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 amic network activity occurring during sleep slow waves.

3 may contribute to the generation of cortical slow waves.

4 r neighboring FS interneurons during post-MD slow waves.

5 ence any change of the dominant frequency of slow waves.

6 Interstitial cells of Cajal (ICC) generate slow waves.

7 including an abnormal elevation of cortical slow waves.

8 together and the EEG displays high-amplitude slow waves.

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

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

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

12 pping to quantify and classify gastroparesis slow-wave abnormalities in spatiotemporal detail.

13 Slow-wave abnormalities were detected by high-resolution

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

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

16 ociated with regional brain atrophy, reduced slow wave activity (SWA) during non-rapid eye movement (

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

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

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

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

21 Hz during rapid eye movement sleep, whereas slow wave activity decreased gradually during non-rapid

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

23 Slow wave activity disruption increases amyloid-beta lev

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

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

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

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

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

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

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

31 siestas than XX females and had higher NREM slow wave activity, a measure of sleep propensity.

32 loss of righting reflex, onset of continuous slow wave activity, and burst suppression; burst-suppres

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

34 tern of discharge irrespective of background slow wave activity.

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

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

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

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

39 neurons can initiate and maintain SWS or EEG slow-wave activity (SWA) in behaving mice.

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

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

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

43 During slow-wave activity (SWA), ChAT+ interneurons, and some P

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

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

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

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

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

49 ver, the spatiotemporal pattern of intrinsic slow-wave activity across the auditory cortical modality

50 ticipants exhibiting more sleep spindles and slow-wave activity after learning the sparse compared wi

51 Recordings from cortical slow-wave activity and global activation states were ana

52 fluctuations, and the modulation of ongoing slow-wave activity by bottom-up and top-down factors pla

53 onto-parietal cortex is involved in abnormal slow-wave activity following temporal lobe seizures.

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

55 provide the first evidence that spindles and slow-wave activity mediate integration of new informatio

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

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

58 broad forebrain coupling takes place during slow-wave activity patterns under either ketamine-xylazi

59 ed averages also showed normalization in the slow-wave activity state (P < 0.05).

60 circuits underlying this intrinsic source of slow-wave activity support coordinated changes in excita

61 The sleeping brain exhibits characteristic slow-wave activity which decays over the course of the n

62 During slow-wave activity, cortical neurons display synchronize

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

64 nt induced a further reduction but increased slow-wave activity.

65 ng revealed new categories of abnormal human slow-wave activity.

66 hift, we found a 'regional' spatial shift in slow-wave activity.

67 plasma melatonin and electroencephalographic slow-wave activity.

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

69 ng periods (p < 0.05) as a result of greater slow wave and rapid eye movement sleep and lower fragmen

70 g increases and becomes more phase-locked to slow wave and spindle oscillations.

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

72 ggest a possible connection between cortical slow waves and behavioural and cognitive changes in a hu

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

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

75 We find that most sleep slow waves and the underlying active and inactive neuron

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

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

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

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

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

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

82 Spindles and slow waves are affected by the recent history of learnin

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

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

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

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

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

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

89 We also find that slow waves can propagate, usually from medial prefrontal

90 cephalography, the investigation of cortical slow waves cannot be easily extended to the whole brain.

91 t anteroposterior propagation of neocortical slow-waves coordinates timing of hippocampal ripples and

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

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

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

95 Recorded slow wave data can be filtered via a range of inbuilt te

96 The steep adolescent decline in the slow wave (delta, 1-4 Hz) electroencephalogram (EEG) of

97 We found that phase coherence in spontaneous slow-wave (delta-theta band) activity was highest betwee

98 that individual differences in spindles and slow waves depend on the white matter microstructure acr

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

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

101 complex partial seizures exhibited increased slow waves distributed to frontal areas with spread to c

102 source imaging to reconstruct the post-ictal slow-wave distribution.

103 tivation more strongly reduces spindles than slow waves during both anesthesia and natural sleep.

104 tivity assessed by the dominant frequency of slow waves during EGG remained within the normal range a

105 t the thalamus finely tunes the frequency of slow waves during non-REM sleep and anesthesia, and thus

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

107 e in spindles and show elevated synchrony by slow waves during sleep.

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 fferentially steeper declines in non-REM EEG slow-wave energy (SWE)-the putative homeostatic marker o

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

117 ional salience of the pictures: the P300 and slow wave event-related potentials (ERPs).

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 The slow wave findings show that information about the relat

122 ring short duration bursts of high-amplitude slow waves followed by longer periods of flat EEG.

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

124 perature were unable to explain the observed slow wave frequency that exceeded accepted normal levels

125 Gastric slow wave frequency was significantly greater than 3 cpm

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

127 dividuals with a steeper rising slope of the slow wave had higher axial diffusivity in the temporal f

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

129 ibution of single neocortical neurons to EEG slow waves have started to be carefully investigated.

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

131 halamocortical neurons strongly entrains EEG slow waves in a narrow frequency band (0.75-1.5 Hz) only

132 esthesia increased the dominant frequency of slow waves in a statistically significant manner (baseli

133 no data on the initiation and propagation of slow waves in gastroparesis because research tools have

134 These events had similar waveforms as slow waves in more distal regions and were coupled to ph

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

136 riefly 'offline' as in sleep, accompanied by slow waves in the local EEG.

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 Abnormalities of slow-wave initiation and conduction occur in gastropares

142 the neocortical and thalamic oscillators of slow waves is required for the full expression of this k

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

144 uality through mechanisms independent of EEG slow waves (<4 Hz), suggesting SK2 signaling as a new po

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

146 interictal generalised 2.5-3.0 Hz spike and slow waves (n=10).

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

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

149 These slow waves of natural sleep are currently considered to

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

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

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

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

154 nscranial electrical stimulation can entrain slow-wave oscillations (SWO) in the human electro-enceph

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

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

157 individual differences in sleep spindle and slow wave parameters were associated with diffusion tens

158 er enhanced neuronal excitability or the EEG slow-wave pattern induced by HFS.

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

160 EEG shifted to a continuous large-amplitude, slow-wave pattern within the 0.5-8.0 Hz bandwidth lastin

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

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

163 ophrenia: fragmented NREM sleep and impaired slow-wave propagation in the model culminate in deficien

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

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

166 equired for observing similar effects on EEG slow waves recorded during anesthesia, a condition in wh

167 kedly (up to 50%) decreases the frequency of slow waves recorded during non-REM sleep in freely movin

168 The most prominent EEG events in sleep are slow waves, reflecting a slow (<1 Hz) oscillation betwee

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

170 Slow waves represent one of the prominent EEG signatures

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

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

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

174 llations of the sleeping brain, spindles and slow waves, show trait-like, within-subject stability an

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

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

177 that result in reduced interference include slow wave sleep (SWS), NMDA receptor antagonists, benzod

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

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

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

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

182 ced REM sleep, while leaving active wake and slow wave sleep relatively intact.

183 and spontaneous ventilation were observed in slow wave sleep time (45 min vs 28 min), rapid eye movem

184 nd suppressed REM sleep time while increased slow wave sleep typifies the inactive phase, findings th

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

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

187 water, however, fur seals exhibit asymmetric slow-wave sleep (ASWS), resembling the unihemispheric sl

188 ry inputs, as in development in utero, or in slow-wave sleep (i.e., throughout the entire lifespan),

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

190 ally sleeping common marmosets, we show that slow-wave sleep (SWS) alters neural responses in the pri

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

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

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

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

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

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

197 to determine wake after sleep onset (WASO), slow-wave sleep (SWS), and rapid eye movement (REM) slee

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

199 e for 48 h in a respiration chamber, whereas slow-wave sleep (SWS), rapid eye movement (REM)-sleep, t

200 d electroencephalogram (EEG) activity during slow-wave sleep (SWS), similar to that observed in all t

201 s, memory consolidation occurs partially via slow-wave sleep (SWS)-dependent replay of activity patte

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

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

204 (50%) in daily wakefulness at the expense of slow-wave sleep (SWS).

205 as positively correlated with the amounts of slow-wave sleep (SWS).

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

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

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

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

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

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

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

213 xtinguished conditioned fear, increased both slow-wave sleep and rapid-eye movement (REM) sleep.

214 s showed differentially smaller increases in slow-wave sleep and smaller reductions in stage 2 sleep

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

216 We propose that rapid eye movement (REM) and slow-wave sleep contribute differently to the formation

217 ced a transient decrease in REM sleep and in slow-wave sleep followed by a slight improvement of slee

218 ng speech understanding, sensory gating, and slow-wave sleep for a subset of elderly individuals.

219 The signature of slow-wave sleep in the electroencephalogram (EEG) is lar

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

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

222 In contrast, slow-wave sleep is more directly involved in the consoli

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

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

225 rospinal fluid Abeta dynamics, decrements in slow-wave sleep may decrease the clearance of Abeta from

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

227 sleep (ASWS), resembling the unihemispheric slow-wave sleep of odontocetes (toothed whales).

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

229 These oscillations occur during slow-wave sleep or at rest.

230 oning, re-exposure to the odorant context in slow-wave sleep promoted stimulus-specific fear extincti

231 ation (TMR) of specific memory traces during slow-wave sleep promotes the emergence of explicit knowl

232 ere positively correlated with the amount of slow-wave sleep that patients obtained between training

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

234 ttern A human IgGs on rapid eye movement and slow-wave sleep time parameters in the inactive phase an

235 s bilaterally placed in the preoptic region, slow-wave sleep time was significantly decreased, but RE

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

237 reactivation of these representations during slow-wave sleep transforms episodic representations into

238 d sounds were re-presented during subsequent slow-wave sleep while participants underwent functional

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

240 assessed for presence of HEP within stage 2, slow-wave sleep, and REM sleep in 40 children with prima

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

242 scillation which occurs predominantly during slow-wave sleep, but may also play a role during awake s

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

244 During slow-wave sleep, cortical neurons display synchronous fl

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

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

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

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

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

250 -cell recordings manifesting Up/Down states (slow-wave sleep, quiet wakefulness), probably as a resul

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

252 During slow-wave sleep, temporal coordination of hippocampal sh

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

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

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

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

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

258 onists induce wakefulness and reduce REM and slow-wave sleep.

259 th one learned sequence were replayed during slow-wave sleep.

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

261 lective memory generalization during REM and slow-wave sleep.

262 , that it also does not arise during natural slow-wave sleep.

263 cting total sleep time, sleep efficiency, or slow-wave sleep.

264 delta oscillations have been associated with slow-wave sleep.

265 d fast-sigma oscillations, especially during slow-wave sleep.

266 ory gating, thalamocortical rhythmicity, and slow-wave sleep.

267 ith performance improvement were specific to slow-wave sleep.

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

269 ivation process for specific memories during slow-wave sleep.

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

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

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

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

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

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

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

277 SDB during non-REM sleep (stage 2: P = 0.03; slow-wave sleep: P = 0.001).

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

279 were often superimposed upon small amplitude slow waves (slow wavesFLC).

280 Slow waves (slow wavesICC) were of greatest amplitude (>

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

282 further define the interrelationships among slow-wave, spindle, and ripple events, indicating that s

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

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

285 s ("drivers") were not modulated by cortical slow waves, suggesting their origin in ascending pathway

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

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

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

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

290 Slow waves (SWs) were of greatest amplitude and frequenc

291 ecrease in synaptic strength associated with slow waves (SWs) would enhance signal-to-noise ratio of

292 the thalamus in slow oscillation, but global slow-wave thalamocortical dynamics have never been exper

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

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

295 centroparietal spindles often occurring with slow-wave up-states, and slow (9-12 Hz) frontal spindles

296 The dominant frequencies of slow waves were compared between the baseline intervals

297 Electrical slow waves were recorded with intracellular microelectro

298 Slow waves were routinely recorded from gastric fundus m

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

300 tures and spatial distribution of post-ictal slow waves with comprehensive spatial coverage.