Maintenance Of Slow Wave Sleep Research Articles

Glucose Induces Slow-Wave Sleep by Exciting the Sleep-Promoting Neurons in the Ventrolateral Preoptic Nucleus: A New Link between Sleep and Metabolism.

Although the brain circuitry underlying vigilance states is well described, the molecular mechanisms responsible for sleep onset remain largely unknown. Combining in vitro and in vivo experiments, we demonstrate that glucose likely contributes to sleep onset facilitation by increasing the excitability of sleep-promoting neurons in the ventrolateral preoptic nucleus (VLPO). We find here that these neurons integrate energetic signals such as ambient glucose directly to regulate vigilance states accordingly. Glucose-induced excitation of sleep-promoting VLPO neurons should therefore be involved in the drowsiness that one feels after a high-sugar meal. This novel mechanism regulating the activity of VLPO neurons reinforces the fundamental and intimate link between sleep and metabolism.

Human longevity is associated with regular sleep patterns, maintenance of slow wave sleep, and favorable lipid profile.

Some individuals are able to successfully reach very old ages, reflecting higher adaptation against age-associated effects. Sleep is one of the processes deeply affected by aging; however few studies evaluating sleep in long-lived individuals (aged over 85) have been reported to date. The aim of this study was to characterize the sleep patterns and biochemical profile of oldest old individuals (N = 10, age 85–105 years old) and compare them to young adults (N = 15, age 20–30 years old) and older adults (N = 13, age 60–70 years old). All subjects underwent full-night polysomnography, 1-week of actigraphic recording and peripheral blood collection. Sleep electroencephalogram spectral analysis was also performed. The oldest old individuals showed lower sleep efficiency and REM sleep when compared to the older adults, while stage N3 percentage and delta power were similar across the groups. Oldest old individuals maintained strictly regular sleep-wake schedules and also presented higher HDL-cholesterol and lower triglyceride levels than older adults. The present study revealed novel data regarding specific sleep patterns and maintenance of slow wave sleep in the oldest old group. Taken together with the favorable lipid profile, these results contribute with evidence to the importance of sleep and lipid metabolism regulation in the maintenance of longevity in humans.

Impact of Sleepiness and Sleep Deficiency on Public Health—Utility of Biomarkers

Sleep disorders and sleep deficiency are important causes of adverse health effects and increased mortality in the United States and worldwide. Sleep deficiency can also result in myriad adverse behavioral consequences, including profound sleepiness, cognitive slowing, automatic behavior, attentional failures and performance degradation, errors, and accidents. It is important to recognize that sleepiness and sleep deficiency are not synonymous.

What are the mechanisms activating the sleep-active neurons located in the preoptic area?

The purpose of this review is to outline the mechanisms responsible for the induction and maintenance of slow-wave sleep (SWS, also named non–rapid eye movement or non-REM sleep). The latest hypothesis on the mechanisms by which cortical activity switches from an activated state during waking to a synchronised state during SWS is presented. It is proposed that the activated cortical state during waking is induced by the activity of multiple waking systems, including the serotonergic, noradrenergic, cholinergic and hypocretin systems located at different subcortical levels. In contrast, the neurons inducing SWS are mainly localized in the ventrolateral preoptic (VLPO) and median preoptic nuclei. These neurons use the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). The notion that the switch from waking to SWS is due to the inhibition of the waking systems by the VLPO sleep-active neurons is introduced. At the onset of sleep, the sleep neurons are activated by the circadian clock localized in the suprachiasmatic nucleus and a powerful hypnogenic factor, adenosine, which progressively accumulates in the brain during waking.

A tryptic hydrolysate from bovine milk α S1-casein improves sleep in rats subjected to chronic mild stress

The putative effects of a tryptic bovine α S1-casein hydrolysate on stress-induced sleep disorders were investigated and their possible link with typical blood stress parameters such as plasma corticosterone concentrations and glycaemia was assessed. Rats were subjected to chronic stress in the form of environmental disturbances, while receiving an oral administration of the α S1-casein hydrolysate (CH). Chronic stress significantly reduced sleep duration in control rats during the first 2 days of the stress period, but stress-induced sleep disturbance was prevented in CH-treated rats. Indeed, CH administration allowed the maintenance of slow wave sleep (SWS) duration and even a slight increase in paradoxical sleep (PS) duration in treated rats. Results on plasma corticosterone concentrations and on glycemia values were inconclusive with respect to the implication of the HPA axis in this study. However, the protective effect of the α S1-casein hydrolysate on sleep during exposure to our chronic mild stress conditions may be mediated by modulation of the central adrenergic response.

Participation of GABAergic Mechanisms of Hypothalamus Ventrolateral Preoptic Area in Regulation of Sleep and Wakefulness and Temperature Homeostasis in the Pigeon Columba livia

A comparative analysis of awakening, somnogenic, and thermoregulating effects of agonists and antagonists of GABAA,B-receptors after microinjections to neuronal populations of ventrolateral preoptic area (VLPA) of hypothalamus was carried out for the first time in representatives of the avian class (pigeon). It has bee established that: (1) VLPA of hypothalamus contains populations of neurons differing by their function and representation of receptor types and participating in control of wakefulness, sleep, and thermoregulation; (2) executive GABAA-ergic mechanisms of maintenance of the slow-wave sleep (SWS) are located predominantly in the caudal part of the hypothalamic VLPA; (3) GABAA,B-ergic mechanisms of control of thermal homeostasis are located predominantly in the caudal part of VLPA. It is suggested that the maintenance of SWS depends on an increase of activity of inhibitory GABAergic VLPA mechanisms leading to inactivation of neuronal networks of wakefulness outside VLPA and on a reduction of activity of the stimulatory aminergic systems present in the preoptic area and outside it.

Functional MRI shows activation of the medial preoptic area during sleep

Changes in the activity of the basal forebrain sleep regulating areas were studied noninvasively in conscious rats by employing functional magnetic resonance imaging (fMRI). Sleep–wakefulness (S–W) stages were identified with the help of electrophysiological recordings carried out simultaneously. An increase in the signal intensity was observed in the medial preoptic area (mPOA) during sleep indicating a heightened activity of neurons in this area. In some rats, there was a decrease in the activity of the fronto-parietal cortex. The sleep-induced increase in activity in the mPOA and decrease in the fronto-parietal cortex are in relation to their levels in the awake state . The findings helped to localize the critical area for the maintenance of slow wave sleep at the mPOA. These results further corroborate some of the previous suggestions based on neurotoxic lesion, chemical stimulation and electrophysiological recordings.

Effects of waking-auditory stimulation on human sleep architecture

Evidence suggests that sleep architecture is affected by endogenous homeostatic mechanisms as well as by behavioral and sensory demands during the prior wakefulness. Regarding the auditory system, sensory deprivation has shown to drastically modify the sleep structure, stressing the relevance of such sensory system for sleep organization. Changes in sleep architecture following prolonged auditory stimulation during prior wakefulness would provide additional support to this hypothesis. In the present study, auditory stimulation was administered over a 6 h period prior to sleep. Sleep parameters obtained from visual scoring were quantified across the total sleep period, for each sleep cycle, and for the two halves of the night, separately. Results showed that 6 h of waking-auditory stimulation were followed by an increase in the duration of slow wave sleep, a shortening of the latency between slow wave sleep periods, and a longer sleep onset latency as compared with the baseline night. In contrast, REM sleep parameters were unaffected by the pre-sleep auditory stimulation. These results indicate that sleep architecture depends on auditory demands during the prior wakefulness, suggesting that the local neural activation underlying auditory stimulation may trigger brain control mechanisms selectively involved in both the slow wave sleep maintenance and organization.

Sleep and suicide in psychiatric patients.

Suicidal patients often report problems with their sleep. Although sleep-related complaints and EEG (electroencephalographic) changes have been seen widely across the spectrum of psychiatric disorders, sleep complaints such as insomnia, hypersomnia, nightmares, and sleep panic attacks are more common in suicidal patients. The subjective quality of sleep as measured by self-rated questionnaires also appears to be more disturbed in suicidal depressive patients. Sleep studies have reported various polysomnographic findings including increased REM (rapid eye movement) time and REM activity in suicidal patients with depression, schizoaffective disorder, and schizophrenia. One mechanism responsible for this possible association between suicide and sleep could be the role of serotonin (5HT). Serotonergic function has been found to be low in patients who attempted and/or completed suicide, particularly those who used violent methods. Aggression dyscontrol appears to be an intervening factor between serotonin and suicide. Additionally, agents that enhance serotonergic transmission decrease suicidal behavior. Serotonin has also been documented to play an important role in onset and maintenance of slow wave sleep and in REM sleep. CSF 5-HIAA levels have been correlated with slow wave sleep in patients with depression as well as schizophrenia. Moreover, 5HT2 receptor antagonists have improved slow wave sleep. Further studies are needed to investigate the possible role of sleep disturbance in suicidal behavior.

Sleep elicited by olfactory tubercle stimulation and the effect of atropine

The effects of high-frequency olfactory tubercle (TbOf) stimulations were studied on the EEG and behaviour of freely-moving cats. The results were as follows: (1) TbOf stimulation elicited sleep similar in every respect to physiological sleep; (2) statistical evaluation of the results showed that primarily the appearance and maintenance of slow wave sleep was facilitated by the stimulations. Stimulations during paradoxical sleep had no effect, but they did promote the recurrence of slow wave sleep after the paradoxical sleep. The effect of stimulations during wakefulness depended on the on-going activity; (3) TbOf stimulation brought about synchronization, which was characterized by a similar arousal threshold as for physiological sleep; and (4) atropine treatment prevented the behavioural effects and did not influence the EEG effects of the stimulations.