Kyoto University · Neuroscience
Professor Yu Hayashi's research lab investigates the neural and molecular mechanisms underlying sleep regulation, with a focus on the developmental origins of sleep-regulating neurons, the bidirectional relationship between sleep and mental health, and the systemic signals that link peripheral fatigue to sleep. The lab employs advanced techniques such as chemogenetics, in vivo two-photon microscopy, and genetic screening in model organisms to dissect how brainstem circuits control sleep-wake states and how stress and neurotransmitter systems like dopamine influence sleep architecture. A key theme is understanding the functional and developmental relationships between distinct neuronal populations that govern sleep, wakefulness, and REM sleep.
Figures are computed from collected data and may differ slightly.
Mammalian sleep comprises rapid eye movement (REM) sleep and non-REM (NREM) sleep. To functionally isolate from the complex mixture of neurons populating the brainstem pons those involved in switching between REM and NREM sleep, we chemogenetically manipulated neurons of a specific embryonic cell lineage in mice. We identified excitatory glutamatergic neurons that inhibit REM sleep and promote NREM sleep. These neurons shared a common developmental origin with neurons promoting wakefulness; both
Patients with depression almost inevitably exhibit abnormalities in sleep, such as shortened latency to enter rapid eye movement (REM) sleep and decrease in electroencephalogram delta power during non-REM sleep. Insufficient sleep can be stressful, and the accumulation of stress leads to the deterioration of mental health and contributes to the development of psychiatric disorders. Thus, it is likely that depression and sleep are bidirectionally related, i.e. development of depression contribute
Sleep is generally viewed as a period of recovery, but how the supply of cerebral blood flow (CBF) changes across sleep/wake states has remained unclear. Here, we directly observe red blood cells (RBCs) within capillaries, where the actual substance exchange between the blood and neurons/glia occurs, by two-photon microscopy. Across multiple cortical areas, average capillary CBF is largely increased during rapid eye movement (REM) sleep, whereas it does not differ between periods of active wakef
Repeated stress is a risk factor for mental disorders and can also lead to sleep disturbances. Although the effects of stress on sleep architecture have been investigated in rodents, the length of the stress exposure period in most studies has been limited to about 10 days, and few studies have analyzed the effects of chronic stress over a longer period. Here we investigated how sleep is affected in a mouse model of depression induced by 3 weeks of daily water immersion and restraint stress (WIR
Sleep is regulated by peripheral tissues under fatigue. The molecular pathways in peripheral cells that trigger systemic sleep-related signals, however, are unclear. Here, a forward genetic screen in C. elegans identifies 3 genes that strongly affect sleep amount: sel-1, sel-11, and mars-1. sel-1 and sel-11 encode endoplasmic reticulum (ER)-associated degradation components, whereas mars-1 encodes methionyl-tRNA synthetase. We find that these machineries function in non-neuronal tissues and that
Despite the established roles of the dopaminergic system in promoting arousal, the effects of loss of dopamine on the patterns of sleep and wakefulness remain elusive. Here, we examined the sleep architecture of dopamine-deficient (DD) mice, which were previously developed by global knockout of tyrosine hydroxylase and its specific rescue in noradrenergic and adrenergic neurons. We found that DD mice have reduced time spent in wakefulness. Unexpectedly, DD mice also exhibited a marked reduction
The mechanisms underlying sleep homeostasis are poorly understood. The nematode <i>Caenorhabditis elegans</i> exhibits 2 types of sleep: lethargus, or developmentally timed, and stress-induced sleep. Lethargus is characterized by alternating cycles of sleep and motion bouts. Sleep bouts are homeostatically regulated, i.e., prolonged active bouts lead to prolonged sleep bouts. Here we reveal that the interneuron ALA is crucial for homeostatic regulation during lethargus. Intracellular Ca<sup>2+</
The molecular mechanism regulating sleep largely remains to be elucidated. In humans, families that carry mutations in <i>TFAP2B</i>, which encodes the transcription factor AP-2β, self-reported sleep abnormalities such as short-sleep and parasomnia. Notably, AP-2 transcription factors play essential roles in sleep regulation in the nematode <i>Caenorhabditis elegans</i> and the fruit fly <i>Drosophila melanogaster</i> Thus, AP-2 transcription factors might have a conserved role in sleep regulati
Mammalian sleep comprises REM and NREM stages, but the regulation mechanisms are unclear. In this issue of Cell Reports, Niwa et al. (2018) comprehensively knocked out cholinergic receptors in mice and found that muscarinic signaling is crucial for REM sleep and possibly important for NREM sleep.
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