IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v15y2024i1d10.1038_s41467-024-50168-5.html
   My bibliography  Save this article

Cortical parvalbumin neurons are responsible for homeostatic sleep rebound through CaMKII activation

Author

Listed:
  • Kazuhiro Kon

    (The University of Tokyo
    Johns Hopkins University School of Medicine)

  • Koji L. Ode

    (The University of Tokyo
    RIKEN Center for Biosystems Dynamics Research (BDR))

  • Tomoyuki Mano

    (The University of Tokyo
    RIKEN Center for Biosystems Dynamics Research (BDR)
    The University of Tokyo
    Okinawa Institute of Science and Technology)

  • Hiroshi Fujishima

    (RIKEN Center for Biosystems Dynamics Research (BDR)
    Kurume University)

  • Riina R. Takahashi

    (The University of Tokyo)

  • Daisuke Tone

    (The University of Tokyo
    RIKEN Center for Biosystems Dynamics Research (BDR))

  • Chika Shimizu

    (RIKEN Center for Biosystems Dynamics Research (BDR))

  • Shinnosuke Shiono

    (The University of Tokyo)

  • Saori Yada

    (The University of Tokyo
    University of Tsukuba)

  • Kyoko Matsuzawa

    (RIKEN Center for Biosystems Dynamics Research (BDR))

  • Shota Y. Yoshida

    (The University of Tokyo
    RIKEN Center for Biosystems Dynamics Research (BDR))

  • Junko Yoshida Garçon

    (RIKEN Center for Biosystems Dynamics Research (BDR)
    Osaka Women’s and Children’s Hospital)

  • Mari Kaneko

    (Chuou-ku)

  • Yuta Shinohara

    (RIKEN Center for Biosystems Dynamics Research (BDR)
    Hokkaido University)

  • Rikuhiro G. Yamada

    (RIKEN Center for Biosystems Dynamics Research (BDR)
    Kurume University)

  • Shoi Shi

    (The University of Tokyo
    RIKEN Center for Biosystems Dynamics Research (BDR)
    University of Tsukuba)

  • Kazunari Miyamichi

    (Chuou-ku)

  • Kenta Sumiyama

    (RIKEN Center for Biosystems Dynamics Research (BDR)
    Nagoya University)

  • Hiroshi Kiyonari

    (Chuou-ku)

  • Etsuo A. Susaki

    (The University of Tokyo
    RIKEN Center for Biosystems Dynamics Research (BDR)
    Juntendo University Graduate School of Medicine)

  • Hiroki R. Ueda

    (The University of Tokyo
    RIKEN Center for Biosystems Dynamics Research (BDR)
    The University of Tokyo
    Kurume University)

Abstract

The homeostatic regulation of sleep is characterized by rebound sleep after prolonged wakefulness, but the molecular and cellular mechanisms underlying this regulation are still unknown. In this study, we show that Ca2+/calmodulin-dependent protein kinase II (CaMKII)-dependent activity control of parvalbumin (PV)-expressing cortical neurons is involved in homeostatic regulation of sleep in male mice. Prolonged wakefulness enhances cortical PV-neuron activity. Chemogenetic suppression or activation of cortical PV neurons inhibits or induces rebound sleep, implying that rebound sleep is dependent on increased activity of cortical PV neurons. Furthermore, we discovered that CaMKII kinase activity boosts the activity of cortical PV neurons, and that kinase activity is important for homeostatic sleep rebound. Here, we propose that CaMKII-dependent PV-neuron activity represents negative feedback inhibition of cortical neural excitability, which serves as the distributive cortical circuits for sleep homeostatic regulation.

Suggested Citation

  • Kazuhiro Kon & Koji L. Ode & Tomoyuki Mano & Hiroshi Fujishima & Riina R. Takahashi & Daisuke Tone & Chika Shimizu & Shinnosuke Shiono & Saori Yada & Kyoko Matsuzawa & Shota Y. Yoshida & Junko Yoshida, 2024. "Cortical parvalbumin neurons are responsible for homeostatic sleep rebound through CaMKII activation," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-50168-5
    DOI: 10.1038/s41467-024-50168-5
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-024-50168-5
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-024-50168-5?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-50168-5. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.