ライフサイエンスコーパス: slow-wave

1 dergo periods of silence phase-locked to the slow wave.

2 ding period-amplitude analysis of individual slow waves.

3 ow waves that are more similar to NREM sleep slow waves.

4 lls, are involved in the generation of sleep slow waves.

5 ve tendency of each hemisphere at generating slow waves.

6 s across neurons, is reflected in the EEG as slow waves.

7 amic network activity occurring during sleep slow waves.

8 may contribute to the generation of cortical slow waves.

9 mpact on the spatiotemporal pattern of sleep slow waves.

10 in the cross-hemispheric traveling of sleep slow waves.

11 state, directly linked to the generation of slow waves.

12 1 caused loss of gastric, but not intestinal slow waves.

13 in in gastric motor activity, with disrupted slow waves, abnormal phasic contractions and delayed gas

14 terstitial cells of Cajal (ICCs) and mapping slow-wave abnormalities in patients with CUNV vs control

15 We found that, on average, slow-wave active states started off within frontal corti

16 learance and affect the relationship between slow wave activity (SWA) and Abeta.

17 y is, in part, driven by impairments of NREM slow wave activity (SWA) and associated overnight memory

18 Slow wave activity (SWA) fluctuated with a 29-min ultrad

19 heimer's disease is OSA leading to decreased slow wave activity (SWA), increased synaptic activity, d

20 and reflected in electroencephalogram (EEG) slow wave activity (SWA, 0.5-4 Hz) during sleep.

21 and sleep, cortical neurons exhibit rhythmic slow wave activity associated with periods of neuronal s

22 ivity pattern and were confirmed for ongoing slow wave activity by independent component and seed-bas

23 Specific disruption of slow wave activity correlated with an increase in amyloi

24 derwent 5-14 days of actigraphy, followed by slow wave activity disruption during polysomnogram, and

25 Slow wave activity disruption increases amyloid-beta lev

26 evidence suggests that electroencephalogram slow wave activity during sleep reflects synaptic potent

27 amic reticular nucleus (TRN) rapidly induces slow wave activity in a spatially restricted region of c

28 In focal epilepsy patients, we examined slow wave activity near and far from the seizure onset z

29 atients also showed local increases in sleep slow wave activity power at scalp locations matching the

30 , patients with epilepsy displayed increased slow wave activity power during non-rapid eye movement s

31 This global increase in slow wave activity power was positively correlated with

32 This local increase in slow wave activity power was positively correlated with

33 Spontaneous slow oscillation-associated slow wave activity represents an internally generated st

34 This effect was specific for slow wave activity, and not for sleep duration or effici

35 ntalized network dynamics were observed; and slow wave activity, dominated by a cortex-wide BOLD comp

36 During slow wave activity, we find a correlation between the oc

37 cortex was engaged in this specific type of slow wave activity.

38 decreased nonrapid eye movement (NREM) sleep slow wave activity.

39 ing slow-wave sleep, electroencephalographic slow-wave activity (0.5-4.5 Hz), and number of low-frequ

40 ruptive" night increased momentary delta and slow-wave activity (ie, during stimulation versus the im

41 ain states, respectively defined by cortical slow-wave activity (SWA) and activation.

42 sures of non-rapid eye movement (NREM) sleep slow-wave activity (SWA) and sleep quality (efficiency)

43 asis of the growing body of evidence linking slow-wave activity (SWA) during sleep to consolidation,

44 Slow-wave activity (SWA) increases with wake duration an

45 cortical synchrony, could explain why sleep slow-wave activity (SWA) is higher after extended wake.

46 Simultaneously, electroencephalographic slow-wave activity (SWA) was significantly decreased and

47 mogenetic activation of SOM+ cells increases slow-wave activity (SWA), slope of individual slow waves

48 contrast to humans, absolute NREM sleep EEG slow-wave activity (SWA, spectral power density between

49 ficantly higher all-night frontal NREM sleep slow-wave activity (SWA: 2-4 Hz), than women, particular

50 The electroencephalographic power of slow-wave activity (SWA; 0.5-4 Hz) in nonrapid eye movem

51 Slow-wave activity (SWA; EEG activity of 1-4.5 Hz) durin

52 dentification and inhibition during cortical slow-wave activity and activation, we report that, in do

53 Previous studies utilized cortical slow-wave activity and/or cortical activation (ACT) unde

54 ntrainment of spindle activity to endogenous slow-wave activity in 66% of electrodes as well as entra

55 This provides a mechanism by which slow-wave activity might bias synapses towards weakening

56 high regularity, regardless of brain state (slow-wave activity or spontaneous activation).

57 During slow-wave activity, cortical neurons display synchronize

58 ic agonist dexmedetomidine that enhances EEG slow-wave activity, increases brain and spinal cord drug

59 acutely after TBI enhanced encephalographic slow-wave activity, markedly reduced diffuse axonal dama

60 plasma melatonin and electroencephalographic slow-wave activity.

61 o decreased density of slow waves-as well as slow-wave activity.

62 n if auditory stimulation is used to enhance slow-wave activity.

63 uration and momentary increases in delta and slow-wave activity.

64 predicted the diminished amplitude of <1 Hz slow-wave-activity, results that were statistically diss

65 , as oppose to simply gate, SWS and cortical slow-wave-activity; (2) armodafinil cannot exert its wak

66 Abnormally high slow waves, alpha/delta intrusions, frequent transitions

67 endoperoxide synthase-2 inhibition increased slow wave amplitudes and reduced frequency of diabetic a

68 und that both the parieto-occipital negative slow wave and the alpha power suppression showed the cha

69 techniques, including automated detection of slow waves and eye movements.

70 y affected the spatiotemporal pattern of the slow waves and maximized memory replay.

71 ccurrence of prominent sleep-like TMS-evoked slow waves and off-periods-reflecting transient suppress

72 rs further suggest an association with sleep slow waves and sleep homeostasis.

73 NREM sleep is distinguished by slow waves and spindles throughout the cerebral cortex a

74 that SOM+ cells can fire immediately before slow waves and their optogenetic stimulation during ON p

75 Interstitial cells of Cajal (ICC) generate slow waves and transduce neurotransmitter signals in the

76 me, total sleep period, sleep efficiency, or slow-wave and rapid eye movement sleep stage duration (P

77 gnitude of which was associated with time in slow-wave and rapid-eye-movement sleep after training.

78 ty were observed between periods of presumed slow-wave and rapid-eye-movement-sleep/active-state, whi

79 precise form of coupling between prefrontal slow-wave and spindle oscillations, which actively dicta

80 low-wave activity (SWA), slope of individual slow waves, and NREM sleep duration; whereas their chemo

81 sely related event, whereas medial-occipital slow waves appear similar to NREM sleep slow waves.SIGNI

82 investigated.SIGNIFICANCE STATEMENT Cortical slow waves are a defining feature of non-rapid eye-movem

83 electrode array, we have shown that fast and slow waves are causally related, so a slowly moving neur

84 Neural slow waves are followed by hemodynamic oscillations, whi

85 Slow waves are locally regulated, and local slow wave dy

86 Slow waves are periodic oscillations in neuronal activit

87 ave sleep-likely due to decreased density of slow waves-as well as slow-wave activity.

88 tween high-frequency activity at >150 Hz and slow wave at 3-4 Hz.

89 Importantly, slow waves behave as traveling waves, and their propagat

90 During sleep slow waves, both GABAergic neurons of the nucleus reticu

91 ely demonstrated that the full expression of slow waves, both of natural sleep and anesthesia, requir

92 spiking, transient stuttering, and transient slow-wave bursting) and 4 steady states (non-adapting sp

93 g spiking, persistent stuttering, persistent slow-wave bursting, and silence).

94 M) sleep, recent work in mice has shown that slow waves can also occur in REM sleep.

95 Local slow waves can appear in various cortical regions in bot

96 onfirm the view that a full understanding of slow waves can only be achieved by considering the thala

97 cs of spikes and their relationship with the slow wave component of non-rapid eye-movement sleep (NR)

98 annels, and was strongly correlated with the slow wave component of NR arousals (r = 0.99, p < 0.0001

99 ied, including lower posterior gamma, higher slow wave connectivity (delta, theta, alpha), higher fro

100 calp electroencephalographic (EEG) bursts of slow waves contrasting with the low-voltage fast desynch

101 ng propofol anesthesia, a high-amplitude EEG slow wave corresponding to a global, stereotypical patte

102 low-amplitude electroencephalographic (EEG) slow wave corresponding to a local pattern of cortical a

103 The latest structure we recorded within the slow-wave cycle was the anterior thalamus, which followe

104 e sleep-wake cycle, LTP, cognition, cortical slow waves, depression, and pain.

105 singly, the prevalence of sleep spindles and slow waves did not systematically vary between day and n

106 In all CPs slow waves displayed a significantly reduced probability

107 tostatin-positive cells-to the generation of slow waves during NREM sleep in freely moving mice.

108 d homeostatic decrease in the slope of sleep slow waves during the night, which in turn predicted red

109 Slow waves are locally regulated, and local slow wave dynamics are important for memory, cognition,

110 Slow-wave dysrhythmias were identified in all 9 subjects

111 .3 bodies/field, respectively; P < .05), but slow-wave dysrhythmias were similar between groups.

112 B complex produce a monotonous high-voltage, slow-wave EEG and eliminate spontaneous behaviors.

113 eralized objects evokes a difference between slow-wave electrophysiological activity observed from co

114 In NREM sleep, slow waves elicited by stimuli appeared to block respons

115 ivity is nested into different phases of the slow wave enabling dynamic coupling or de-coupling of th

116 d and was related to locally lower values of slow-wave energy during preceding sleep, an electrophysi

117 we find a correlation between the occurring slow wave events and the strength of functional connecti

118 The individual slow wave events were used for an event-related analysis

119 tereotypical episodes of neuronal activity - slow wave events.

120 gly, replay was linked to the coincidence of slow-wave events and bursts of spindle activity.

121 antly higher in SH, and was related to local slow-wave flow-motion activity over multiple spatial and

122 Doubling the frequency of slow waves for one month with optogenetics resulted in i

123 mited to primary olfactory structures during slow-wave forebrain states.

124 ck of the CC does not lead to differences in slow-wave generation across brain hemispheres.SIGNIFICAN

125 ency coupling analyses demonstrated that the slow wave governs a precise temporal coordination of sle

126 rlying fast and local modulation of cortical slow waves has not been identified.

127 led a lateralized parieto-occipital negative slow wave (i.e., the contralateral delay activity) and l

128 ion (CSD) is the propagation of a relatively slow wave in cortical brain tissue that is linked to a n

129 re sensitive to anoctamin-1 antagonists than slow waves in adult muscles.

130 acy of anoctamin-1 antagonists in inhibiting slow waves in adult small intestinal muscles suggest tha

131 te the role of optogenetically induced sleep slow waves in an animal model of ischemic stroke and ide

132 channel protein anoctamin-1 leads to loss of slow waves in gastric and intestinal muscles.

133 ntial for the cross-hemispheric traveling of slow waves in human sleep, which is in line with the ass

134 Slow waves in intestinal muscles of juvenile mice were m

135 Slow waves in neural activity contribute to memory conso

136 deletion of Ano1 in mice resulted in loss of slow waves in smooth muscle of small intestine.

137 Furthermore, slow waves in the older mice were characterized by incre

138 ics of individual electroencephalogram (EEG) slow waves in young and elderly humans.

139 ir chemogenetic inhibition decreases SWA and slow-wave incidence without changing time spent in NREM

140 d, for the first time, the parameters of EEG slow waves, including their incidence, amplitude, durati

141 ep slow waves.SIGNIFICANCE STATEMENT The EEG slow wave is typically considered a hallmark of nonrapid

142 designed plasmonic crystal and exploiting a slow-wave lattice resonance and spontaneous thermal plas

143 fied subtypes (sawtooth and medial-occipital slow waves) may reflect distinct generation mechanisms a

144 ow regional cortical disruption, mediated by slow wave modulation of broadband activity, changes duri

145 We found that broadband slow-wave modulation enveloped posterior cortex when sub

146 nd rodents [4, 7] have shown that NREM sleep slow waves most often involve only a subset of brain reg

147 cortical cooling might be used to manipulate slow-wave network activity and induce neuromodulator-ind

148 ase, we retrospectively tested whether sleep slow waves, objectively quantified with polysomnography,

149 minar recordings in freely moving mice, that slow waves occur regularly during REM sleep, but only in

150 Although the EEG slow wave of sleep is typically considered to be a hallm

151 The slow waves of non-rapid eye movement (NREM) sleep reflec

152 established, new evidence suggests that the slow waves of non-rapid eye movement sleep may function

153 Slow waves of non-REM sleep are suggested to play a role

154 brain hemispheres.SIGNIFICANCE STATEMENT The slow waves of NREM sleep behave as traveling waves, and

155 it did not have a significant impact on the slow waves or memory performance after sleep.

156 o significant effects on the distribution of slow-wave origin probability across hemispheres.

157 tion or inhibition of AANs led to diminished slow-wave oscillation, significant loss of sleep, and sh

158 hase amplitude coupling between the phase of slow wave oscillations (0.1-1 Hz) and amplitude of broad

159 EEG, including alpha oscillations (8-12 Hz), Slow Wave Oscillations (SWO, 0.1-1.5 Hz), and dose-depen

160 ed with the quality of nonrapid eye movement slow wave oscillations during recovery sleep, and by way

161 A new study finds sleep-dependent slow wave oscillations in the fruit fly, which act to in

162 The coupled interaction between slow-wave oscillations and sleep spindles during non-rap

163 In contrast, non-rapid eye movement (NREM) slow-wave oscillations offer an ameliorating, anxiolytic

164 udy, we provide evidence that enhancement of slow-wave oscillatory activity in the delta-frequency ra

165 reversible disruption of the thalamocortical slow-wave pattern rhythmicity and the appearance of fast

166 me that this memory benefit was predicted by slow-wave phase at the time of stimulation.

167 nd impact to applications in explorations of slow wave physics.

168 Slow wave potentials (SWPs) are damage-induced electrica

169 ps have been implicated in the generation of slow wave potentials (SWPs), damage-induced membrane dep

170 nt to trigger root-to-shoot Ca(2+) waves and slow wave potentials (SWPs).

171 rons at the frequency of slow waves restores slow wave power, halts deposition of amyloid plaques and

172 Slow-wave propagation profiles were defined by high-reso

173 s also revealed a residual cross-hemispheric slow-wave propagation that may rely on alternative pathw

174 t the main responsible for cross-hemispheric slow-wave propagation.

175 ationship between white matter integrity and slow-wave propagation.

176 s with CUNV, including the identification of slow-wave re-entry.

177 usly cease firing, the neuronal basis of the slow wave, remains unknown.

178 These slow waves resemble those seen in sleep, as cortical uni

179 rtical pyramidal neurons at the frequency of slow waves restores slow wave power, halts deposition of

180 al is related to these active periods of the slow wave rhythm.

181 sely, mild heating increased thalamocortical slow-wave rhythmicity.

182 ddition, the ensuing interictal up states of slow wave rhythms are more intense in epileptic than con

183 ital slow waves appear similar to NREM sleep slow waves.SIGNIFICANCE STATEMENT The EEG slow wave is t

184 s share specialized forms of sleep including slow wave sleep (SWS) and rapid eye movement sleep (REM)

185 Cortical activity during slow wave sleep (SWS) differs from that during REM sleep

186 ar activity of cortical neurons while during slow wave sleep (SWS) these neurons show synchronous alt

187 tuned for hippocampal ensemble spike data in slow wave sleep (SWS), even in the absence of prior beha

188 Slow wave sleep (SWS), the deepest sleep stage hallmarke

189 and humans has suggested the existence of a slow wave sleep (SWS)-promoting/electroencephalogram (EE

190 ly observed in electrophysiogical studies of slow wave sleep (SWS).

191 ep in an unusual manner, with unihemispheric slow wave sleep (USWS) and suppressed REM sleep, it is u

192 en RR neurons and SPW-R events in subsequent slow wave sleep was diminished.

193 and REM sleep than in quiet wakefulness and slow wave sleep, behavioral states that differ with resp

194 During quiescence and slow wave sleep, bouts of synchronized activity represen

195 depression, revealing not only a decrease in Slow Wave Sleep, but also a disinhibition of REM (rapid

196 share many features with the down states of slow wave sleep.

197 ave ripples observed in quiet wakefulness or slow wave sleep.

198 ved in the cortex and the hippocampus during slow wave sleep.

199 occur during both behavior (awake SWRs) and slow-wave sleep (sleep SWRs).

200 z EEG slow oscillation (SO) is a hallmark of slow-wave sleep (SWS) and is critically involved in slee

201 However, only in slow-wave sleep (SWS) beta- and gamma-oscillations are a

202 respond to 6-h sleep deprivation (SD) with a slow-wave sleep (SWS) EEG delta (1.0 to 4.0 Hz) power re

203 Slow-wave sleep (SWS) is characterized by synchronized n

204 Slow-wave sleep (SWS) is known to contribute to memory c

205 Slow oscillations during slow-wave sleep (SWS) may facilitate memory consolidatio

206 Slow-wave sleep (SWS) was characterized by low neural fi

207 thening of associated neural circuits during slow-wave sleep (SWS), a process known as "cellular cons

208 ENT Convincing evidence supports the role of slow-wave sleep (SWS), and the relevance of close tempor

209 points, including paradoxical sleep (PS) and slow-wave sleep (SWS), as well as the circadian rhythmic

210 traces are spontaneously reactivated during slow-wave sleep (SWS), leading to the consolidation of r

211 the unmarked reward zone to patterns during slow-wave sleep (SWS).

212 paradoxical sleep (PS; aka REM) than during slow-wave sleep (SWS).

213 fulness, but in the reverse direction during slow-wave sleep (SWS).

214 motor memory after targeted reactivation in slow-wave sleep (SWS).

215 ial role in the induction and maintenance of slow-wave sleep (SWS).

216 aking or rapid eye movement (REM) sleep from slow-wave sleep (SWS).

217 These results suggest that enhancing slow-wave sleep acutely after trauma may have a benefici

218 Ebselen decreased slow-wave sleep and affected emotional processing by inc

219 spent in rapid eye movement (REM) sleep and slow-wave sleep and an increase in muscle tone during RE

220 During slow-wave sleep and deep anesthesia, the rat hippocampus

221 ave sleep, share commonalities with those of slow-wave sleep and paradoxical or rapid eye movement sl

222 ia-activated neurons (AANs) strongly promote slow-wave sleep and potentiates GA, whereas conditional

223 Slow-wave sleep and rapid eye movement (or paradoxical)

224 egative affect stage, there is a decrease in slow-wave sleep and some limited recovery in REM sleep w

225 ane potential oscillations are slower during slow-wave sleep and under anesthesia.

226 eye movement sleep (all P < 0.001), whereas slow-wave sleep duration was preserved (Poverfeeding x s

227 the production of sharp-wave ripples during slow-wave sleep in a unilateral or bilateral manner, res

228 se supports a potentially beneficial role of slow-wave sleep in neurodegeneration.

229 However, the importance of slow-wave sleep in Parkinson disease is unknown.

230 n chronically sleep restricted subjects, low slow-wave sleep intensity over the right prefrontal cort

231 Slow-wave sleep is a marker of sleep need, but its prese

232 indicate that the control of unihemispheric slow-wave sleep is likely to be a function of interponti

233 synchronization of cortical activity during slow-wave sleep is still controversial, with some studie

234 Slow-wave sleep is thought to be important for retuning

235 first time, a mechanistic explanation of how slow-wave sleep may promote consolidation of recent memo

236 s showing the mean and standard deviation of slow-wave sleep MI of neighboring non-epileptic channels

237 (active) and Down (quiescent) states during slow-wave sleep or anesthesia.

238 We propose that during slow-wave sleep the tight functional coupling between GA

239 hypothesis is that neurons fire less during slow-wave sleep to recover from the "fatigue" accrued du

240 Slow-wave sleep was associated with delta-band sequences

241 e postreserpine days, sleep was dominated by slow-wave sleep with fast intrusions and reduced hierarc

242 During subsequent slow-wave sleep within an afternoon nap, we presented ha

243 ty and beta-cell function, for time spent in slow-wave sleep, and for EEG spectral power in the delta

244 ivity and temperature patterns, increases in slow-wave sleep, and shifts in EEG spectral power, sever

245 ng of HA neurons during wakefulness promotes slow-wave sleep, but not rapid eye movement sleep, durin

246 e time awake during the night, a decrease in slow-wave sleep, decreases in delta electroencephalogram

247 rst half of the night, which is dominated by slow-wave sleep, did not improve recall.

248 ogic markers of sleep homeostasis, including slow-wave sleep, electroencephalographic slow-wave activ

249 sleepwalking, i.e. the partial arousal from slow-wave sleep, is today well-documented, the detailed

250 empirical functional changes observed during slow-wave sleep, namely a global shift of the brain's dy

251 During subsequent slow-wave sleep, one sound was unobtrusively presented t

252 nimal studies support the hypothesis that in slow-wave sleep, replay of waking neocortical activity u

253 ule scale relationships disintegrated during slow-wave sleep, suggesting that grid modules function a

254 o sleep states, rapid eye movement sleep and slow-wave sleep, to offline memory processing.

255 the first half of the night is dominated by slow-wave sleep, whereas during the second half, rapid e

256 sleep and anesthesia regimens that induce a slow-wave sleep-like state.

257 icipants, patients had significantly reduced slow-wave sleep-likely due to decreased density of slow

258 ocampal local field potentials (LFPs) during slow-wave sleep-related to motor-bursts (micro-arousals)

259 f hippocampal projections within mPFC during slow-wave sleep.

260 al decrease in effective interactions during slow-wave sleep.

261 rousal but to rapidly and selectively induce slow-wave sleep.

262 ot occur with MECIII input inhibition during slow-wave sleep.

263 ity in healthy humans during wakefulness and slow-wave sleep.

264 f stimulation in memory consolidation during slow-wave sleep.

265 during wakefulness, to a stable focus during slow-wave sleep.

266 ll brain nodes to best match wakefulness and slow-wave sleep.

267 play of cortical cell spike sequences during slow-wave sleep.

268 s deviations from perfect balance, mostly in slow-wave sleep.

269 ef periods of desynchronization prevalent in slow-wave sleep.

270 is important for this transformation during slow-wave sleep.

271 during waking and accelerated tenfold during slow-wave sleep.

272 derlies the generation of sharp waves during slow-wave sleep.

273 and its role in sharp-wave generation during slow-wave sleep.

274 sufficient to rapidly and selectively induce slow-wave sleep.SIGNIFICANCE STATEMENT The function of m

275 (PZ(Vgat)) neurons in behaving mice produces slow-wave-sleep (SWS), even in the absence of sleep defi

276 nd (iii) progressive increases in individual slow wave slope and frontal fast oscillation power.

277 Slow waves (slow wavesSMC) were recorded from LSMCs and

278 ults predicted a temporal dispersion of this slow wave-spindle coupling, impairing overnight memory c

279 been suggested to occur more broadly during slow-wave states (including sleep) throughout the forebr

280 form of mammalian sleep, with unihemispheric slow waves, suppressed REM sleep, and continuous bodily

281 These oscillations are reminiscent of sleep slow waves (SW) and suggestive of a role for sleep in br

282 ke rest, the neocortex generates large-scale slow-wave (SW) activity.

283 Unilateral odor cues locally modulated slow-wave (SW) power such that regional SW power increas

284 Sleep slow waves (SWs) change considerably throughout normal a

285 hypothesis that tone depends upon electrical slow waves (SWs) initiated in intramuscular interstitial

286 t tone depends upon generation of electrical slow waves (SWs) initiated in intramuscular interstitial

287 Slow waves (SWs) produced by interstitial cells of Cajal

288 Incidentally, we also found that slow waves tend to originate more often in the right tha

289 ent on the coordinated interplay of cortical slow waves, thalamo-cortical sleep spindles and hippocam

290 e is the P3b event-related potential, a late slow wave that appears when observers are aware of a sti

291 ls and a medial-occipital cluster containing slow waves that are more similar to NREM sleep slow wave

292 a are associated with spontaneous electrical slow waves that are thought to originate in pacemaker ce

293 Cortical slow waves, the hallmark of NREM sleep, reflect near-syn

294 s callosum in the cortical spreading of NREM slow waves through the study of a rare population of tot

295 found that higher accumulated power of sleep slow waves was associated with slower motor progression,

296 The slow waves were not affected by apyrase, or by the P2 re

297 During sleep, slow waves were reduced, and gamma oscillations amplifie

298 During non-REM sleep the EEG is dominated by slow waves which result from synchronized UP and DOWN st

299 is interrupted by transient inactive states (slow waves) while the hippocampal alternations reflect a

300 In both CPs and HSs, the incidence of large slow waves within individual NREM epochs tended to diffe