Sleep-wake cycle mechanisms Mecanismos do ciclo sono-vigília (original) (raw)
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Current understanding on the neurobiology of sleep and wakefulness
The modern concept of sleep and wakefulness has evolved from the landmark discovery of ascending reticular activating system by Moruzzi and Magoun in 1949. The other major contributions have come from the electrophysiological studies of sleep–wake states following the discovery of electroencephalogram by Hans Berger in 1929. Research studies over the past 60 years have provided us an enormous understanding on the neural basis of sleep–wake states and their regulatory mechanisms. By shuttling through the two behavioral states of sleep and wake, brain coordinates many complex functions essential for cellular homeostasis and adaptation to environment. This review brie fl y summarizes the current awareness on the dynamicity of brain mechanisms of sleep and wakefulness as well as the newer concepts of the biological functions of sleep.
The Neurobiology of Sleep–Wake Systems: An Overview
Narcolepsy, 2011
Following studies of patients with postinfluenza encephalitis, the neuropathologist von Economo reported that inflammatory lesions of the preoptic area (POA) were often associated with insomnia and therefore proposed that the POA was critical for the production of normal sleep [1]. Then, Ranson in monkeys, Nauta in rats, and McGinty in cats showed that POA lesions induce a profound and persistent insomnia . It was later shown in cats that POA electrical stimulation induces EEG slow-wave activity and sleep (SWS) . Finally, putative sleep-promoting neurons displaying an elevated discharge rate during SWS compared to waking (W), diffusely distributed within a large region encompassing the horizontal limb of the diagonal bands of Broca and the lateral preoptic area-substantia innominata were recorded in freely moving cats . Altogether, these studies indicate that the POA is a unique brain structure containing neurons that directly promote sleep.
Seminars in Neurology, 2009
The neurobiology of sleep and narcolepsy is reviewed. Non-rapid eye movement (NREM) sleep is generated by neurons in the preoptic region of the hypothalamus and adjacent basal forebrain. Lesions in these regions cause insomnia. Stimulation of these regions rapidly produces sleep onset. The key brain structure for generating REM sleep is the pons and adjacent portions of the midbrain. Damage to the pons and/or caudal midbrain can cause abnormalities in REM sleep. The persistent sleepiness of narcolepsy is a result of a loss of hypocretin function.
Sleep Medicine Clinics
Behavioral states alternate between wakefulness and sleep, which is further subdivided into rapid-eye-movement sleep and non-rapid-eye-movement sleep. Waking and sleep states are highly complex processes that are elegantly orchestrated by fine-tuned neurochemical changes, including the neurotransmitters and neuromodulators glutamate, acetylcholine,-amino-butyric acid, norepinephrine, dopamine, serotonin, histamine, hypocretin, melanin concentrating hormone, adenosine, and melatonin. However, as highlighted in this brief overview, no single neurotransmitter or neuromodulator, but rather their complex interactions within organized neuronal ensembles, regulate waking and sleep states and drive their transitions. Dysregulation of and medications interfering with these neurochemical systems lead to sleep-wake disorders and functional changes of wakefulness and sleep. The neurochemical pathways presented here, thus, are aimed to provide a conceptual framework for the understanding of the effects of currently used medications on wakefulness and sleep.
Brain mechanisms that control sleep and waking
Naturwissenschaften, 2004
This review paper presents a brief historical survey of the technological and early research that laid the groundwork for recent advances in sleep-waking research. A major advance in this field occurred shortly after the end of World War II with the discovery of the ascending reticular activating system (ARAS) as the neural source in the brain stem of the waking state. Subsequent research showed that the brain stem activating system produced cortical arousal via two pathways: a dorsal route through the thalamus and a ventral route through the hypothalamus and basal forebrain. The nuclei, pathways, and neurotransmitters that comprise the multiple components of these arousal systems are described. Sleep is now recognized as being composed of two very different states: rapid eye movements (REMs) sleep and non-REM sleep. The major findings on the neural mechanisms that control these two sleep states are presented. This review ends with a discussion of two current views on the function of sleep: to maintain the integrity of the immune system and to enhance memory consolidation. This article is based in part on material in the book "The neural control of sleep and waking" (J. Siegel, 2002).
Neurochemical aspects of sleep regulation with specific focus on slow-wave sleep
World Journal of Biological Psychiatry, 2010
The purpose of this review is to outline the mechanisms responsible for the succession of the three vigilance states, namely waking, non rapid eye movement (nonREM) and REM (paradoxical) sleep over 24 h. The latest hypothesis on the mechanisms by which cortical activity switches from an activated state during waking to a synchronised state during nonREM sleep 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 nonREM sleep are all localized in a single small nucleus named the ventrolateral preoptic nucleus (VLPO) situated above the optic chiasm. These neurons all contain the inhibitory neurotransmitter γ -aminobutyric acid. The notion that the switch from waking to nonREM sleep 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 hypnogenic factor, adenosine, which progressively accumulates in the brain during waking. World J Biol Psychiatry Downloaded from informahealthcare.com by University Claude Bernard Lyon 1 on 07/30/10 For personal use only.
The neurotransmitters of sleep and wake, a physiological reviews series
Sleep Medicine Reviews, 2013
Although many questions remain about the key functions of sleep and wakefulness (W), recent studies have revealed much detailed information about this process. Non-rapid-eye-movement sleep (NREMS), rapid-eye-movement sleep (REMS) and W are regulated by several neurotransmitter systems and a number of diffusable or circulating factors. Strategies aimed at determining their role in the regulation of sleep and W have included electrophysiological, genetic, neurochemical and neuropharmacological approaches. The central nervous system (CNS) structures involved in the promotion of the waking state are located in the brainstem, hypothalamus and basal forebrain (BFB). The nuclei found in the brainstem include neurons containing serotonin [5-HT: dorsal raphe nucleus (DRN), median raphe nucleus (MRN)]; norepinephrine [NE: locus coeruleus]; dopamine [DA: ventral tegmental area (VTA), substantia nigra pars compacta (SNc), ventral periaqueductal gray matter (vPAG); and acetylcholine [ACh (W-on): laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT)]. The structures located in the hypothalamus include cells containing histamine [HA: tuberomammillary nucleus (TMN)]; and orexin [OX: posterior lateral hypothalamus around the fornix (LH)]. The cholinergic and glutamatergic neurons of the BFB involved in the regulation of W are located predominantly in the diagonal band, substantia innominata and medial septal area. 1,2
Updates Regarding Neurocircuits and Neurotransmitters Involved in the Regulation of Wakefulness
Sohag Medical Journal
Sleep is a universal phenomenon that is observed not only in humans but also in birds, fishes, and flies even in simpler organisms such as worms also we spend about 8 hours each day in sleep which represents nearly one-third of our life. All these observations indicate the physiological importance of sleep. study of sleep mechanisms requires the first study of the mechanisms, neurocircuits, and neurotransmitters involved in the promotion of wakefulness. Observation of Von Economo in 1930 of patients affected by "encephalitis lethargica", an epidemic that causes widespread and prolonged sleepiness most of the day, opened the door for the study of the brain regions responsible for wakefulness. Researchers recognized now many brain regions that are responsible for wakefulness and other brain regions responsible for the induction of different types of sleep. This review will try to discuss the most recent mechanisms and neural circuits involved in the promotion of wakefulness.
Sleep-wake mechanisms and basal forebrain circuitry
Frontiers in Bioscience-landmark, 2003
The seminal studies by von Economo in humans (1) and by Nauta (2) in rats implicated specific basal forebrain areas at the preoptic level as important in sleep regulation. In the last two decades, studies employing recording of single neurons and monitoring of sleep parameters with subsequent chemical and electron microscopic identification of the synaptic input-output relations of these recorded neurons, provided an increasingly detailed understanding of the function of specific neurotransmitters and corresponding chemically specific neuronal circuits in the forebrain in relation to sleep-wake states.