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1 an open upper airway become hypotonic during REM sleep.
2 ay closure when asleep, in particular during REM sleep.
3 psychological disorders marked by fragmented REM sleep.
4 in REM sleep relative to quiet waking or non-REM sleep.
5 with larger responses during SWS than during REM sleep.
6 mechanism for upper airway hypotonia during REM sleep.
7 positively correlated across wakefulness and REM sleep.
8 active exclusively in the DOWN state of non-REM sleep.
9 um in cognitive functions and that of MCH in REM sleep.
10 ated in KO compared with OE mice in NREM and REM sleep.
11 context for memory consolidation during non-REM sleep.
12 ong-range correlations break down during non-REM sleep.
13 d maintain breathing automaticity during non-REM sleep.
14 on of GABAergic PPT neurons slightly reduced REM sleep.
15 presence and absence of dreaming in NREM and REM sleep.
16 s wakefulness and also reduces NREM and also REM sleep.
17 cephalon leads to decreases in both NREM and REM sleep.
18 kefulness from propofol anesthesia, NREM and REM sleep.
19 ed a key site for regulating wakefulness and REM sleep.
20 usands of downstates and spindles during non-REM sleep.
21 g, whereas lesions of the PPT in cats reduce REM sleep.
22 cingulate cortex (ACC) and the DLPFC during REM sleep.
23 , these long timescales are abrogated in non-REM sleep.
24 ally different gating mechanisms in NREM and REM sleep.
25 nd evoked delta activity, and an increase in REM sleep.
26 hat regulate the EEG and motor components of REM sleep.
27 cated neurons more selectively active during REM sleep.
28 t (REM) sleep, and to a lesser degree during REM sleep.
29 trol of locomotion, muscle tone, waking, and REM sleep.
30 to be a bihemispheric sleeper that expresses REM sleep.
31 T during NREM sleep was sufficient to induce REM sleep.
32 low-voltage fast desynchronized activity of REM sleep.
33 ay be involved in cognitive processes during REM sleep.
34 these neurons in sleep selectively promotes REM sleep.
35 l areas in non-rapid eye movement (NREM) and REM sleep.
36 in mice has shown that it can also occur in REM sleep.
37 n of hypoglossal motor neurons (HMNs) during REM sleep.
38 has shown that slow waves can also occur in REM sleep.
39 ring sleep, particularly rapid eye movement (REM) sleep.
40 tribute to forgetting in rapid eye movement (REM) sleep.
41 ep, in particular during rapid-eye-movement (REM) sleep.
42 eye movement (NREM) and rapid eye movement (REM) sleep.
43 hypopnea indices during rapid eye movement (REM) sleep.
44 s restricted primarily to periods of active (REM) sleep.
45 vioral states, including rapid eye-movement (REM) sleep.
46 y was related to time in rapid eye movement (REM) sleep.
47 cephalogram (EEG) during rapid eye movement (REM) sleep.
48 onic twitches of the whiskers during active (REM) sleep.
49 ine which species 'have' rapid eye movement (REM) sleep.
50 that are reactivated during REM, but not non-REM, sleep.
51 hat occur during non-rapid-eye-movement (non-REM) sleep(1-8) and whose disruption impairs spatial mem
52 Response thresholds were also greater in REM sleep (10 mW) compared to non-REM and waking (3 to 5
53 haviors, including rapid eye movement sleep (REM sleep), a sleep phase when the brain is as active as
54 rs exclusively and abundantly during active (REM) sleep, a particularly prominent state in early deve
55 Cholinergic REM Induction Test revealed that REM sleep abnormalities can be mimicked by administratio
61 ns, which were wake- and rapid eye movement (REM) sleep-active, produced wakefulness through projecti
62 mulations of LH MCH neural activity increase REM sleep after long-term withdrawal with important diff
64 ABNs that are reactivated during subsequent REM sleep against a backdrop of overall reduced ABN acti
65 Compared to NREM sleep, IEDs location in REM sleep also showed a higher concordance with electrog
67 silencing of this sparse ABN activity during REM sleep alters the structural remodeling of spines on
69 ly, such a decline was associated with lower REM sleep amounts, supporting a role for REM sleep in ov
70 Almost all antidepressant agents suppress REM sleep and a time-and-dose-response relationship betw
71 g revealed dynamic network activation during REM sleep and activation of a subset of the neurons duri
72 led dynamic activation of MCH neurons during REM sleep and activation of a subset of the same neurons
81 ortex, naive participants were awakened from REM sleep and responded to a questionnaire on bodily sen
82 ely, there was no direct correlation between REM sleep and SCRs, indicating that REM may only modulat
84 ls for the regulation of rapid eye movement (REM) sleep and non-REM sleep, how mutual inhibition betw
85 n of glycine-induced non-rapid eye movement (REM) sleep and shortened NREM sleep latency with a simul
87 o induce spindles during rapid-eye movement (REM) sleep and wakefulness-behavioral states that do not
89 were found to be synchronously active during REM sleep, and also during the exploration of novel obje
92 olidation), the neural circuits that control REM sleep, and how dysfunction of REM sleep mechanisms u
93 the number of oxygen desaturation events in REM sleep, and increased ventilation in non-REM and REM
94 d processing in the prefrontal region during REM sleep, and inhibited neural activation in the untrai
95 alcium spikes increased substantially during REM sleep, and the blockade of these calcium spikes prev
96 ence of dreams in human sleep, especially in REM sleep, and the detection of physiologically similar
98 uring quiet wake and non-rapid eye movement (REM) sleep, and to a lesser degree during REM sleep.
99 that dendritic calcium spikes arising during REM sleep are important for pruning and strengthening ne
100 et out to determine whether movements during REM sleep are processed by different motor networks than
102 Although quiet wake and rapid eye movement (REM) sleep are characterized by similar, long timescales
103 R1-KO) mice showed no significant changes in REM sleep as a function of T(a), even with increased sle
105 -eye-movement (NREM) and rapid-eye-movement (REM) sleep, as well as increased sleep fragmentation.
106 e anatomical, cellular and synaptic basis of REM sleep atonia control is a critical step for treating
108 l Jouvet used the term paradoxical to define REM sleep because of the simultaneous occurrence of a co
109 Patients with Parkinson's disease (PD) and REM sleep behavior disorder (RBD) show mostly unimpaired
110 nsylvania Smell Identification Test (UPSIT), REM Sleep Behavior Disorder screening questionnaire (RBD
113 valence, and survival of rapid eye movement (REM) sleep behavior disorder (RBD) in patients who devel
114 The presence of probable rapid eye movement (REM) sleep behavior disorder was strongly associated wit
118 including obstructive sleep apnoea (apnea), REM sleep behaviour disorder (RBD) and narcolepsy with c
122 ores, higher depression scores and increased REM sleep behaviour disorder symptoms compared to patien
123 d with Parkinson's disease--in patients with REM sleep behaviour disorder without Parkinson's disease
124 ients with polysomnography-proven idiopathic REM sleep behaviour disorder, 26 cases with early Parkin
125 with Parkinson's disease in individuals with REM sleep behaviour disorder, a condition associated wit
126 s of dementia and parkinsonism in idiopathic REM sleep behaviour disorder: a multicentre study' by Po
128 ean (SD) 19.2 (12.7) vs 6.1 (5.7); p<0.001), REM-sleep behaviour disorder screening questionnaire (me
132 n contrast, the E/I balance decreased during REM sleep but only after pre-sleep training, and the dec
133 was stronger during waking compared with non-REM sleep but stronger during non-REM sleep among deep-l
134 mice, that slow waves occur regularly during REM sleep, but only in primary sensory and motor areas a
135 ted in the generation of rapid eye movement (REM) sleep, but the underlying circuit mechanisms remain
136 spindles throughout the cerebral cortex and REM sleep by an "activated," low-voltage fast electroenc
137 on of negative delta (1-4 Hz) waves in human REM sleep by analyzing high-density EEG sleep recordings
138 ol the upper airway muscles are inhibited in REM sleep by the combination of monoaminergic disfacilit
139 has been identified with rapid eye-movement (REM) sleep, characterized by wake-like, globally 'activa
140 day SF procedure that selectively fragmented REM sleep, cholinergic output neurons (ChNs) in the mHb
141 llations were calculated during movements in REM sleep compared with movements in the waking state an
142 tentials revealed elevated beta power during REM sleep compared with NREM sleep and beta power in REM
143 nots, and more on the diverse expression of REM sleep components over development and across species
144 interrogation of brain circuitry linked with REM sleep control, in turn revealing how REM sleep mecha
146 on regulation, we hypothesized that restless REM sleep could interfere with the overnight resolution
148 263397 increased waking and reduced NREM and REM sleep, decreased gamma power during wake and NREM, a
149 ormance gains independent of learning, while REM sleep decreases plasticity to stabilize learning in
151 ing of complex representations necessary for REM sleep-dependent memory consolidation.SIGNIFICANCE ST
154 in deep NREM sleep and, importantly, also in REM sleep, despite the recovery of wake-like neural acti
155 nerated movements produced during active (or REM) sleep, differ from wake movements in that they reli
156 results not only demonstrate that selective REM sleep disturbance leads to hyperactivity of mHb ChNs
163 r trauma exposure was sufficient to increase REM sleep duration during both the Light and Dark Phase,
165 at wild-type (WT) mice dynamically increased REM sleep durations specifically during warm T(a) pulsin
167 d within species, the potential functions of REM sleep (e.g., memory consolidation), the neural circu
174 the discovery of REM sleep, the diversity of REM sleep expression across and within species, the pote
175 ed with T(a) warming, showing an increase in REM sleep expression beyond what T(a) warming in yellow
180 e hypoglossal motor nucleus (MoXII) restores REM sleep genioglossus activity, highlighting the import
183 on of rapid eye movement (REM) sleep and non-REM sleep, how mutual inhibition between specific pathwa
187 inhibited by glycinergic transmission during REM sleep, hypoglossal motoneurons that control the uppe
188 p regulates emotional memory, and persistent REM sleep impairment after cocaine withdrawal negatively
190 eficient for neurotensin exhibited increased REM sleep, implicating the involvement of the neuropepti
192 al, giving clinical relevance to the role of REM sleep in emotion regulation in insomnia, depression,
194 These findings reveal an important role of REM sleep in experience-dependent synapse elimination an
196 erefore, delta waves are an integral part of REM sleep in humans and the two identified subtypes (saw
201 des evidence that nocturnal movements during REM sleep in Parkinson's disease (PD) patients are not p
202 motor task is learned, indicating a role for REM sleep in pruning to balance the number of new spines
203 on a template derived from the expression of REM sleep in the adults of a small number of mammalian s
204 Our findings provide evidence for a role for REM sleep in the maintenance of cellular representations
205 ring NREM sleep and reward processing during REM sleep in the reward group but not in the no-reward g
206 kefulness and suppresses rapid-eye movement (REM) sleep in mice and rats and reduces cataplexy in two
207 ovement (NREM) sleep and rapid eye movement (REM) sleep, in six medication-refractory focal epilepsy
209 eam mentation occurs during both non-REM and REM sleep, indicates that all mammals have the potential
213 d in healthy adult individuals, we show that REM sleep is characterized by prominent delta waves also
215 ing signal for postural muscle atonia during REM sleep is thought to originate from glutamatergic neu
223 arcolepsy, a disorder of rapid eye movement (REM) sleep, is characterized by excessive daytime sleepi
224 pheric slow wave sleep (USWS) and suppressed REM sleep, it is unclear whether the mysticete whales sh
225 t, which is dominated by rapid eye movement (REM) sleep, led to better discrimination between fear-re
226 Initial hopes that these abnormalities of REM sleep may serve as differential-diagnostic markers f
227 dy suggest that baseline rapid eye movement (REM) sleep may serve a protective function against enhan
228 ith REM sleep control, in turn revealing how REM sleep mechanisms themselves impact processes such as
229 at control REM sleep, and how dysfunction of REM sleep mechanisms underlie debilitating sleep disorde
231 able entrainment of spindle power during non-REM sleep, nor of theta power during resting wakefulness
232 ic stimulation promotes both wakefulness and REM sleep, optogenetic stimulation of these neurons in s
234 preferentially increases rapid eye movement (REM) sleep over non-REM (NREM) sleep across species.
236 may not be continuously available during non-REM sleep, permitting the cortex to control thalamic spi
238 ults indicate that higher baseline levels of REM sleep predict reduced fear-related activity in, and
239 rence of dreaming during rapid eye movement (REM) sleep prompts interest in the role of REM sleep in
241 these neurons selectively in sleep enhances REM sleep quality and quantity after long-term withdrawa
242 p compared with NREM sleep and beta power in REM sleep reached levels similar as in the waking state.
244 movement - rapid eye movement (REM) cycling, REM sleep reduction or loss, and REM sleep instruction i
247 understood how cocaine experience may alter REM sleep regulatory machinery, and what may serve to im
248 cataplexy, nighttime sleep disturbances, and REM-sleep-related phenomena (sleep paralysis, hallucinat
249 ccurred in all recorded neurons (n = 106) in REM sleep relative to quiet waking or non-REM sleep.
250 matergic neurons are maximally active during REM sleep (REM-max), while the majority of GABAergic neu
255 As previously reported in our analysis of REM sleep responses, we found different patterns of chan
257 alidated to be a specific proxy for restless REM sleep (selective fragmentation: R = 0.57, P < 0.001;
259 related to EEG oscillatory parameters of non-REM sleep serving as markers of sleep-dependent memory c
261 received auditory cueing during NREM but not REM sleep showed impaired fear memory upon later present
262 of electroencephalographic activation during REM sleep similar to that observed during the performanc
264 pectral slope discriminates wakefulness from REM sleep solely based on the neurophysiological brain s
265 oglossal motor output in-vivo and identifies REM sleep specific suppression of net motor excitability
268 eye movement (NREM) and rapid eye movement (REM) sleep, strongly consolidating the waking state for
269 tion between complexity and motor indices in REM sleep suggests drastically different gating mechanis
270 and-dose-response relationship between total REM sleep suppression and therapeutic response to treatm
271 levels and provide a possible mechanism for REM sleep suppression of upper airway muscle activity.SI
272 vity was greater in exploratory behavior and REM sleep than in quiet wakefulness and slow wave sleep,
275 s the historical origins of the discovery of REM sleep, the diversity of REM sleep expression across
276 during phasic REM sleep but not during tonic REM sleep, the latter resembling relaxed wakefulness.
279 during training enhanced rapid eye movement (REM) sleep time, increased oscillatory activities for re
282 a period of rapid eye movement (REM) and non-REM sleep, was absent in all animals in which 5-HT defic
283 nce, that dream mentation only occurs during REM sleep, we conclude that it is unlikely that monotrem
284 This finding may help explain why, during REM sleep, we remain disconnected from the environment e
285 st activity map of individual neurons during REM sleep, we use deep-brain calcium imaging in unrestra
286 When dreaming during rapid eye movement (REM) sleep, we can perform complex motor behaviors while
289 neural circuits to opportunistically express REM sleep when the need for thermoregulatory defense is
290 by non-rapid eye movement (NREM) sleep or by REM sleep, whether it results from plasticity increases
291 show mostly unimpaired motor behavior during REM sleep, which contrasts strongly to coexistent noctur
292 cortex interferes with dream movement during REM sleep, which is consistent with a causal contributio
293 rimarily occurred during rapid-eye movement (REM) sleep, which is notable because REM is associated w
294 ostasis, KO mice accrued only half the extra REM sleep wild-type (WT) littermates obtained during rec
296 ur results suggest that elevated submentalis REM sleep without atonia appears to be a potentially use
297 r operating characteristic curves determined REM sleep without atonia cutoffs distinguishing synuclei
299 utility of quantitative rapid eye movement (REM) sleep without atonia analysis in the submentalis an
300 Spindles and SWRs were initiated during non-REM sleep, yet the changes were incorporated in the netw