ライフサイエンスコーパス: REM sleep

1 t (REM) sleep, and to a lesser degree during REM sleep.

2 ong-range correlations break down during non-REM sleep.

3 trol of locomotion, muscle tone, waking, and REM sleep.

4 to be a bihemispheric sleeper that expresses REM sleep.

5 d maintain breathing automaticity during non-REM sleep.

6 T during NREM sleep was sufficient to induce REM sleep.

7 nt of the pontomedullary network controlling REM sleep.

8 ut reduced fR only during quiet wake and non-REM sleep.

9 ons of this area have had varying effects on REM sleep.

10 ut reduced fR only during quiet wake and non-REM sleep.

11 VT but raised fR only in quiet wake and non-REM sleep.

12 why central sleep apnoea is less frequent in REM sleep.

13 or agonist) in the SubC virtually eliminated REM sleep.

14 ency and produced sighs and arousal from non-REM sleep.

15 eversed theta flow was most prominent during REM sleep.

16 btherapeutic levels for 3 minutes during non-REM sleep.

17 to suppress SWS and promote wakefulness and REM sleep.

18 t induces wake transitions from both SWS and REM sleep.

19 obably serve to promote muscle atonia during REM sleep.

20 ocampal theta oscillations that characterize REM sleep.

21 ed the relationship between FPS response and REM sleep.

22 y stimulation, sighing, and arousal from non-REM sleep.

23 tion, both of which are cardinal features of REM sleep.

24 riance in startle retention accounted for by REM sleep.

25 g non-REM or transitions between non-REM and REM sleep.

26 vorexant induced sleep largely by increasing REM sleep.

27 O) of rats induced long-lasting increases in REM sleep.

28 on of GABAergic PPT neurons slightly reduced REM sleep.

29 the circuitry regulating motor atonia during REM sleep.

30 presence and absence of dreaming in NREM and REM sleep.

31 s wakefulness and also reduces NREM and also REM sleep.

32 cephalon leads to decreases in both NREM and REM sleep.

33 ed a key site for regulating wakefulness and REM sleep.

34 usands of downstates and spindles during non-REM sleep.

35 g, whereas lesions of the PPT in cats reduce REM sleep.

36 cingulate cortex (ACC) and the DLPFC during REM sleep.

37 , these long timescales are abrogated in non-REM sleep.

38 ally different gating mechanisms in NREM and REM sleep.

39 um in cognitive functions and that of MCH in REM sleep.

40 ated in KO compared with OE mice in NREM and REM sleep.

41 context for memory consolidation during non-REM sleep.

42 hat regulate the EEG and motor components of REM sleep.

43 cated neurons more selectively active during REM sleep.

44 eye movement (NREM) and rapid eye movement (REM) sleep.

45 y was related to time in rapid eye movement (REM) sleep.

46 uch as wheel running and rapid eye movement (REM) sleep.

47 ral to the regulation of rapid eye movement (REM) sleep.

48 ine in the regulation of rapid-eye-movement (REM) sleep.

49 ws decreased activity in rapid eye movement (REM) sleep.

50 hypopnea indices during rapid eye movement (REM) sleep.

51 s restricted primarily to periods of active (REM) sleep.

52 vioral states, including rapid eye-movement (REM) sleep.

53 ehavioral arousal during SWS, but not during REM sleep, a result in contrast to the previously report

54 rs exclusively and abundantly during active (REM) sleep, a particularly prominent state in early deve

55 In infant rats during active (or REM) sleep--a behavioral state that predominates in earl

56 t with being presynaptic to the phenotype of REM sleep-active SLD neurons.

57 apnea-hypopnea index in REM (AHIREM) and non-REM sleep (AHINREM), respectively.

58 on the other night, CPAP was reduced only in REM sleep, allowing REM OSA to recur.

59 In addition, REM sleep also promotes local learning-dependent activit

60 Moreover, REM sleep also strengthens and maintains newly formed sp

61 ly, such a decline was associated with lower REM sleep amounts, supporting a role for REM sleep in ov

62 n between cortical areas is disrupted in non-REM sleep and anesthesia.

63 PPN lesion induced a transient decrease in REM sleep and in slow-wave sleep followed by a slight im

64 bition of pharyngeal motoneurons accompanies REM sleep and is a cause of hypoventilation and obstruct

65 evailing thought, the DLPFC is active during REM sleep and likely interacting with other areas.

66 ave suggested that lesions or dysfunction in REM sleep and motor control circuitry in the pontomedull

67 beta activity before and during movements in REM sleep and NREM sleep.

68 MCH into the DRN resulted in an increase in REM sleep and produce a depressive-like effect.

69 Hypoventilation can occur in REM sleep and progress into non-REM sleep, with continuo

70 ibition reduced breathing equally during non-REM sleep and quiet wake.

71 activity that occurs from wakefulness to non-REM sleep and reduces airway collapsibility.

72 ely, there was no direct correlation between REM sleep and SCRs, indicating that REM may only modulat

73 olidation is differentially mediated by both REM sleep and SWS.

74 EG signatures of non-rapid eye movement (non-REM) sleep and are thought to play an important role in

75 ls for the regulation of rapid eye movement (REM) sleep and non-REM sleep, how mutual inhibition betw

76 n of glycine-induced non-rapid eye movement (REM) sleep and shortened NREM sleep latency with a simul

77 duction in time spent in rapid eye movement (REM) sleep and slow-wave sleep and an increase in muscle

78 o induce spindles during rapid-eye movement (REM) sleep and wakefulness-behavioral states that do not

79 , with unihemispheric slow waves, suppressed REM sleep, and continuous bodily movement.

80 olidation), the neural circuits that control REM sleep, and how dysfunction of REM sleep mechanisms u

81 accessory respiratory muscles, reduction in REM sleep, and loss of normal REM atonia in some individ

82 by diminished frontal connectivity, reduced REM sleep, and poorer performance.

83 Together with few episodic memory traces in REM sleep, and REM sleep deprivation affecting hippocamp

84 uring quiet wake and non-rapid eye movement (REM) sleep, and to a lesser degree during REM sleep.

85 that dendritic calcium spikes arising during REM sleep are important for pruning and strengthening ne

86 et out to determine whether movements during REM sleep are processed by different motor networks than

87 Slow waves of non-REM sleep are suggested to play a role in shaping synapt

88 Although quiet wake and rapid eye movement (REM) sleep are characterized by similar, long timescales

89 hin the DRN is involved in the regulation of REM sleep as well as in the pathophysiology of depressiv

90 ion in the reinforcement of transitions into REM sleep, as evidenced by increases in non-REM-to-REM s

91 -eye-movement (NREM) and rapid-eye-movement (REM) sleep, as well as increased sleep fragmentation.

92 e anatomical, cellular and synaptic basis of REM sleep atonia control is a critical step for treating

93 EM neurons are regulated and in turn produce REM sleep atonia.

94 The HCVR is reduced during REM sleep because fR is no longer under chemoreceptor co

95 se metabolism is distinct for non-REM versus REM sleep because of differences in sleep-state-dependen

96 l Jouvet used the term paradoxical to define REM sleep because of the simultaneous occurrence of a co

97 ntribution to the tidal volume during phasic REM sleep becomes a critical vulnerability, resulting in

98 Patients with Parkinson's disease (PD) and REM sleep behavior disorder (RBD) show mostly unimpaired

99 nephrine levels, slow resting heart rate, no REM sleep behavior disorder, and preserved smell.

100 certain phenomenological aspects observed in REM sleep behavior disorder.

101 Rapid eye movement (REM) sleep behavior disorder (RBD) is a failure of the c

102 The presence of probable rapid eye movement (REM) sleep behavior disorder was strongly associated wit

103 including obstructive sleep apnoea (apnea), REM sleep behaviour disorder (RBD) and narcolepsy with c

104 Concomitant REM sleep behaviour disorder (RBD) is commonly observed

105 nderlie debilitating sleep disorders such as REM sleep behaviour disorder and narcolepsy.

106 Both patients with REM sleep behaviour disorder and Parkinson's disease dem

107 Individuals with REM sleep behaviour disorder are at significantly higher

108 uitry in the pontomedullary structures cause REM sleep behaviour disorder phenomenology, and degenera

109 he presence of probable RBD (pRBD) using the REM Sleep Behaviour Disorder Screening Questionnaire (RB

110 ores, higher depression scores and increased REM sleep behaviour disorder symptoms compared to patien

111 d with Parkinson's disease--in patients with REM sleep behaviour disorder without Parkinson's disease

112 ese structures might explain the presence of REM sleep behaviour disorder years or decades before the

113 n the four patients with REM sleep recorded, REM sleep behaviour disorder).

114 ients with polysomnography-proven idiopathic REM sleep behaviour disorder, 26 cases with early Parkin

115 with Parkinson's disease in individuals with REM sleep behaviour disorder, a condition associated wit

116 Apathy, REM sleep behaviour disorder, anosmia, hypersalivation,

117 Rapid eye movement (REM) sleep behaviour disorder (RBD) is characterised by

118 and 24% versus 10% scored above cut-off for REM-sleep behaviour disorder (p=0.008).

119 er risk using proxies, including smell loss, REM-sleep behaviour disorder and reduced tapping speed,

120 hat is specifically associated with restless REM sleep (beta = 0.31, P < 10(-26)).

121 developments in our current understanding of REM sleep biology and pathobiology.

122 This pattern is present during phasic REM sleep but not during tonic REM sleep, the latter res

123 oning during stage 2 and rapid eye movement (REM) sleep but not following aversive conditioning durin

124 emained across all sleep stages (N1, N2, and REM sleep), but with an incomplete structure; compared w

125 mice, that slow waves occur regularly during REM sleep, but only in primary sensory and motor areas a

126 also contains neurons that are active during REM sleep, but whether they play a causal role in REM sl

127 ted in the generation of rapid eye movement (REM) sleep, but the underlying circuit mechanisms remain

128 spindles throughout the cerebral cortex and REM sleep by an "activated," low-voltage fast electroenc

129 finalistic behaviours, normalisation of non-REM sleep by the end of the night, and, in the four pati

130 he waking rat and during rapid eye movement (REM) sleep by simultaneously recording local field and s

131 During quiet resting and non-REM sleep, C1 cell stimulation (20 s, 2-20 Hz) increased

132 During hypoxia (awake) or REM sleep, C1 cell stimulation increases BP but no longe

133 has been identified with rapid eye-movement (REM) sleep, characterized by wake-like, globally 'activa

134 llations were calculated during movements in REM sleep compared with movements in the waking state an

135 tentials revealed elevated beta power during REM sleep compared with NREM sleep and beta power in REM

136 ncreased sleep spindle density and decreased REM sleep compared with placebo and sodium oxybate (Xyre

137 ght, with 28.4% of the variance in increased REM sleep consolidation from baseline accounted for by s

138 uisition phase was associated with increased REM sleep consolidation that night, with 28.4% of the va

139 Rapid eye movement (REM) sleep constitutes a distinct "third state" of consc

140 interrogation of brain circuitry linked with REM sleep control, in turn revealing how REM sleep mecha

141 uced contribution of RTN to breathing during REM sleep could explain why certain central apnoeas are

142 on regulation, we hypothesized that restless REM sleep could interfere with the overnight resolution

143 263397 increased waking and reduced NREM and REM sleep, decreased gamma power during wake and NREM, a

144 This REM sleep-dependent elimination of new spines facilitate

145 few episodic memory traces in REM sleep, and REM sleep deprivation affecting hippocampus-independent

146 in deep NREM sleep and, importantly, also in REM sleep, despite the recovery of wake-like neural acti

147 ed transitions from SWS to wakefulness or to REM sleep did not significantly differ from that of natu

148 of mnemonics to be dreamlike, nor does their REM sleep differ from mnemonic-naive control subjects.

149 nerated movements produced during active (or REM) sleep, differ from wake movements in that they reli

150 ontradict an isomorphism between features of REM sleep dreaming and mnemonic principles.

151 thesis about the lack of rapid eye movement (REM)-sleep dreaming leading to loss of personal identity

152 This result suggests that transmission of REM sleep drive to the SubC is acetylcholine-independent

153 h selectively decreased the fragmentation of REM sleep during their inactive (light) phase without ch

154 d within species, the potential functions of REM sleep (e.g., memory consolidation), the neural circu

155 models controlled for OSA events during non-REM sleep, either by statistical adjustment or by strati

156 Recently, restless rapid-eye-movement (REM) sleep emerged as a robust signature of sleep in ins

157 We therefore propose that, in REM sleep, endogenously generated processes compete with

158 ber of REM sleep episodes and did not change REM sleep episode duration.

159 non-REM (NREM) sleep increased the number of REM sleep episodes and did not change REM sleep episode

160 Hence, the periodic occurrence of REM sleep episodes and dreaming may be regarded as a rec

161 n increase in muscle tone during REM and non-REM sleep episodes and in the number of awakenings and m

162 ergic neurons rapidly and reliably initiated REM sleep episodes and prolonged their durations, wherea

163 corporated in the network over the following REM sleep epoch.

164 spatio-temporal physiological signatures of REM sleep, especially in humans.

165 Although wake and rapid eye movement (REM) sleep exhibit long timescales, these long-range cor

166 Animals with improved REM sleep exhibited decreased incubation of cocaine crav

167 thdrawal from cocaine, animals with improved REM sleep exhibited reduced accumulation of CP-AMPARs in

168 the discovery of REM sleep, the diversity of REM sleep expression across and within species, the pote

169 spindle-like oscillations; and (3) increased REM sleep expression.

170 tween the hippocampus and the BLA during non-REM sleep following training.

171 uggest that sleep difficulties, specifically REM sleep fragmentation, may play a mechanistic role in

172 transition to waking or rapid eye movement (REM) sleep from slow-wave sleep (SWS).

173 REM sleep frontal high delta power was a negative correl

174 olinergic neurotransmission to contribute to REM sleep generation has been established, the role of c

175 leep, but whether they play a causal role in REM sleep generation remains unclear.

176 ainstem is both necessary and sufficient for REM sleep generation, and the neural circuits in the pon

177 olinergic inputs are not majorly involved in REM sleep generation, they may perform a minor function

178 um (PPT) and laterodorsal tegmentum (LDT) in REM sleep generation.

179 Initial theories of rapid eye movement (REM) sleep generation posited that induction of the stat

180 Together, these findings indicate that REM sleep has multifaceted functions in brain developmen

181 tial navigational memory, a similar role for REM sleep has never been examined in humans.

182 hanisms and functions of rapid-eye-movement (REM) sleep have occurred over the past decade.

183 on of rapid eye movement (REM) sleep and non-REM sleep, how mutual inhibition between specific pathwa

184 In REM sleep, however, this relationship was reversed.

185 During quiet wake or non-REM sleep, hypercapnia (3 or 6% FI,CO2 ) increased both

186 During quiet wake or non-REM sleep, hypercapnia increased both breathing frequenc

187 ncy (fR ) and tidal volume (VT ) whereas, in REM sleep, hypercapnia increased VT exclusively.

188 I,CO2 ) increased both fR and VT whereas, in REM sleep, hypercapnia increased VT exclusively.

189 of HEP within stage 2, slow-wave sleep, and REM sleep in 40 children with primarily mild to moderate

190 rk across individuals, suggesting a role for REM sleep in affective brain recalibration.

191 dual antagonists, MK-1064 increases NREM and REM sleep in dogs without inducing cataplexy.

192 al, giving clinical relevance to the role of REM sleep in emotion regulation in insomnia, depression,

193 Given the role of REM sleep in emotion regulation, we hypothesized that re

194 frequency of slow waves recorded during non-REM sleep in freely moving, naturally sleeping-waking ra

195 ing and safety signal learning on subsequent REM sleep in healthy adults.

196 conclusion, we demonstrate a novel role for REM sleep in human memory formation and highlight a sign

197 from the ventral medulla powerfully promotes REM sleep in mice.

198 likely to play a role in the suppression of REM sleep in odontocete cetaceans.

199 wer REM sleep amounts, supporting a role for REM sleep in overnight emotional processing.

200 des evidence that nocturnal movements during REM sleep in Parkinson's disease (PD) patients are not p

201 motor task is learned, indicating a role for REM sleep in pruning to balance the number of new spines

202 ovides a novel way of addressing the role of REM sleep in spatial navigational memory with a physiolo

203 he developmental role of rapid eye movement (REM) sleep in children.

204 exclusively and abundantly during active (or REM) sleep in mammals, especially in early development [

205 uggest the importance of rapid eye movement (REM) sleep in spatial navigational memory, a similar rol

206 haracteristics during quiet wake, non-REM or REM sleep, including variable dependence on PCO2.

207 Stimulation during REM sleep increased BP, but had no effect on EEG or brea

208 Characteristics of these REM sleep increases were identical to those resulting fr

209 c boutons in the PnO are responsible for the REM sleep induction by GABA(A) receptor antagonists thro

210 During active (or REM) sleep, infant mammals exhibit myoclonic twitches of

211 t stimulation in the lower gamma band during REM sleep influences ongoing brain activity and induces

212 This mechanism is the major cause of REM sleep inhibition at a pharyngeal motor pool critical

213 M) cycling, REM sleep reduction or loss, and REM sleep instruction in wakefulness.

214 phasic P-wave activity, during post-training REM sleep is critical for consolidation of fear extincti

215 The brain circuitry governing REM sleep is located in the pontine and medullary brains

216 ing signal for postural muscle atonia during REM sleep is thought to originate from glutamatergic neu

217 e of cholinergic inputs in the generation of REM sleep is ultimately undetermined as the critical tes

218 this sudden amelioration of motor control in REM sleep is unknown, however.

219 Rapid eye movement (REM) sleep is a distinct brain state characterized by ac

220 Rapid eye movement (REM) sleep is a recurring part of the sleep-wake cycle c

221 Rapid eye movement (REM) sleep is an important component of the natural slee

222 during the second half, rapid eye movement (REM) sleep is more predominant.

223 We conclude that sleep, especially REM sleep, is causal to successful consolidation of dang

224 arcolepsy, a disorder of rapid eye movement (REM) sleep, is characterized by excessive daytime sleepi

225 pheric slow wave sleep (USWS) and suppressed REM sleep, it is unclear whether the mysticete whales sh

226 iciency, sleep onset and rapid eye movement [REM] sleep latencies, non-REM and REM sleep stages, and

227 t, which is dominated by rapid eye movement (REM) sleep, led to better discrimination between fear-re

228 ocus supporting short-latency induction of a REM sleep-like state following local application of a GA

229 bachol into the dorsomedial pons produces an REM sleep-like state with muscle atonia and cortical act

230 hibition of genioglossus activity throughout REM sleep; likewise, with G-protein-coupled inwardly rec

231 dy suggest that baseline rapid eye movement (REM) sleep may serve a protective function against enhan

232 ith REM sleep control, in turn revealing how REM sleep mechanisms themselves impact processes such as

233 at control REM sleep, and how dysfunction of REM sleep mechanisms underlie debilitating sleep disorde

234 both necessary and sufficient for generating REM sleep muscle atonia.

235 In REM sleep, neurons of the sublaterodorsal tegmental nucl

236 able entrainment of spindle power during non-REM sleep, nor of theta power during resting wakefulness

237 eep Cohort Study with at least 30 minutes of REM sleep obtained from overnight in-laboratory polysomn

238 The capability to induce REM sleep on command may offer a powerful tool for inves

239 We also examined the effects of changes in REM sleep on retention of fear and safety learning.

240 During REM sleep, on the phenomenological level, this composite

241 ow wave sleep (SWS) differs from that during REM sleep or waking states.

242 undifferentiated non-rapid-eye-movement [non-REM] sleep or poorly structured stage N2, simple movemen

243 re fitted to explore the association between REM sleep OSA and prevalent hypertension in the entire c

244 d with SWS (P < 0.05) and WASO compared with REM sleep (P < 0.05).

245 may not be continuously available during non-REM sleep, permitting the cortex to control thalamic spi

246 Except in REM sleep, phasic RTN stimulation entrained and shortene

247 In addition, REM sleep physiology across the sleep-rested night signi

248 states, but with a greater likelihood after REM sleep, potentially due to an observed increase in ba

249 ults indicate that higher baseline levels of REM sleep predict reduced fear-related activity in, and

250 Here we show that REM sleep prunes newly formed postsynaptic dendritic spi

251 or is in autorhythmic mode (anaesthesia, non-REM sleep, quiet wake).

252 argues for generic information processing in REM sleep rather than linking episodic memory traces.

253 p compared with NREM sleep and beta power in REM sleep reached levels similar as in the waking state.

254 of the night, and, in the four patients with REM sleep recorded, REM sleep behaviour disorder).

255 REM disruption via this method caused REM sleep reduction and significantly fragmented any rem

256 movement - rapid eye movement (REM) cycling, REM sleep reduction or loss, and REM sleep instruction i

257 The findings suggest that restless REM sleep reflects a process that interferes with the ov

258 esopontine tegmentum have been implicated in REM sleep regulation, but lesions of this area have had

259 matergic neurons are maximally active during REM sleep (REM-max), while the majority of GABAergic neu

260 wake cycle, yet the mechanisms that regulate REM sleep remain incompletely understood.

261 underlying mechanisms of rapid eye movement (REM) sleep remain unclear.

262 ons showed that they were most active during REM sleep (REMmax), and during wakefulness they were pre

263 In both NREM and REM sleep, reports of dream experience were associated w

264 alidated to be a specific proxy for restless REM sleep (selective fragmentation: R = 0.57, P < 0.001;

265 related to EEG oscillatory parameters of non-REM sleep serving as markers of sleep-dependent memory c

266 received auditory cueing during NREM but not REM sleep showed impaired fear memory upon later present

267 of electroencephalographic activation during REM sleep similar to that observed during the performanc

268 cantly lower in children with SDB during non-REM sleep (stage 2: P = 0.03; slow-wave sleep: P = 0.001

269 knowledge of the physiology of NREM and then REM sleep stages and their ordered succession.

270 movement [REM] sleep latencies, non-REM and REM sleep stages, and wakefulness after sleep onset); an

271 When SFA is minimal (in waking or REM sleep state, high ACh) patterns of activity are loca

272 robiological features of rapid eye movement (REM) sleep suggest more functions than only elaborative

273 tion between complexity and motor indices in REM sleep suggests drastically different gating mechanis

274 ation of ch-BF neurons during wakefulness or REM sleep sustained the cortical activation.

275 rapid eye movement (SOREM) periods in BIISS, REM sleep tends to arise from stage 2 sleep (non-REM (NR

276 enioglossus activity from wakefulness to non-REM sleep that occurred on the placebo night.

277 During non-REM sleep the EEG is dominated by slow waves which resul

278 part of the brain - may function to control REM sleep, the brain state that underlies dreaming.

279 s the historical origins of the discovery of REM sleep, the diversity of REM sleep expression across

280 during phasic REM sleep but not during tonic REM sleep, the latter resembling relaxed wakefulness.

281 ives wakefulness, whereas inhibition reduces REM sleep theta activity.

282 tently contribute to motor inhibition during REM sleep through descending projections to motor-relate

283 eep, as evidenced by increases in non-REM-to-REM sleep transition duration and failure rate during ch

284 rst half of the sleep period leaving most of REM sleep untreated.

285 e during wakefulness and rapid eye movement (REM) sleep (wake/REM active) than during non-REM (NREM)

286 However, REM sleep was not reduced by scopolamine microperfusion

287 SDB severity during REM and non-REM sleep was quantified using the apnea-hypopnea index

288 Yet until now, cortical activity during REM sleep was thought to be homogenously wake-like.

289 Overnight REM sleep was, in turn, related to overnight retention o

290 a period of rapid eye movement (REM) and non-REM sleep, was absent in all animals in which 5-HT defic

291 This finding may help explain why, during REM sleep, we remain disconnected from the environment e

292 When dreaming during rapid eye movement (REM) sleep, we can perform complex motor behaviors while

293 nt for both the induction and maintenance of REM sleep, which are probably mediated in part by inhibi

294 show mostly unimpaired motor behavior during REM sleep, which contrasts strongly to coexistent noctur

295 rimarily occurred during rapid-eye movement (REM) sleep, which is notable because REM is associated w

296 e interaction of dDpMe and SLD in control of REM sleep, while also indicating operation of mechanisms

297 fy the independent association of OSA during REM sleep with prevalent and incident hypertension.

298 can occur in REM sleep and progress into non-REM sleep, with continuous desaturation and hypercarbia.

299 ing, non-rapid eye movement sleep [NREM] and REM sleep) within an ultradian cycle.

300 n and significantly fragmented any remaining REM sleep without affecting total sleep time, sleep effi

301 g (W) and paradoxical sleep (PS, also called REM sleep), yet also in promoting PS with muscle atonia.

302 Spindles and SWRs were initiated during non-REM sleep, yet the changes were incorporated in the netw