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Jacques Montplaisir - One of the best experts on this subject based on the ideXlab platform.
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REM Sleep behaviour disorder
Nature reviews. Disease primers, 2018Co-Authors: Yves Dauvilliers, Carlos H. Schenck, Pierre-hervé Luppi, Alex Iranzo, Giuseppe Plazzi, Jacques Montplaisir, Ronald B. Postuma, Bradley F. BoeveAbstract:Rapid eye movement (REM) Sleep behaviour disorder (RBD) is a parasomnia that is characterized by loss of muscle atonia during REM Sleep (known as REM Sleep without atonia, or RSWA) and abnormal behaviours occurring during REM Sleep, often as dream enactments that can cause injury. RBD is categorized as either idiopathic RBD or symptomatic (also known as secondary) RBD; the latter is associated with antidepressant use or with neurological diseases, especially α-synucleinopathies (such as Parkinson disease, dementia with Lewy bodies and multiple system atrophy) but also narcolepsy type 1. A clinical history of dream enactment or complex motor behaviours together with the presence of muscle activity during REM Sleep confirmed by video polysomnography are mandatory for a definite RBD diagnosis. Management involves clonazepam and/or melatonin and counselling and aims to suppress unpleasant dreams and behaviours and improve bedpartner quality of life. RSWA and RBD are now recognized as manifestations of an α-synucleinopathy; most older adults with idiopathic RBD will eventually develop an overt neurodegenerative syndrome. In the future, studies will likely evaluate neuroprotective therapies in patients with idiopathic RBD to prevent or delay α-synucleinopathy-related motor and cognitive decline. Rapid eye movement (REM) Sleep behaviour disorder (RBD) is characterized by a loss of muscle atonia and abnormal behaviours during REM Sleep. This Primer discusses the epidemiology, pathophysiology, diagnosis and management of RBD as well as the relationship and implications of the relationship between idiopathic RBD and neurodegenerative disease.
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REM Sleep behaviour disorder
Nature reviews Disease primers, 2018Co-Authors: Yves Dauvilliers, Pierre-hervé Luppi, Alex Iranzo, Giuseppe Plazzi, Jacques Montplaisir, Ronald B. Postuma, Carlos Schenck, Bradley F. BoeveAbstract:Rapid eye movement (REM) Sleep behaviour disorder (RBD) is a parasomnia that is characterized by loss of muscle atonia during REM Sleep (known as REM Sleep without atonia, or RSWA) and abnormal behaviours occurring during REM Sleep, often as dream enactments that can cause injury. RBD is categorized as either idiopathic RBD or symptomatic (also known as secondary) RBD; the latter is associated with antidepressant use or with neurological diseases, especially α-synucleinopathies (such as Parkinson disease, dementia with Lewy bodies and multiple system atrophy) but also narcolepsy type 1. A clinical history of dream enactment or complex motor behaviours together with the presence of muscle activity during REM Sleep confirmed by video polysomnography are mandatory for a definite RBD diagnosis. Management involves clonazepam and/or melatonin and counselling and aims to suppress unpleasant dreams and behaviours and improve bedpartner quality of life. RSWA and RBD are now recognized as manifestations of an α-synucleinopathy; most older adults with idiopathic RBD will eventually develop an overt neurodegenerative syndrome. In the future, studies will likely evaluate neuroprotective therapies in patients with idiopathic RBD to prevent or delay α-synucleinopathy-related motor and cognitive decline.
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breakdown in REM Sleep circuitry underlies REM Sleep behavior disorder
Trends in Neurosciences, 2014Co-Authors: J Peever, Pierre-hervé Luppi, Jacques MontplaisirAbstract:During rapid eye movement (REM) Sleep, skeletal muscles are almost paralyzed. However, in REM Sleep behavior disorder (RBD), which is a rare neurological condition, muscle atonia is lost, leaving afflicted individuals free to enact their dreams. Although this may sound innocuous, it is not, given that patients with RBD often injure themselves or their bed-partner. A major concern in RBD is that it precedes, in 80% of cases, development of synucleinopathies, such as Parkinson's disease (PD). This link suggests that neurodegenerative processes initially target the circuits controlling REM Sleep. Clinical and basic neuroscience evidence indicates that RBD results from breakdown of the network underlying REM Sleep atonia. This finding is important because it opens new avenues for treating RBD and understanding its link to neurodegenerative disorders.
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REM Sleep parasomnias.
Handbook of clinical neurology, 2011Co-Authors: Jacques Montplaisir, Jean-françois Gagnon, Ronald B. Postuma, Mélanie VendetteAbstract:Publisher Summary This chapter focuses on Sleep behavior disorder (RBD). Rapid eye movement (REM) Sleep parasomnias are disorders in which undesirable physical phenomena occur predominantly during REM Sleep. REM parasomnias encompass abnormal Sleep-related movements, behavior, emotions, and dreaming. Three conditions are commonly identified as REM Sleep parasomnias, namely REM Sleep behavior disorder (RBD), recurrent isolated Sleep paralysis, and nightmare disorder. RBD is accompanied by electromyographic (EMG) abnormalities in REM Sleep, consisting of excess muscle tone and/or phasic EMG activity. Behaviors can range from simple motor activities such as laughing, talking, shouting, or excessive body and limb jerking to complex behavior such as gesturing, punching, kicking, sitting up, leaping from bed, and running. A characteristic feature of RBD is the occurrence of specific and somewhat stereotyped dream content irrespective of individual psychological profiles. Another polygraphic characteristic of RBD is the presence of periodic leg movements in Sleep (PLMS). RBD is divided into primary and secondary forms.
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REM Sleep characteristics in narcolepsy and REM Sleep behavior disorder.
Sleep, 2007Co-Authors: Yves Dauvilliers, Sylvie Rompré, Dominique Petit, Jean-françois Gagnon, Mélanie Vendette, Jacques MontplaisirAbstract:Study Objectives: To assess the presence of polysomnographic characteristics of REM Sleep behavior disorder (RBD) in narcolepsy; and to quantify REM Sleep parameters in patients with narcolepsy, in patients with “idiopathic” RBD, and in normal controls.
J Peever - One of the best experts on this subject based on the ideXlab platform.
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REM Sleep Behavior Disorder: The Link Between Synucleinopathies and REM Sleep Circuits
Rapid-Eye-Movement Sleep Behavior Disorder, 2018Co-Authors: Dillon Mckenna, J PeeverAbstract:Normal REM Sleep is characterized by vivid dreaming, rapid eye movements, and wake-like cortical activity that are accompanied by generalized skeletal muscle paralysis. A defined network of brainstem nuclei control REM Sleep motor paralysis, and abnormal control of this network is thought to underlie the excessive and often violent movements in REM Sleep behavior disorder (RBD). A major concern associated with RBD is that the majority of patients (80–90%) without identified comorbidities eventually develop some form of synucleinopathy, primarily Parkinson’s disease, dementia with Lewy bodies, or multiple system atrophy. This group of diseases is linked to aggregates of the misfolded endogenous protein alpha-synuclein (αSyn). The high level of association between RBD and later synucleinopathy has led to the hypothesis that RBD itself is an early symptom of developing synucleinopathies that arise from degeneration of the brainstem circuitry that normally suppresses muscle activity in REM Sleep. Indeed, animal models show that the integrity of this region is required for normal muscle paralysis across species, and human synucleinopathy patients display αSyn aggregates and signs of degeneration within the brainstem REM Sleep network. In this chapter, we outline the clinical and basic science evidence supporting the hypothesis that RBD is caused by synucleinopathy progressing through the brainstem regions that regulate muscle paralysis in normal REM Sleep. Understanding RBD progression is vital as it could lead to neuroprotective strategies against later synucleinopathy development.
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The Biology of REM Sleep
Current biology : CB, 2017Co-Authors: J Peever, Patrick M. FullerAbstract:Considerable advances in our understanding of the mechanisms and functions of rapid-eye-movement (REM) Sleep have occurred over the past decade. Much of this progress can be attributed to the development of new neuroscience tools that have enabled high-precision interrogation of brain circuitry linked with REM Sleep control, in turn revealing how REM Sleep mechanisms themselves impact processes such as sensorimotor function. This review is intended to update the general scientific community about the recent mechanistic, functional and conceptual developments in our current understanding of REM Sleep biology and pathobiology. Specifically, this review outlines the historical origins of the discovery of REM Sleep, the diversity of REM Sleep expression across and within species, the potential functions of REM Sleep (e.g., memory consolidation), the neural circuits that control REM Sleep, and how dysfunction of REM Sleep mechanisms underlie debilitating Sleep disorders such as REM Sleep behaviour disorder and narcolepsy.
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REM Sleep at its core circuits neurotransmitters and pathophysiology
Frontiers in Neurology, 2015Co-Authors: Jimmy J. Fraigne, Zoltan A. Torontali, Matthew B Snow, J PeeverAbstract:REM Sleep is generated and maintained by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain and hypothalamus. Within these circuits lies a core region that is active during REM Sleep, known as the subcoeruleus nucleus (SubC) or sublaterodorsal nucleus. It is hypothesized that glutamatergic SubC neurons regulate REM Sleep and its defining features such as muscle paralysis and cortical activation. REM Sleep paralysis is initiated when glutamatergic SubC activate neurons in the ventral medial medulla (VMM), which causes release of GABA and glycine onto skeletal motoneurons. REM Sleep timing is controlled by activity of GABAergic neurons in the ventrolateral periaqueductal gray (vlPAG) and dorsal paragigantocellular reticular nucleus (DPGi) as well as melanin-concentrating hormone (MCH) neurons in the hypothalamus and cholinergic cells in the laterodorsal (LDT) and pedunculo-pontine tegmentum (PPT) in the brainstem. Determining how these circuits interact with the SubC is important because breakdown in their communication is hypothesized to underlie cataplexy/narcolepsy and REM Sleep behaviour disorder (RBD). This review synthesizes our current understanding of mechanisms generating healthy REM Sleep and how dysfunction of these circuits contributes to common REM Sleep disorders such as cataplexy/narcolepsy and RBD.
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breakdown in REM Sleep circuitry underlies REM Sleep behavior disorder
Trends in Neurosciences, 2014Co-Authors: J Peever, Pierre-hervé Luppi, Jacques MontplaisirAbstract:During rapid eye movement (REM) Sleep, skeletal muscles are almost paralyzed. However, in REM Sleep behavior disorder (RBD), which is a rare neurological condition, muscle atonia is lost, leaving afflicted individuals free to enact their dreams. Although this may sound innocuous, it is not, given that patients with RBD often injure themselves or their bed-partner. A major concern in RBD is that it precedes, in 80% of cases, development of synucleinopathies, such as Parkinson's disease (PD). This link suggests that neurodegenerative processes initially target the circuits controlling REM Sleep. Clinical and basic neuroscience evidence indicates that RBD results from breakdown of the network underlying REM Sleep atonia. This finding is important because it opens new avenues for treating RBD and understanding its link to neurodegenerative disorders.
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Cholinergic involvement in control of REM Sleep paralysis.
The Journal of physiology, 2014Co-Authors: Zoltan A. Torontali, Richard L. Horner, Kevin P. Grace, J PeeverAbstract:REM Sleep, also known as dreaming Sleep, is marked by intense cortical activation and absence of skeletal muscle tone, so-called REM Sleep paralysis (atonia). It is commonly believed that REM Sleep paralysis functions to prevent movement during vivid dreams. Indeed, REM Sleep behaviour disorder – a neurological condition marked by violent dream enactment – results from loss of REM Sleep paralysis. For the last 50 years, biologists have focused on the identification of brain mechanisms responsible for REM Sleep. A majority of evidence suggests that a brainstem region known as the sublaterodorsal nucleus (SLD), also called the subcoeruleus, is important for REM Sleep generation (Jouvet 1962). However, there is uncertainty concerning the chemical mechanisms by which the SLD triggers REM Sleep phenomena. For example, some data suggest that cholinergic modulation of SLD cells underlies REM Sleep generation, whereas, other data suggest that GABAergic disinhibition and glutamatergic excitation of SLD cells are critical for REM Sleep control (Boissard et al. 2002; Lu et al. 2006). The recent study by Weng et al. (2014) provides a potentially new framework for understanding REM Sleep control by showing that both cholinergic and glutamatergic processes operating within the SLD could be important for triggering REM Sleep paralysis.
H C Heller - One of the best experts on this subject based on the ideXlab platform.
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Monoaminergic and cholinergic modulation of REM-Sleep timing in rats.
Brain research, 1995Co-Authors: J H Benington, H C HellerAbstract:The effects on Sleep structure of systemic administration of benchmark cholinergic, serotonergic, and noradrenergic antagonists (QNB, ritanserin, metergoline, and prazosin) were characterized in rats using a new technique for identifying transitions (NRTs) from non-REM (NREM) Sleep to REM Sleep. In agreement with previous studies, all agents tested reduced REM-Sleep expression (by 36-86%). In addition, the serotonergic and noradrenergic antagonists reduced NRT frequency (by 58-81%). The cholinergic antagonist QNB had no effect on NRT frequency. These findings suggest that blockade of serotonergic or noradrenergic receptors increases the interval between REM-Sleep episodes, perhaps reducing the rate of accumulation of REM-Sleep propensity. Blockade of cholinergic receptors, by contrast, decreases REM-Sleep expression by interfering with REM-Sleep maintenance, not by modulating REM-Sleep timing. These conclusions are contrary to the predictions of a number of published models of REM-Sleep timing.
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REM-Sleep propensity accumulates during 2-h REM-Sleep deprivation in the rest period in rats.
Neuroscience letters, 1994Co-Authors: Joel H. Benington, M C Woudenberg, H C HellerAbstract:Two-hour, highly-selective, rest-period, rapid-eye-movement (REM)-Sleep deprivation (RD) was performed on rats to characterize the time-course of the homeostatic response to REM-Sleep loss. RD caused a dramatic and progressive increase in the frequency of attempts to enter REM Sleep, suppressed non-REM Sleep EEG delta power, and (in late rest period trials) was followed by a rebound increase in REM-Sleep expression.
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REM-Sleep timing is controlled homeostatically by accumulation of REM-Sleep propensity in non-REM Sleep
American Journal of Physiology-Regulatory Integrative and Comparative Physiology, 1994Co-Authors: J H Benington, H C HellerAbstract:Sleep structure in the rat was characterized during uninterrupted full-day recordings using an analytic procedure that identifies rapid eye movement (REM) Sleep episodes based on REM-Sleep-onset electroencephalograph phenomena, hence independently of REM-Sleep duration. The data were used to determine whether REM-Sleep timing is controlled homeostatically or by an oscillatory mechanism. The findings and conclusions are that 1) non-REM (NREM) Sleep episode duration is positively correlated with prior REM-Sleep episode duration, suggesting that REM-Sleep expression is permissive of NREM Sleep; 2) mean NREM-Sleep episode duration decreases after repeated brief REM-Sleep episodes ( 30 s), suggesting that REM-Sleep propensity increases progressively within episodes of NREM Sleep; and 5) the diurnal cycle of REM-Sleep expression primarily reflects modulation in the efficiency of REM-Sleep maintenance. These findings support the hypothesis that REM-Sleep timing is controlled by accumulation of REM-Sleep propensity during NREM Sleep.
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REM-Sleep timing is controlled homeostatically by accumulation of REM-Sleep propensity in non-REM Sleep.
The American journal of physiology, 1994Co-Authors: J H Benington, H C HellerAbstract:Sleep structure in the rat was characterized during uninterrupted full-day recordings using an analytic procedure that identifies rapid eye movement (REM) Sleep episodes based on REM-Sleep-onset electroencephalograph phenomena, hence independently of REM-Sleep duration. The data were used to determine whether REM-Sleep timing is controlled homeostatically or by an oscillatory mechanism. The findings and conclusions are that 1) non-REM (NREM) Sleep episode duration is positively correlated with prior REM-Sleep episode duration, suggesting that REM-Sleep expression is permissive of NREM Sleep; 2) mean NREM-Sleep episode duration decreases after repeated brief REM-Sleep episodes (< 30 s), also suggesting that discharge of REM-Sleep propensity is essential for NREM-Sleep expression; 3) REM-Sleep episode duration is independent of prior Sleep history, suggesting that REM-Sleep maintenance is controlled by factors other than accumulated REM-Sleep propensity; 4) brief REM-Sleep episodes occur progressively more frequently over the course of the NREM-Sleep interval between sustained REM-Sleep episodes (> 30 s), suggesting that REM-Sleep propensity increases progressively within episodes of NREM Sleep; and 5) the diurnal cycle of REM-Sleep expression primarily reflects modulation in the efficiency of REM-Sleep maintenance. These findings support the hypothesis that REM-Sleep timing is controlled by accumulation of REM-Sleep propensity during NREM Sleep.
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Does the function of REM Sleep concern non-REM Sleep or waking?
Progress in neurobiology, 1994Co-Authors: Joel H. Benington, H C HellerAbstract:We have hypothesized that REM Sleep is functionally and homeostatically related to NREM Sleep rather than to waking. In other words, REM Sleep rather than to waking. In other words, REM Sleep occurs in response to NREM-Sleep expression and compensates for some process that takes place during NREM Sleep. Under normal conditions, the need for REM Sleep does not accrue during waking. The primary basis for this hypothesis is the fact that REM-Sleep expression is a function of prior NREM-Sleep expression. That is, REM Sleep follows NREM Sleep within Sleep periods, REM-Sleep episodes occur at intervals determined by the amount of NREM-Sleep time elapsed, and total time spent in REM Sleep is consistently about 1/4 of prior NREM-Sleep time, regardless of how much time is spent in NREM Sleep. Our experimental tests of the hypothesis support it. (1) REM-Sleep propensity accumulates quite rapidly during a 2-hr interval spent predominantly in NREM Sleep. (2) The timing of individual REM-Sleep episodes is controlled homeostatically, by accumulation within NREM Sleep of a propensity for REM Sleep. The NREM Sleep-related model of REM-Sleep regulation (Fig. 1) explains a number of phenomena of REM-Sleep expression, including the frequent and periodic occurrence of REM-Sleep episodes throughout Sleep periods, that have been accommodated by the waking-related model but are not functionally accounted for by it. In our opinion, the NREM Sleep-related model of REM-Sleep regulation recommends itself partly by its simplicity. According to the waking-related model, two independent and competing Sleep propensities accumulate during waking and are discharged in two distinct Sleep states that perform different waking-related recovery processes. One behaviour, Sleep, is thought to perform two independent and competing functions that alternate at regular intervals. In the NREM Sleep-related model of REM-Sleep regulation, Sleep debt simply reflects a need for NREM Sleep. That is, the cerebrally less activated state of NREM Sleep enables some form of restoration made necessary by the cerebrally activated state of waking. Periodic occurrence of REM-Sleep episodes is explained without postulating an oscillatory mechanism to gate expression of NREM Sleep versus REM Sleep. In assessing the comparative merits of the waking-related and NREM Sleep-related models of REM-Sleep regulation, one should consider the influence of time-worn habits of thought.(ABSTRACT TRUNCATED AT 400 WORDS)
Adrián Ocampo-garcés - One of the best experts on this subject based on the ideXlab platform.
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REM Sleep-dependent short-term and long-term hourglass processes in the ultradian organization and recovery of REM Sleep in the rat.
Sleep, 2020Co-Authors: Adrián Ocampo-garcés, Alejandro Bassi, Enzo Brunetti, Jorge L. Estrada, Ennio A. VivaldiAbstract:STUDY OBJECTIVES To evaluate the contribution of long-term and short-term REM Sleep homeostatic processes to REM Sleep recovery and the ultradian organization of the Sleep wake cycle. METHODS Fifteen rats were Sleep recorded under a 12:12 LD cycle. Animals were subjected during the rest phase to two protocols (2T2I or 2R2I) performed separately in non-consecutive experimental days. 2T2I consisted of 2 h of total Sleep deprivation (TSD) followed immediately by 2 h of intermittent REM Sleep deprivation (IRD). 2R2I consisted of 2 h of selective REM Sleep deprivation (RSD) followed by 2 h of IRD. IRD was composed of four cycles of 20-min RSD intervals alternating with 10 min of Sleep permission windows. RESULTS REM Sleep debt that accumulated during deprivation (9.0 and 10.8 min for RSD and TSD, respectively) was fully compensated regardless of cumulated NREM Sleep or wakefulness during deprivation. Protocol 2T2I exhibited a delayed REM Sleep rebound with respect to 2R2I due to a reduction of REM Sleep transitions related to enhanced NREM Sleep delta-EEG activity, without affecting REM Sleep consolidation. Within IRD permission windows there was a transient and duration-dependent diminution of REM Sleep transitions. CONCLUSIONS REM Sleep recovery in the rat seems to depend on a long-term hourglass process activated by REM Sleep absence. Both REM Sleep transition probability and REM Sleep episode consolidation depend on the long-term REM Sleep hourglass. REM Sleep activates a short-term REM Sleep refractory period that modulates the ultradian organization of Sleep states.
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REM Sleep phase preference in the crepuscular Octodon degus assessed by selective REM Sleep deprivation.
Sleep, 2013Co-Authors: Adrián Ocampo-garcés, Felipe Westermeyer Hernández, Adrian G. PalaciosAbstract:STUDY OBJECTIVES To determine rapid eye movement (REM) Sleep phase preference in a crepuscular mammal (Octodon degus) by challenging the specific REM Sleep homeostatic response during the diurnal and nocturnal anticrepuscular rest phases. DESIGN We have investigated REM Sleep rebound, recovery, and documented REM Sleep propensity measures during and after diurnal and nocturnal selective REM Sleep deprivations. SUBJECTS Nine male wild-captured O. degus prepared for polysomnographic recordings. INTERVENTIONS Animals were recorded during four consecutive baseline and two separate diurnal or nocturnal deprivation days, under a 12:12 light-dark schedule. Three-h selective REM Sleep deprivations were performed, starting at midday (zeitgeber time 6) or midnight (zeitgeber time 18). MEASUREMENTS AND RESULTS Diurnal and nocturnal REM Sleep deprivations provoked equivalent amounts of REM Sleep debt, but a consistent REM Sleep rebound was found only after nocturnal deprivation. The nocturnal rebound was characterized by a complete recovery of REM Sleep associated with an augment in REM/total Sleep time ratio and enhancement in REM Sleep episode consolidation. CONCLUSIONS Our results support the notion that the circadian system actively promotes REM Sleep. We propose that the Sleep-wake cycle of O. degus is modulated by a chorus of circadian oscillators with a bimodal crepuscular modulation of arousal and a unimodal promotion of nocturnal REM Sleep
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Short-term homeostasis of REM Sleep assessed in an intermittent REM Sleep deprivation protocol in the rat.
Journal of sleep research, 2002Co-Authors: Adrián Ocampo-garcés, Ennio A. VivaldiAbstract:An intermittent rapid eye movement (REM) Sleep deprivation protocol was applied to determine whether an increase in REM Sleep propensity occurs throughout an interval without REM Sleep comparable with the spontaneous Sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light–dark schedule were subjected to an intermittent REM Sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM Sleep permission window alternating with a 20-min REM Sleep deprivation window. REM Sleep increased throughout the protocol, so that total REM Sleep in the two REM Sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM Sleep transitions were already increased in the second deprivation window. Attempted transitions to REM Sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM Sleep changed in correspondence to the amount of REM Sleep in the permission window in-between. Our results suggest that: (i) REM Sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM Sleep; (ii) it diminishes during REM Sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM Sleep. These results are consistent with a homeostatic REM Sleep regulatory mechanism that operates in the time scale of spontaneous Sleep cycle.
Ennio A. Vivaldi - One of the best experts on this subject based on the ideXlab platform.
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REM Sleep-dependent short-term and long-term hourglass processes in the ultradian organization and recovery of REM Sleep in the rat.
Sleep, 2020Co-Authors: Adrián Ocampo-garcés, Alejandro Bassi, Enzo Brunetti, Jorge L. Estrada, Ennio A. VivaldiAbstract:STUDY OBJECTIVES To evaluate the contribution of long-term and short-term REM Sleep homeostatic processes to REM Sleep recovery and the ultradian organization of the Sleep wake cycle. METHODS Fifteen rats were Sleep recorded under a 12:12 LD cycle. Animals were subjected during the rest phase to two protocols (2T2I or 2R2I) performed separately in non-consecutive experimental days. 2T2I consisted of 2 h of total Sleep deprivation (TSD) followed immediately by 2 h of intermittent REM Sleep deprivation (IRD). 2R2I consisted of 2 h of selective REM Sleep deprivation (RSD) followed by 2 h of IRD. IRD was composed of four cycles of 20-min RSD intervals alternating with 10 min of Sleep permission windows. RESULTS REM Sleep debt that accumulated during deprivation (9.0 and 10.8 min for RSD and TSD, respectively) was fully compensated regardless of cumulated NREM Sleep or wakefulness during deprivation. Protocol 2T2I exhibited a delayed REM Sleep rebound with respect to 2R2I due to a reduction of REM Sleep transitions related to enhanced NREM Sleep delta-EEG activity, without affecting REM Sleep consolidation. Within IRD permission windows there was a transient and duration-dependent diminution of REM Sleep transitions. CONCLUSIONS REM Sleep recovery in the rat seems to depend on a long-term hourglass process activated by REM Sleep absence. Both REM Sleep transition probability and REM Sleep episode consolidation depend on the long-term REM Sleep hourglass. REM Sleep activates a short-term REM Sleep refractory period that modulates the ultradian organization of Sleep states.
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Short-term homeostasis of REM Sleep assessed in an intermittent REM Sleep deprivation protocol in the rat.
Journal of sleep research, 2002Co-Authors: Adrián Ocampo-garcés, Ennio A. VivaldiAbstract:An intermittent rapid eye movement (REM) Sleep deprivation protocol was applied to determine whether an increase in REM Sleep propensity occurs throughout an interval without REM Sleep comparable with the spontaneous Sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light–dark schedule were subjected to an intermittent REM Sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM Sleep permission window alternating with a 20-min REM Sleep deprivation window. REM Sleep increased throughout the protocol, so that total REM Sleep in the two REM Sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM Sleep transitions were already increased in the second deprivation window. Attempted transitions to REM Sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM Sleep changed in correspondence to the amount of REM Sleep in the permission window in-between. Our results suggest that: (i) REM Sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM Sleep; (ii) it diminishes during REM Sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM Sleep. These results are consistent with a homeostatic REM Sleep regulatory mechanism that operates in the time scale of spontaneous Sleep cycle.
