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

Autor: Kon K; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.; Kennedy Krieger Institute, Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA., Ode KL; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan., Mano T; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan.; Department of Information Physics and Computing, Graduate School of Information Science and Technology, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.; Computational Neuroethology Unit, Okinawa Institute of Science and Technology, Onna, Okinawa, Japan., Fujishima H; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan.; Department of Systems Biology, Institute of Life Science, Kurume University, Kurume, Fukuoka, Japan., Takahashi RR; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan., Tone D; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan., Shimizu C; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan., Shiono S; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan., Yada S; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.; International Institute for Integrative Sleep Medicine (IIIS), University of Tsukuba, Tsukuba, Ibaraki, Japan., Matsuzawa K; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan., Yoshida SY; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan., Yoshida Garçon J; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan.; Department of Molecular Embryology, Research Institute, Osaka Women's and Children's Hospital, Izumi, Osaka, Japan., Kaneko M; Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Biosystems Dynamics Research (BDR), Chuou-ku, Kobe, Hyogo, Japan., Shinohara Y; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan.; Division of Molecular Psychoimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan., Yamada RG; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan.; Department of Systems Biology, Institute of Life Science, Kurume University, Kurume, Fukuoka, Japan., Shi S; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan.; International Institute for Integrative Sleep Medicine (IIIS), University of Tsukuba, Tsukuba, Ibaraki, Japan., Miyamichi K; Laboratory for Comparative Connectomics, RIKEN Center for Biosystems Dynamics Research (BDR), Chuou-ku, Kobe, Hyogo, Japan., Sumiyama K; Laboratory for Mouse Genetic Engineering, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan.; Laboratory of Animal Genetics and Breeding, Graduate School of Bioagricultural Sciences, Nagoya University, Chikusa-ku, Nagoya, Japan., Kiyonari H; Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Biosystems Dynamics Research (BDR), Chuou-ku, Kobe, Hyogo, Japan., Susaki EA; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan.; Department of Biochemistry and Systems Biomedicine, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan., Ueda HR; Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan. uedah-tky@umin.ac.jp.; Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research (BDR), Suita, Osaka, Japan. uedah-tky@umin.ac.jp.; Department of Information Physics and Computing, Graduate School of Information Science and Technology, The University of Tokyo, Bunkyo-ku, Tokyo, Japan. uedah-tky@umin.ac.jp.; Department of Systems Biology, Institute of Life Science, Kurume University, Kurume, Fukuoka, Japan. uedah-tky@umin.ac.jp.
Jazyk: angličtina
Zdroj: Nature communications [Nat Commun] 2024 Jul 18; Vol. 15 (1), pp. 6054. Date of Electronic Publication: 2024 Jul 18.
DOI: 10.1038/s41467-024-50168-5
Abstrakt: 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 Ca 2+ /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.
(© 2024. The Author(s).)
Databáze: MEDLINE
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