
JournalNature
Volume380
Issue number6575
DOIs
Publication statusPublished - Apr 1996

Keywords

  • Animals
  • Circadian Rhythm/genetics
  • Circadian Rhythm/physiology
  • Mice
  • Mice, Inbred C57BL
  • Motor Activity
  • Mutation
  • Prion Diseases/genetics
  • Prion Diseases/physiopathology
  • Prions/genetics
  • Sleep/genetics
  • Sleep/physiology

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