ライフサイエンスコーパス: REM

1 REM sleep frontal high delta power was a negative correl

2 REM-CA is an unconventional lipid-binding motif that con

3 REMs are the best-characterized nanodomain markers via a

4 REMs were also tested for oxyanion separation.

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

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

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

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

9 during waking and paradoxical sleep (PS; aka REM) than during slow-wave sleep (SWS).

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

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

12 linear association between intelligence and REM anterior beta power was found in females but not mal

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

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

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

16 263397 increased waking and reduced NREM and REM sleep, decreased gamma power during wake and NREM, a

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

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

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

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

21 ally different gating mechanisms in NREM and REM sleep.

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

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

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

25 a symbiotic relationship between non-REM and REM stages of sleep in the homeostatic regulation of neu

26 nificantly different between NREM states and REM.

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

28 to suppress SWS and promote wakefulness and REM sleep.

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

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

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

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

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

34 Outcomes in Parkinson's Disease (SCOPA-AUT), REM (Rapid Eye Movement) Sleep Behavior Disorder Single-

35 Building on this finding, baseline REM measurements may serve as a noninvasive biomarker fo

36 vement (REM) sleep, which is notable because REM is associated with increased cholinergic tone and ch

37 the MTL, exhibit reduced firing rates before REMs as well as transient increases in firing rate immed

38 s revealed a significant association between REM AHI categories and the development of hypertension (

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

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

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

42 ot enter REM, suggesting involvement of both REM and NREM sleep.

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

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

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

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

47 nt of the pontomedullary network controlling REM sleep.

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

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

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

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

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

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

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

55 cated neurons more selectively active during REM sleep.

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

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

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

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

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

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

62 However, whether presenting a CS during REM or NREM sleep enhances or extinguishes fear memory h

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

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

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

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

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

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

69 eversed theta flow was most prominent during REM sleep.

70 ticosubthalamic coherence was reduced during REM and NREM movements.

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

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

73 SDB severity during REM and non-REM sleep was quantified using the apnea-hyp

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

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

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

77 o observed in participants who did not enter REM, suggesting involvement of both REM and NREM sleep.

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

79 to be a bihemispheric sleeper that expresses REM sleep.

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

81 ta oscillations is similarly reset following REMs in sleep and wakefulness, and after controlled visu

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

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

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

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

86 nes, and optimal reactivity was achieved for REMs composed of high purity Ti4O7.

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

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

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

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

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

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

93 type noise is shown to decrease from 3.08 in REM and 2.58 in NonREM to a value of 1.99 in the Waking

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

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

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

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

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

99 ss than or equal to 5, a twofold increase in REM AHI was associated with 24% higher odds of hypertens

100 quantified using the apnea-hypopnea index in REM (AHIREM) and non-REM sleep (AHINREM), respectively.

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

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

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

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

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

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

107 certain phenomenological aspects observed in REM sleep behavior disorder.

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

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

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

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

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

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

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

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

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

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

118 p (via polysomnography), including increased REM and NREM sleep.

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

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

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

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

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

124 Transient, spindle-like "REM beta tufts" are described in the EEG of healthy subj

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

126 = 4 to 6, reactive electrochemical membrane (REM) for water treatment.

127 hich was entered into random effects models (REM) to compare CC with NC, CC with DC, and DC with NC.

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

129 sleep and increases both rapid eye movement (REM) and non-REM (NREM) sleep in rats at OX2R occupancie

130 ty (siesta), a period of rapid eye movement (REM) and non-REM sleep, was absent in all animals in whi

131 non-rapid eye movement - rapid eye movement (REM) cycling, REM sleep reduction or loss, and REM sleep

132 sustained inhibition of rapid eye movement (REM) in vivo.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 eye movement (NREM) and rapid eye movement (REM), characterized by quiescence and reduced responsive

159 was lower than Awake and rapid eye movement (REM).

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

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

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

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

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

165 between memories during rapid eye movement [REM] dreams followed by indexation and network junction

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

167 Are rapid eye movements (REMs) in sleep associated with visual-like activity, as

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

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

170 reases both rapid eye movement (REM) and non-REM (NREM) sleep in rats at OX2R occupancies higher than

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

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

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

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

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

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

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

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

179 ence of a symbiotic relationship between non-REM and REM stages of sleep in the homeostatic regulatio

180 d drop in functional connectivity during non-REM (NREM) sleep can be explained by a decrease in coupl

181 inergic neurons in the PPT or LDT during non-REM (NREM) sleep increased the number of REM sleep episo

182 REM) sleep (wake/REM active) than during non-REM (NREM) sleep, and activation of each cell type rapid

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

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

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

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

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

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

189 context for memory consolidation during non-REM sleep.

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

191 d maintain breathing automaticity during non-REM sleep.

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

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

194 B and glucose metabolism is distinct for non-REM versus REM sleep because of differences in sleep-sta

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

196 soscopic level and is globally weaker in non-REM (NREM) sleep and anesthesia than wakefulness, it is

197 However, dreaming also occurs in non-REM (NREM) sleep, characterized by prominent low-frequen

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

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

200 REM sleep, as evidenced by increases in non-REM-to-REM sleep transition duration and failure rate du

201 bition reduced wakefulness and increased non-REM (NREM) sleep.

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

203 apid eye movement [REM] sleep latencies, non-REM and REM sleep stages, and wakefulness after sleep on

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

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

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

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

208 ogram (EEG) correlate of sleep pressure, non-REM delta power, failed to increase.

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

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

211 erent characteristics during quiet wake, non-REM or REM sleep, including variable dependence on PCO2.

212 In individuals with non-REM AHI less than or equal to 5, a twofold increase in R

213 , reduction in REM sleep, and loss of normal REM atonia in some individuals may partially protect aga

214 LGN during poststimulus NREM sleep (but not REM or wake) disrupts coherence between LGN and V1 and a

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

216 was significantly correlated with amount of REM, but was also observed in participants who did not e

217 Analyses of REM-CA mutants by single particle tracking demonstrate t

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

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

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

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

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

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

224 By contrast, the effect of REM was to reduce firing rates across the entire rate sp

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

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

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

228 e probably mediated in part by inhibition of REM-suppressing GABAergic neurons in the ventrolateral p

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

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

231 re significantly attenuated after a night of REM disruption without changes in psychomotor vigilance.

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

233 e in baseline excitability during periods of REM compared with other brains states also characterized

234 and advance our understanding of the role of REM and NREM sleep in memory consolidation.

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

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

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

238 n the control of USWS and the suppression of REM in the odontocete cetaceans are present in the minke

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

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

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

242 e results demonstrate the extreme promise of REMs for water treatment applications.

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

244 Our data show that only REM-rich sleep during the second half of the night promo

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

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

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

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

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

250 activated after a small number of images or REMs exhibit delayed increases in firing rates.

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

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

253 etal-mediated group transfer polymerization (REM-GTP) of polar monomers and is composed of three main

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

255 ive OX2R antagonism is sufficient to promote REM and NREM sleep across species, similarly to that see

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

257 R-REM in nursing homes is highly prevalent.

258 R-REM was identified through resident interviews, staff in

259 7 of 2011 residents experienced at least 1 R-REM event; the total 1-month prevalence was 20.2% (95% C

260 All R-REM cases may not have been detected; resident and staff

261 Because R-REM can cause injury or death, strategies are urgently n

262 Resident-to-resident elder mistreatment (R-REM) in nursing homes can cause physical and psychologic

263 associated with higher estimated rates of R-REM.

264 Verbal R-REM is most common, but physical mistreatment also occur

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

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

267 on of GABAergic PPT neurons slightly reduced REM sleep.

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

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

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

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

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

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

274 knowledge of the synaptic basis by which SLD REM neurons are regulated and in turn produce REM sleep

275 , and particularly rapid eye movement sleep (REM), has been implicated in the modulation of neural ac

276 urons are maximally active during REM sleep (REM-max), while the majority of GABAergic neurons are ma

277 ditory CS was re-presented during subsequent REM or NREM sleep.

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

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

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

281 between REM sleep and SCRs, indicating that REM may only modulate fear acquisition indirectly.

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

283 Our results suggest that REMs during sleep rearrange discrete epochs of visual-li

284 The REMs were synthesized from tubular asymmetric TiO2 ultra

285 This REM sleep-dependent elimination of new spines facilitate

286 dicate OH(*) were produced only on the Ti4O7 REM and not on less reduced phases (e.g., Ti6O11).

287 A-GTP) of vinylphosphonates in comparison to REM-GTP, and properties of poly(vinylphosphonate)s.

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

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

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

291 We show that two REM transcription factors, VALKYRIE (VAL) and VERDANDI (

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

293 The mechanism of vinylphosphonate REM-GTP is discussed in detail for initiation and propag

294 ess and rapid eye movement (REM) sleep (wake/REM active) than during non-REM (NREM) sleep, and activa

295 During sleep and wakefulness, REM onsets are associated with distinct intracranial pot

296 Individuals with REM sleep behaviour disorder are at significantly higher

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

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

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

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