Neuroscience: A Distributed Neural Network Controls REM Sleep

Peever, John H.; Fuller, Patrick M.

doi:10.1016/j.cub.2015.11.011

Cited by 48 publications

(30 citation statements)

References 158 publications

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“…It is our working hypothesis that RBD is caused by synucleinopathic degeneration of this 2‐part brain stem circuit (Fig. ), and this assertion is supported by the fact that lesions of the so‐called “REM sleep circuit” can cause RBD‐like motor behaviors in both animals (cats, rats, mice) and humans …”

Section: Mechanisms Controlling Rem Sleep Paralysismentioning

confidence: 93%

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Degeneration of rapid eye movement sleep circuitry underlies rapid eye movement sleep behavior disorder

McKenna

Peever

2017

Movement Disorders

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During healthy rapid eye movement sleep, skeletal muscles are actively forced into a state of motor paralysis. However, in rapid eye movement sleep behavior disorder-a relatively common neurological disorder-this natural process is lost. A lack of motor paralysis (atonia) in rapid eye movement sleep behavior disorder allows individuals to actively move, which at times can be excessive and violent. At first glance this may sound harmless, but it is not because rapid eye movement sleep behavior disorder patients frequently injure themselves or the person they sleep with. It is hypothesized that the degeneration or dysfunction of the brain stem circuits that control rapid eye movement sleep paralysis is an underlying cause of rapid eye movement sleep behavior disorder. The link between brain stem degeneration and rapid eye movement sleep behavior disorder stems from the fact that rapid eye movement sleep behavior disorder precedes, in the majority (∼80%) of cases, the development of synucleinopathies such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, which are known to initially cause degeneration in the caudal brain stem structures where rapid eye movement sleep circuits are located. Furthermore, basic science and clinical evidence demonstrate that lesions within the rapid eye movement sleep circuits can induce rapid eye movement sleep-specific motor deficits that are virtually identical to those observed in rapid eye movement sleep behavior disorder. This review examines the evidence that rapid eye movement sleep behavior disorder is caused by synucleinopathic neurodegeneration of the core brain stem circuits that control healthy rapid eye movement sleep and concludes that rapid eye movement sleep behavior disorder is not a separate clinical entity from synucleinopathies but, rather, it is the earliest symptom of these disorders. © 2017 International Parkinson and Movement Disorder Society.

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Section: Mechanisms Controlling Rem Sleep Paralysismentioning

confidence: 93%

“…Therefore, the subcoeruleus nucleus and ventromedial medulla constitute “the core” REM sleep circuit, with glutamate cells in the subcoeruleus nucleus functioning as the “master REM sleep switch” (Fig. ).…”

Section: Mechanisms Controlling Rem Sleep Paralysismentioning

confidence: 99%

Degeneration of rapid eye movement sleep circuitry underlies rapid eye movement sleep behavior disorder

McKenna

Peever

2017

Movement Disorders

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“…In mammals, slow waves are generated by thalamocortical interactions [Steriade et al, 1993;Lemieux et al, 2014]. REM sleep-related cortical activation, reduction in muscle tone, and eye movements are all controlled by the brainstem [Siegel, 2011;Luppi et al, 2013;Weber et al, 2015] and its interactions with a network of other brain structures throughout the neuroaxis [Jego et al, 2013;Luppi et al, 2015;Peever and Fuller, 2016].…”

Section: Introductionmentioning

confidence: 99%

Sleep-Related Electrophysiology and Behavior of Tinamous (<b><i>Eudromia elegans</i></b>): Tinamous Do Not Sleep Like Ostriches

Tisdale¹,

Vyssotski²,

Lesku³

et al. 2017

Brain Behav Evol

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The functions of slow wave sleep (SWS) and rapid eye movement (REM) sleep, distinct sleep substates present in both mammals and birds, remain unresolved. One approach to gaining insight into their function is to trace the evolution of these states through examining sleep in as many taxonomic groups as possible. The mammalian and avian clades are each composed of two extant groups, i.e., the monotremes (echidna and platypus) and therian (marsupial and eutherian [or placental]) mammals, and Palaeognaths (cassowaries, emus, kiwi, ostriches, rheas, and tinamous) and Neognaths (all other birds) among birds. Previous electrophysiological studies of monotremes and ostriches have identified a unique “mixed” sleep state combining features of SWS and REM sleep unlike the well-delineated sleep states observed in all therian mammals and Neognath birds. In the platypus this state is characterized by periods of REM sleep-related myoclonic twitching, relaxed skeletal musculature, and rapid eye movements, occurring in conjunction with SWS-related slow waves in the forebrain electroencephalogram (EEG). A similar mixed state was also observed in ostriches; although in addition to occurring during periods with EEG slow waves, reduced muscle tone and rapid eye movements also occurred in conjunction with EEG activation, a pattern typical of REM sleep in Neognath birds. Collectively, these studies suggested that REM sleep occurring exclusively as an integrated state with forebrain activation might have evolved independently in the therian and Neognath lineages. To test this hypothesis, we examined sleep in the elegant crested tinamou (Eudromia elegans), a small Palaeognath bird that more closely resembles Neognath birds in size and their ability to fly. A 24-h period was scored for sleep state based on electrophysiology and behavior. Unlike ostriches, but like all of the Neognath birds examined, all indicators of REM sleep usually occurred in conjunction with forebrain activation in tinamous. The absence of a mixed REM sleep state in tinamous calls into question the idea that this state is primitive among Palaeognath birds and therefore birds in general.

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“…Due to the similarities of the EEG spectrum and muscle atonia features, cataplexy has long been considered as a REM sleep intrusion into waking or abnormal REM sleep during waking (Luppi et al, 2011;Roth et al, 1969). Indeed, studies have found that cataplexy and REM sleep share some common neural substrates (Dauvilliers et al, 2014;Peever et al, 2016;Thakkar et al, 1999). Thus, MCH neurons, an important REM sleepregulating hub, are thought to trigger intrusions of REM sleep bouts into waking in the absence of orexin, consequently resulting in cataplexy.…”

Section: Discussionmentioning

confidence: 99%