The Neurobiology of Sleep

Siegel, Jerome M.

doi:10.1055/s-0029-1237118

Cited by 85 publications

(60 citation statements)

References 148 publications

(189 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Based on studies of unihemispheric sleep in marine mammals, it is widely appreciated that the minimal unit for sleep expression may not encompass the entire brain [59]. However, defining which parts of the brain engage in sleep expression is a challenge.…”

Section: Local Sleepmentioning

confidence: 99%

Thalamocortical dynamics of sleep: Roles of purinergic neuromodulation

Halassa

2011

Seminars in Cell & Developmental Biology

View full text Add to dashboard Cite

Thalamocortical dynamics, the millisecond to second changes in activity of thalamocortical circuits, are central to perception, action and cognition. Generated by local circuitry and sculpted by neuromodulatory systems, these dynamics reflect the expression of vigilance states. In sleep, thalamocortical dynamics are thought to mediate “offline” functions including memory consolidation and synaptic scaling. Here, I discuss thalamocortical sleep dynamics and their modulation by the ascending arousal system and locally-released neurochemicals. I focus on modulation of these dynamics by electrically-silent astrocytes, highlighting the role of purinergic signaling in this glial form of communication. Astrocytes modulate cortical slow oscillations, sleep behavior, and sleep-dependent cognitive function. The discovery that astrocytes can modulate sleep dynamics and sleep-related behaviors suggests a new way of thinking about the brain, in which integrated circuits of neurons and glia control information processing and behavioral output.

show abstract

Section: Local Sleepmentioning

confidence: 99%

Thalamocortical dynamics of sleep: Roles of purinergic neuromodulation

Halassa

2011

Seminars in Cell & Developmental Biology

View full text Add to dashboard Cite

show abstract

“…The firing rate of cortical neurons has generally been reported to be reduced during NREM relative to wakefulness and REM (5,6). A few studies have reported cortical neurons with the opposite pattern.…”

mentioning

confidence: 99%

A role for cortical nNOS/NK1 neurons in coupling homeostatic sleep drive to EEG slow wave activity

Morairty

Dittrich

Pasumarthi

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

121

View full text Add to dashboard Cite

Although the neural circuitry underlying homeostatic sleep regulation is little understood, cortical neurons immunoreactive for neuronal nitric oxide synthase (nNOS) and the neurokinin-1 receptor (NK1) have been proposed to be involved in this physiological process. By systematically manipulating the durations of sleep deprivation and subsequent recovery sleep, we show that activation of cortical nNOS/NK1 neurons is directly related to non-rapid eye movement (NREM) sleep time, NREM bout duration, and EEG δ power during NREM sleep, an index of preexisting homeostatic sleep drive. Conversely, nNOS knockout mice show reduced NREM sleep time, shorter NREM bouts, and decreased power in the low δ range during NREM sleep, despite constitutively elevated sleep drive. Cortical NK1 neurons are still activated in response to sleep deprivation in these mice but, in the absence of nNOS, they are unable to up-regulate NREM δ power appropriately. These findings support the hypothesis that cortical nNOS/NK1 neurons translate homeostatic sleep drive into up-regulation of NREM δ power through an NO-dependent mechanism.T he electrical activity of the cerebral cortex has been used to distinguish sleep vs. wakefulness since the earliest EEG studies of sleep (1). Several neural circuits have been implicated in the synchronization and desynchronization of cortical activity that distinguish non-rapid eye movement sleep (NREM) from wakefulness and rapid eye movement sleep (REM). Input from the basal forebrain (BF), likely from both cholinergic and noncholinergic neurons, is critical for the desynchronized EEG characteristic of wakefulness and REM (2, 3). Synchronization of the EEG during NREM depends on thalamic as well as intrinsic cortical oscillators (4).The firing rate of cortical neurons has generally been reported to be reduced during NREM relative to wakefulness and REM (5, 6). A few studies have reported cortical neurons with the opposite pattern. For example, 4 of 177 neurons in the monkey orbitofrontal cortex increased their firing rates during NREM (7). In the cat parietal cortex, 25% of neurons discharged in phase with NREM slow waves during up states but ceased firing during quiet wakefulness (8).Using Fos immunohistochemistry as a marker of cellular activity, we described a population of cortical GABAergic interneurons that are activated during sleep in three species (9, 10). These neurons express neuronal nitric oxide synthase (nNOS) and thus likely release nitric oxide (NO) as well as GABA (11). The percentage of activated cortical nNOS neurons was proportional to NREM δ energy (NRDE), the product of NREM time and NREM EEG δ power. Because NREM time and δ power increase in response to prolonged wakefulness through a regulated process referred to as sleep homeostasis, NRDE is an electrophysiological marker of homeostatic sleep "drive." Consequently, activation of cortical nNOS neurons during sleep seems to be related to the sleep need that accrues during wakefulness.Cortical nNOS neurons receive cholinergic (12), monoamin...

show abstract

“…Multiple monoamines, including dopamine (DA), serotonin, norepinephrine, and histamine, as well as acetylcholine and the neuropeptide, hypocretin [ 28 ] , appear to be involved in the modulation of the sleep-wake cycle. Serotonin and DA both function to promote waking and to inhibit slowwave sleep and/or rapid eye movement sleep [ 29 ] .…”

Section: Sleep Physiologymentioning

confidence: 99%

Insomnia in Parkinson’s Disease

Moro-de-Casillas

Riley

2012

Parkinson’s Disease and Nonmotor Dysfunction

View full text Add to dashboard Cite

The International Classi fi cation of Sleep Disorders (ICSD) de fi nes insomnia simply as "dif fi culty in initiating and/or maintaining sleep". Other de fi nitions exist, and there is no clear consensus in this matter. The core elements of insomnia are an inadequate quantity or quality of sleep, with both nocturnal and daytime consequences. Traditionally, insomnia has been subgrouped into sleep-onset insomnia, sleep-maintaining insomnia, and insomnia with early morning awakening; however, there is extensive overlap, and most insomniacs fi t into more than one subgroup.Sleep disorders, particularly in the elderly, are strongly associated with increased morbidity and mortality, signi fi cant limitations in activities of daily living, and impaired quality of life. Aside from the obvious complications of daytime fatigue and somnolence, insomniacs have an increased incidence of psychiatric disorders such as depression and anxiety, increased use of over-the-counter medications and alcohol, and a higher incidence of accidents and unemployment. Chronic sleep loss has multisystem consequences and may represent a risk factor for obesity, insulin resistance, and Type 2 diabetes. However, the brunt of negative effects of sleep deprivation is borne by the brain. Chronic insomnia independently predicts incident cognitive decline in older men, but it also has been suggested that some degree of apparent age-related cognitive decline may be due to treatable insomnia.

show abstract

The Neurobiology of Sleep

Cited by 85 publications

References 148 publications

Thalamocortical dynamics of sleep: Roles of purinergic neuromodulation

Thalamocortical dynamics of sleep: Roles of purinergic neuromodulation

A role for cortical nNOS/NK1 neurons in coupling homeostatic sleep drive to EEG slow wave activity

Insomnia in Parkinson’s Disease

Contact Info

Product

Resources

About