Topic
Slow-wave sleep
About: Slow-wave sleep is a research topic. Over the lifetime, 6543 publications have been published within this topic receiving 320663 citations. The topic is also known as: deep sleep.
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TL;DR: A dose-dependent dissociation of effects on behaviour and motor control was revealed and the sleep-waking cycle was affected; the duration of REM sleep showed a consistent dose-related reduction although the total sleeping time was not considerably altered.
92 citations
TL;DR: Although reports of dreaming are sometimes elicited on awakenings from NREM sleep, the frequency of such reports is less than the frequency for REM period awakenings, and the quality of these reports are less "dream-like" than thequality of REM period reports.
Abstract: The cyclic occurrence of REM periods (sleep characterized by a low voltage, desynchronized EEG pattern, and rapid eye movements) 1,3 and the association of these periods with reports of dreaming 1,4,6,7,9,10,14 have been well established. With the exception of narcoleptic sleep, 5,13 and the sleep of amphetamine addicts subjected to drug withdrawal, 12 REM periods do not occur during nocturnal sleep until after the passage of approximately 45 minutes of NREM sleep (periods characterized by EEG sleep spindle and/or δ-activity and the absence of rapid eye movements). Although reports of dreaming are sometimes elicited on awakenings from NREM sleep, the frequency of such reports is less than the frequency for REM period awakenings, and the quality of these reports is less "dream-like" than the quality of REM period reports. 6,14 Therefore, one would expect, upon hearing vivid, well-recalled, thematically organized dreams, that they were experienced during
92 citations
TL;DR: The study points out the topical role of enhanced activation and arousal instability not only in the first part of the night (mismatch between objective and subjective sleep onset) but also in the misperception of consecutive objective awakenings which are subjectively grouped together as a single prolonged event.
92 citations
TL;DR: Lesion analysis revealed that the candidate structures for PS erectile control include both the lateral preoptic area (LPOA) and ventral division of the bed nucleus of the stria terminalis; however, lesions of the LPOA were the most effective in disruptingPS erectile activity.
Abstract: Penile erections are a characteristic phenomenon of paradoxical sleep (PS), or rapid eye movement sleep. Although the neural mechanisms of PS-related erections are unknown, the forebrain likely plays a critical role (Schmidt et al., 1999). The preoptic area is implicated in both sleep generation and copulatory mechanisms, suggesting it may be a primary candidate in PS erectile control. Continuous recordings of penile erections, body temperature, and sleep-wake states were performed before and up to 3 weeks after ibotenic acid lesions of the preoptic forebrain in three groups of rats. Neurotoxic lesions involving the medial preoptic area (MPOA) and anterior hypothalamus (n = 5) had no significant effects on either erectile activity or sleep-wake architecture. In contrast, bilateral lesions of the lateral preoptic region, with (n = 4) or without (n = 5) MPOA involvement, resulted in a significant decrease in the number of erections per hour of PS, number of PS-related erections, and PS phases exhibiting an erection. Lesion analysis revealed that the candidate structures for PS erectile control include both the lateral preoptic area (LPOA) and ventral division of the bed nucleus of the stria terminalis; however, lesions of the LPOA were the most effective in disrupting PS erectile activity. LPOA lesioning also resulted in a long-lasting insomnia, characterized by the significant increase in wakefulness and decrease in slow wave sleep (SWS). PS architecture and waking-state erections remained unchanged after lesion in all groups. These data identify an essential role of the LPOA in both PS-related erectile mechanisms and SWS generation. Moreover, higher erectile mechanisms appear to be context-specific because LPOA lesioning selectively disrupted PS-related erections while leaving waking-state erections intact.
92 citations
TL;DR: The short (s-) allele of the 5-HTTLPR is found to be significantly more frequent in patients suffering from insomnia than in control individuals, which contributes to the understanding of the pathophysiology of primary insomnia and suggests a biological basis between the prevalent comorbidity ofPrimary insomnia and other psychiatric disorders.
Abstract: PRIMARY INSOMNIA, ACCORDING TO DSM-IV, IS ONE OF THE MOST FREQUENT SLEEP DISORDERS, WITH A PREVALENCE OF 3%1,2 AND IS CHARACTERIZED BY difficulties initiating or maintaining sleep or nonrestorative sleep causing distress or impairment. The presence of learned, sleep-preventing associations, such as conditioned arousal to sleep-related cues and evidence for increased somatized tension are additional criteria for psychophysiological insomnia in the International Classification of Sleep Disorders (ICSD).
Large family and twin studies have consistently shown that insomnia is under strong genetic influence: first-degree relatives of patients with primary insomnia are at a 6.65-fold increased risk to develop insomnia themselves.3,4 Among other factors, anxious-ruminative personality traits5 and occurrence of stressful life events contribute to the onset and perpetuation of insomnia.6 Thus, primary insomnia may be regarded as a potential consequence of gene-environment interaction.
Primary insomnia and other insomnia diagnoses show an association with mood disorders, with insomnia typically appearing before the onset of depression.1 Therefore, insomnia could either be a risk factor for depression, or insomnia and affective disorders could share a common background, e.g., as a spectrum of stress-related disorders.
There is a longstanding discussion on the role of serotonin (5-HT) in the regulation of sleep.7,8 In rodents and cats, it has been shown that typical, but not all9 serotonergic raphe neurons discharge regularly during waking, at slower rates during slow wave sleep, and cease firing during paradoxical sleep,10 which indicates serotonergic activity being related to wakefulness. In addition to this possible REM sleep inhibitory action, sleep facilitatory effects have also been reported,11 likely due to the multitude of postsynaptic receptors, which mediate different responses. In particular, studies in humans support the 5HT2- receptor to be involved in slow wave sleep regulation.12,13 Accordingly, several 5-HT2A receptor antagonists or inverse agonists are currently being tested in randomized controlled trials for treatment of primary insomnia,14 which underscores 5-HT's role in the regulation of sleep.
The key regulator of serotonin in the synapse, and therefore of overall serotonergic activity, is the 5-HT transporter (5-HTT). The presynaptic 5-HTT is the target of most antidepressants. A frequent variant of the 5-HTT gene (SLC6A4,17q11.2) is a 44 base-pair insertion/deletion polymorphism in the 5′ regulatory region of the 5-HTT gene; and it affects gene transcription and transporter density in transfected cells. SLC6A4 genotype, usually grouped into “short” (s)- and “long” (l)-alleles, has been studied extensively with regard to psychiatric phenotypes and has been found to be associated with a variety of stress-related psychiatric conditions, such as trait anxiety15,16 and risk for affective disorders,17 especially in interaction with environmental adversity.18,19 Moreover, the 5-HTTLPR s-allele has also been found associated with poor sleep quality in chronic stress20 and worsened insomnia in depressed patients being treated with fluoxetine.21 Based on these findings and on the role of psychosocial stress in pathophysiological concepts of primary insomnia,22 we hypothesized that s-allele of 5-HTTLPR would be associated with primary insomnia.
92 citations