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; Hiroki R. Ueda

doi:10.1038/s41467-024-50168-5

NeuroscienceNature CommunicationsJul 18, 2024

Peer-reviewed journal article

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

Kazuhiro Kon iD, Koji L. Ode iD, Tomoyuki Mano iD, Hiroshi Fujishima iD, Riina R. Takahashi, Daisuke Tone, Chika Shimizu, Shinnosuke Shiono, Saori Yada iD, Kyoko Matsuzawa, Shota Y. Yoshida iD, Junko Yoshida Garçon, Mari Kaneko iD, Yuta Shinohara, Rikuhiro G. Yamada iD, Shoi Shi iD, Kazunari Miyamichi iD, Kenta Sumiyama iD, Hiroshi Kiyonari iD, Etsuo A. Susaki iD, Hiroki R. Ueda iD

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. We show here that CaMKII-dependent activity control of parvalbumin (PV)-expressing cortical neurons is involved in sleep homeostasis regulation. 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. 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.

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