Dementia Japan34: 154-162, 2020

Ca²⁺-dependent sleep control in mammals

Koji L. Ode¹⁾, Hiroki R. Ueda¹⁾²⁾

¹⁾Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo
²⁾Laboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research

Sleep is fundamental to the functioning of the central nervous system.　However, the mechanism underlying the homeostasis of sleep remains unclear.　Several lines of evidence indicate that cortical neuron assemblies have a unique property that elicits a firing pattern called slow oscillation, which is observed in the NREM sleep.　Genetic studies showed that ion channels and pumps potentially involved in the slow oscillation regulate the sleep duration or sleep depth.　In addition, several neuronal kinases were shown to promote sleep, and conversely, the phosphoproteomics profile of synaptic protein is dynamically altered by the sleep-wake cycle.　Interestingly, many of these sleep-controlling proteins are involved in the calcium signaling of neurons, suggesting that the calcium and downstream phosphorylation signaling inside the neuron encode the sleep homeostasis.

Address correspondence to Dr. Hiroki R. Ueda, Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo（7-3-1 Hongo, Bunkyo-Ku, Tokyo 113-0033, Japan）