We used Hori’s EEG stages to quantitatively describe EEG changes during the sleep onset period (SOP).We have also described the significance of psychophysiological approaches to the wake-sleep transition period, the topographical characteristics of EEG activities in the SOP, and temporal dynamics of the relationship between the waking period before sleep onset and the progress of sleep onset. We expect helpful information providing insights into the consciousness, emotions, behaviors, and brain functions in the waking and sleeping states from investigating the SOP using EEG stages of sleep onset as the primary index and correlating it with behavioral and subjective indexes.

Brain imaging studies have revealed that brain regions related to emotions, such as the ventromedial prefrontal cortex (vmPFC) and amygdala, are activated during rapid-eye-movement (REM) sleep. In addition, the pre-REM negativity (PRN), a brain potential indicated by current source density analysis to originate from the vmPFC and amygdala, appears before REMs during REM sleep. The hypotheses proposed on roles of emotion-related brain activation during REM sleep include the consolidation of conditioned fear and extinction, emotional memory consolidation, dissipation of emotional charge, and optimization of waking behavior in emotional responses, the last of which requires more experimental evidence. This review presents an overview of human emotion-related brain activities during REM sleep and their roles in waking emotional processing. Specifically, the hypothesis that memories of decision-making under uncertain conditions are reprocessed during REM sleep and biases the next day’s decision-making in favor of appropriate long-term choices is discussed. This hypothesis provides a framework for investigating the role of REM sleep in optimizing waking emotional behavior.

“Why do we sleep?” It is a question that has intrigued researchers for more than a century; however, the exact reason remains enigmatic. A growing body of evidence suggests that sleep plays a vital role in learning and memory. Non-rapid eye movement (NREM) sleep has been investigated intensively. Several major models elucidating the role of NREM sleep in learning and memory have been proposed, including the active learning consolidation and synaptic homeostatic hypotheses. Nevertheless, the role of REM sleep has remained controversial. In this review, I have discussed recent studies describing the functions of NREM and REM sleep in human visual perceptual learning, demonstrated to represent a type of adult brain plasticity. I have provided novel insights into the mechanisms underlying REM sleep-induced stabilization of visual perceptual learning. I have also highlighted technical advances in human sleep research, including the role of simultaneous magnetic resonance spectroscopy and polysomnography, which facilitate the noninvasive investigation of adult human brain plasticity during sleep.

Difficulty in falling asleep could be caused by physiological and cognitive arousal, including anxiety and worry. However, it is unclear which part of the sleep onset process is affected by cognitive arousal. This study examined the effects of the effort to fall asleep on the sleep onset process represented by nine EEG stages. Healthy male university students (N=9, aged 21 to 23 years) without any sleep-related complaints participated in the study on two experimental nights. They were instructed to sleep when they felt sleepy (Neutral condition) or try to sleep as soon as possible (Effort condition). Results indicated the prolonged EEG Stage 1(the alpha wave train) and Stage 4(EEG flattening) in the Effort condition. These results suggest that the effort to fall asleep affects only the early part of the sleep onset process in which the arousal system has reduced activity.

The exact functions of the K-complex are under investigation; however, the K-complex, unique to Stage 2 sleep, reportedly plays a role in arousal induction and sleep protection. Event-related potentials (ERPs),appearing when externally evoked K-complexes are observed, have a monomodal (N300-P900 or N550-P900) or a bimodal (N300-P400-N550-P900) morphology. Studies have indicated the involvement of P400 in these morphological differences. P400 reflects information processing about external stimuli, which decays or disappears as sleep-depth increases. We compared the ERP waveforms and the functions of auditory evoked K-complex by dividing Stage 2 sleep of the first sleep cycle into first and second half sections. Results indicated that P400 amplitude attenuated in the second compared to the first half. Concomitantly, we observed a bimodal (N300-P400-N550-P900) ERP waveform in the first half, whereas a monomodal (N300-P900) waveform was observed in the second half of the first sleep cycle. These findings suggest that the function of the K-complex in the first half of Stage 2 sleep might predominantly be arousal induction, whereas its function in the second half is sleep protection.

Diurnal variation of sleepiness consists of daytime sleepiness increasing ca. 6 to 8 hours after waking up and nocturnal sleepiness before bedtime. Nocturnal sleepiness is associated with the circadian rhythms of core body temperature which strongly controls the central circadian pacemaker. However, the underlying mechanism involved in the source of daytime sleepiness is still unknown. Therefore, we examined the relationship between the diurnal rhythm of body temperature, autonomic nervous activities, and subjective/objective sleepiness in strictly controlled laboratory conditions. As a result, most subjects showed 2–5 h fluctuation in sleepiness. A significant correlation was found between the sleepiness, body temperature, autonomic functions in the 1–3 h after wake-up and 1–3 h before bedtime, whereas the fluctuations of daytime sleepiness were not in parallel with the diurnal changes in the temperature and autonomic functions. In sum, the ultradian rhythms during the daytime might be independent of the circadian rhythms of body temperature and autonomic function, whereas sleepiness in the morning and before the bedtime is mainly regulated by the circadian pacemaker.