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

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 Garçon, Mari Kaneko, Yuta Shinohara, Rikuhiro G. Yamada, Shoi Shi, Kazunari Miyamichi, Kenta Sumiyama, Hiroshi Kiyonari, Etsuo A. Susaki and Hiroki R. Ueda ()
Additional contact information
Kazuhiro Kon: The University of Tokyo
Koji L. Ode: The University of Tokyo
Tomoyuki Mano: The University of Tokyo
Hiroshi Fujishima: RIKEN Center for Biosystems Dynamics Research (BDR)
Riina R. Takahashi: The University of Tokyo
Daisuke Tone: The University of Tokyo
Chika Shimizu: RIKEN Center for Biosystems Dynamics Research (BDR)
Shinnosuke Shiono: The University of Tokyo
Saori Yada: The University of Tokyo
Kyoko Matsuzawa: RIKEN Center for Biosystems Dynamics Research (BDR)
Shota Y. Yoshida: The University of Tokyo
Junko Yoshida Garçon: RIKEN Center for Biosystems Dynamics Research (BDR)
Mari Kaneko: Chuou-ku
Yuta Shinohara: RIKEN Center for Biosystems Dynamics Research (BDR)
Rikuhiro G. Yamada: RIKEN Center for Biosystems Dynamics Research (BDR)
Shoi Shi: The University of Tokyo
Kazunari Miyamichi: Chuou-ku
Kenta Sumiyama: RIKEN Center for Biosystems Dynamics Research (BDR)
Hiroshi Kiyonari: Chuou-ku
Etsuo A. Susaki: The University of Tokyo
Hiroki R. Ueda: The University of Tokyo

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: 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.

Date: 2024
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DOI: 10.1038/s41467-024-50168-5

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