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1 matergic neurons causes a strong increase in wakefulness.
2 impairment in settings that involve extended wakefulness.
3 z) and gamma-band activity (30-80 Hz) during wakefulness.
4 pants (4 females) studied during 40-hours of wakefulness.
5 ation of this pathway in vivo rapidly drives wakefulness.
6 relative to wild-type controls during quiet wakefulness.
7 responsive, then reversed upon emergence to wakefulness.
8 ularly after more than 10 hours of scheduled wakefulness.
9 , the VTA has a role in regulating sleep and wakefulness.
10 eep-wake cycles with highest activity during wakefulness.
11 ep onset, sleep fragmentation, and increased wakefulness.
12 internal clock and by the duration of prior wakefulness.
13 ctivity changes during transitions to active wakefulness.
14 stabilized after sleep but diminished after wakefulness.
15 onset of muscle weakness or paralysis during wakefulness.
16 uction or loss, and REM sleep instruction in wakefulness.
17 g of synapses that have been built up during wakefulness.
18 rement for the maintenance of arousal during wakefulness.
19 le to study somnambulism behaviorally during wakefulness.
20 strength of the peaks with EEG-defined sleep/wakefulness.
21 with impaired behavioral performance during wakefulness.
22 onnected to mental ability both in sleep and wakefulness.
23 hown to depend on EEG-defined stage of sleep/wakefulness.
24 y young and older volunteers under extendend wakefulness.
25 urons and their specific role in maintaining wakefulness.
26 REM sleep, nor of theta power during resting wakefulness.
27 rousal and promote the maintenance of normal wakefulness.
28 d was observed, even after 4 days of induced wakefulness.
29 nic REM sleep, the latter resembling relaxed wakefulness.
30 ans, this occurs during sleep but not during wakefulness.
31 delta power spectrum and slightly decreased wakefulness.
32 he decisive role of the LTD and PPT in sleep-wakefulness.
33 ice increases local acetylcholine levels and wakefulness.
34 ffects on spiking activity across periods of wakefulness.
35 ral cortex, rather than to induce behavioral wakefulness.
36 emporal reactivated patterns in SWS or quiet wakefulness.
37 e and acetylcholine are highly active during wakefulness.
38 oral functions, such as control of sleep and wakefulness.
39 dividual neurons and the cortical LFP during wakefulness.
40 hcrt) are necessary for normal regulation of wakefulness.
41 e performance of a voluntary movement during wakefulness.
42 normal waking day, but also during overnight wakefulness.
43 e EEG and metabolic consequences of extended wakefulness.
44 , but not to the thalamus, mediate PB-driven wakefulness.
45 aracterized by hypersomnolence during normal wakefulness.
46 mice with an exceptional amount of sustained wakefulness.
47 paralysis, hallucinations) that intrude into wakefulness.
48 ring sleep and 'desynchronized' state during wakefulness.
49 in 11 healthy volunteers during 1 h of quiet wakefulness.
50 ntal or parietal cortices, failed to restore wakefulness.
51 exin signals, which rapidly fluctuate during wakefulness.
52 e changes in our nighttime sleep and daytime wakefulness.
53 on, compared to comparable amounts of active wakefulness.
54 g postsleep EEG were recorded during resting wakefulness.
55 vel circuits in the mouse brain that promote wakefulness.
56 some fragments are eliminated slowly during wakefulness.
57 e preserved after sleep but diminished after wakefulness.
58 lutamate cells impaired the consolidation of wakefulness.
59 ve during rapid eye movement (REM) sleep and wakefulness.
60 sleep, whereas their inactivation increased wakefulness.
61 generators of the alpha rhythm during quiet wakefulness.
63 (5-HT or serotonin), and modulates sleep and wakefulness(5) by activating two high-affinity G-protein
64 integrin activation compared with nocturnal wakefulness, a mechanism possibly underlying some of the
66 ifically, the same neurons shaping sleep and wakefulness actually do influence the anesthetic state i
68 and month 3 by polysomnography end points of wakefulness after persistent sleep onset and latency to
69 o placebo on subjective total sleep time and wakefulness after persistent sleep onset at night 1/week
71 ross the circadian cycle, during 42 hours of wakefulness and after recovery sleep, in 33 healthy part
72 ess, whereas TAAR1 partial agonism increases wakefulness and also reduces NREM and also REM sleep.
73 system are elevated in schizophrenia during wakefulness and are also induced in the N-methyl-D-aspar
75 he laboratory, the operational way to assess wakefulness and consciousness is through responsiveness.
77 tive in blocking spindles but increased both wakefulness and cortical delta/gamma activity, as well a
78 visual cortical neurons, even during active wakefulness and decision making.SIGNIFICANCE STATEMENT A
79 d-EEG recordings of 12 healthy adults during wakefulness and deep (N3-)sleep, characterised by differ
80 Cortical state changes also occur at full wakefulness and during rapid cognitive acts, such as per
82 apeutic option for the treatment of impaired wakefulness and excessive sleepiness in patients with na
83 duced silencing of Kiss1(ARH) neurons shifts wakefulness and food consumption to the light phase and
84 regulator of behavioral arousal, sleep, and wakefulness and has been an area of intense research eff
85 tamine (HA) system, implicated in supporting wakefulness and higher brain function, but has been diff
86 ergic projections to cortex directly control wakefulness and illustrates the utility of "opto-dialysi
87 ly, in mice, ablation of the raphe increases wakefulness and impairs the homeostatic response to slee
89 s continue to live under extended periods of wakefulness and ingestion events, daily eating pattern o
90 itical for maintaining normal daily cycle of wakefulness and involving astrocyte-neuron metabolic int
95 riment 1, n = 39), and during sleep-deprived wakefulness and non-rapid eye movement sleep (experiment
98 from non-rapid eye movement (NREM) sleep to wakefulness and produces sustained arousal, higher locom
99 Conversely, chemogenetic inhibition opposed wakefulness and promoted NREM sleep, even in the face of
101 off, when sleep pressure was high, promoted wakefulness and reduced both REM and non-REM sleep witho
102 usions: Solriamfetol significantly increased wakefulness and reduced sleepiness in participants with
103 ereas chemogenetic stimulation promotes both wakefulness and REM sleep, optogenetic stimulation of th
108 pace function in intact rodent models during wakefulness and sleep, and MRI in humans has enabled per
114 oratory behavior and REM sleep than in quiet wakefulness and slow wave sleep, behavioral states that
118 AAR1 partial agonist RO5263397 also promoted wakefulness and suppressed nonrapid eye movement sleep.
119 ation, in contrast, initiated and maintained wakefulness and suppressed sleep and sleep-related nesti
121 strated that these state transitions between wakefulness and unconsciousness were rapid and unstable.
122 been typically observed following prolonged wakefulness and widely used as a sleep homeostasis indic
124 leep-wake cycle, sensory gain control during wakefulness, and consider evidence for cholinergic suppo
128 ty: locomotion, nonlocomotor movement, quiet wakefulness, and sleep; transitions occurred not randoml
130 neurons is necessary for the maintenance of wakefulness, and their silencing not only impairs arousa
131 y cortical substates during quiet and active wakefulness, and transitions in population activity duri
135 wing exposure to intermittent hypoxia during wakefulness are positively associated with loop gain and
138 SBT and are extubated reach higher levels of wakefulness as indicated by the ORP, suggesting abnormal
139 lated brain regions that mediate arousal and wakefulness as well as the effect of opioids in sleep-re
140 Key secondary endpoints were maintenance of wakefulness assessed on the basis of the Oxford Sleep Re
141 relative to wild-type controls during quiet wakefulness at baseline and at elevated core body temper
143 es during rapid-eye movement (REM) sleep and wakefulness-behavioral states that do not naturally expr
146 mation from the cortex to hippocampus during wakefulness, but in the reverse direction during slow-wa
147 ila, where brain activity appears similar to wakefulness, but responsiveness to external sensory stim
148 n-class agent utilizing histamine to improve wakefulness by acting as an antagonist/inverse agonist o
149 sistently dysregulated patterns of sleep and wakefulness by blunting serotonergic signaling in the la
150 suggest that GABAergic VTA neurons may limit wakefulness by inhibiting the arousal-promoting VTA glut
151 reotypical electroencephalography pattern of wakefulness by simply imposing a change in the extracell
152 two dominant mutations that affect sleep and wakefulness by using an electroencephalogram/electromyog
153 homeostatic recovery sleep, indicating that wakefulness can be dissociated from accrual of sleep nee
158 strate that hippocampal astrocytes sense the wakefulness-dependent activity of septal cholinergic fib
159 delivery to prefrontal cortex (PFC) restored wakefulness despite continuous administration of the gen
160 hich cholinergic stimulation of PFC produced wakefulness despite continuous exposure to a general ane
161 luding Arntl/Bmal1, suggesting that enforced wakefulness directly impacts the molecular clock machine
162 ured subjects in various states of conscious wakefulness, disconnected consciousness, and unconscious
163 glutamatergic neurons that increase sleep or wakefulness does not substantively influence anesthetic
164 : 63.6 (1.3) y)] underwent 40-h of sustained wakefulness during 3 balanced crossover segments, once u
170 arousal and that their inhibition suppresses wakefulness, even in the face of ethologically relevant
171 Human ventilatory activity persists, during wakefulness, even when hypocapnia makes it unnecessary.
173 Rationale: Abnormal patterns of sleep and wakefulness exist in mechanically ventilated patients.
175 afish that generates short-term increases in wakefulness followed by sustained rebound sleep after wa
176 ypothalamus, which promote the transition to wakefulness from non-rapid eye movement (NREM) and rapid
177 BF-PV neurons produced rapid transitions to wakefulness from non-rapid eye movement (NREM) sleep but
178 ree component of neural activity, delineates wakefulness from propofol anesthesia, NREM and REM sleep
179 Critically, the spectral slope discriminates wakefulness from REM sleep solely based on the neurophys
180 nder homeostatic control, whereby increasing wakefulness generates sleep need and triggers sleep driv
182 Rapid variations in cortical state during wakefulness have a strong influence on neural and behavi
183 increases transitions between NREM sleep and wakefulness, implicating cholinergic projections to cort
184 ingly, burst optogenetic stimulation induces wakefulness in accordance with previously described burs
186 d eye movement sleep, and slightly increased wakefulness in both light and dark phases, whereas inhib
187 leep, which was consistent with decreases in wakefulness in C57BL/6Slac mice compared with their own
188 ation) before and after periods of sleep and wakefulness in humans (female and male participants).
190 amine-associated receptor 1 (TAAR1) promote wakefulness in mice and rats, we evaluated whether TAAR1
193 suppressed despite pharmacologically induced wakefulness in the presence of anesthetic, with restorat
195 ribe the main modulatory drives of sleep and wakefulness, including homeostatic, circadian, and motiv
196 nputs inhibiting VTA(Vgat) neurons intensify wakefulness (increased activity, enhanced alertness and
197 y, which was similar to that observed during wakefulness induced after carbachol delivery to PFC.
201 ctive sleep-promoting neurons that translate wakefulness into the depolarization of a sleep-active ne
202 cquisition of recovery sleep after prolonged wakefulness is an important issue in sleep research.
203 ORP), to determine whether abnormal sleep or wakefulness is associated with the outcome of spontaneou
209 systems and circuits that regulate sleep and wakefulness is often disrupted as part of the pathophysi
210 during REM sleep and during evening resting wakefulness is related to affective experiences in REM s
211 type-specific silencing of HA neurons during wakefulness is sufficient to not only impair arousal but
212 tion circuit for sleep-wake control in which wakefulness is supported by separate arousal and action
214 ed on is unclear because it is not known how wakefulness is translated into sleep-active neuron depol
217 in non-REM (NREM) sleep and anesthesia than wakefulness, it is unknown how neuronal communication is
218 xcitation far better than inhibition; during wakefulness, it predicted them equally well, and visual
219 d in patients with heart failure (HF) during wakefulness, its persistence in an upright position is s
220 ction of sleep onset latency and increase in wakefulness later in the night may be related to the acu
223 fluctuations in population synchrony during wakefulness modulate the accuracy of sensory encoding an
224 isomic Ts65Dn mouse model of DS during quiet wakefulness, natural sleep, and the performance of a mem
225 tion that the human ventilatory drive during wakefulness often results from a corticosubcortical coop
226 the effect of voluntary wheel running during wakefulness on neuronal activity in the motor and somato
232 e (up) and silent (down) states during quiet wakefulness or NREM sleep regulate fundamental cortical
234 of the PB was highly effective in extending wakefulness over 4 days, although subsequent PB activati
235 tonic (median, 96% [86-120] vs. 75% [50-92] wakefulness; P = 0.01) but not phasic genioglossus activ
239 global neuronal activity during drug-induced wakefulness predicted the amount of subsequent rebound s
241 nd that acute silencing of HA neurons during wakefulness promotes slow-wave sleep, but not rapid eye
243 e of calcium transients was increased during wakefulness relative to an extremely low rate during ane
247 ng and decision making, control of sleep and wakefulness, sensory salience including pain, and the ph
248 tion of intermittent hypoxia during hours of wakefulness should be combined with continuous positive
249 12 sequential hours-capturing both sleep and wakefulness should be obtained to sufficiently sample th
250 rom a metabolic standpoint, induced extended wakefulness significantly reduced body weight and leptin
251 external driven stimulation in, for example, wakefulness, sleep, coma, or neuropsychiatric diseases.
252 e patients: 72 vegetative state/unresponsive wakefulness state (VS/UWS), 36 minimally-conscious state
253 y conscious state (MCS) and the unresponsive wakefulness syndrome (UWS) is a persistent clinical chal
254 getative state (VS)-also coined unresponsive wakefulness syndrome (UWS)-and minimally conscious state
255 (DoC) such as vegetative state/unresponsive wakefulness syndrome (VS/UWS) or minimally conscious sta
256 27 patients in vegetative state/unresponsive wakefulness syndrome (VS/UWS; n = 70) and minimally cons
257 te compared to vegetative state/unresponsive wakefulness syndrome encompassed bilateral auditory and
258 sed to be vigilant but unaware (Unresponsive Wakefulness Syndrome) and 17 patients revealing signs of
259 8 patients (11 vegetative state/unresponsive wakefulness syndrome, VS/UWS, and 7 minimally conscious
261 e algorithmically identify a theta-dominated wakefulness (TDW) substate underlying motivated behavior
262 ep latency <25 minutes on the Maintenance of Wakefulness Test (MWT), Epworth Sleepiness Scale (ESS) s
264 rate fluctuations) was globally stronger in wakefulness than in NREM sleep (with distinct traits for
267 r the FG hypothesis and propose that, during wakefulness, the degradation of accumulating fragments i
269 aled that short Abeta oligomers induce acute wakefulness through Adrenergic receptor b2 (Adrb2) and P
270 id eye movement (REM) sleep-active, produced wakefulness through projections to the nucleus accumbens
271 e Drosophila model to map starvation-induced wakefulness to a single pair of peptidergic neurons and
272 ability to reversibly switch the brain from wakefulness to a state of unconsciousness, knowing how a
274 this novel and noninvasive model of induced wakefulness to explore the EEG and metabolic consequence
276 enioglossus muscle activity that occurs from wakefulness to non-REM sleep and reduces airway collapsi
277 rmal reduction of genioglossus activity from wakefulness to non-REM sleep that occurred on the placeb
278 state of arousal leading to transition from wakefulness to sleep and it is further considered to be
280 k and suggest that a transitional state from wakefulness to unconsciousness is not a continuous proce
281 ween damped to sustained oscillations during wakefulness, to a stable focus during slow-wave sleep.
284 sleep/wake cycle prior to 24 h of continual wakefulness under highly controlled environmental condit
285 less, the clinical measures of awareness and wakefulness upon which differential diagnosis rely were
291 The increase that was observed after 52 h of wakefulness was restored to control levels during a 14-h
292 n of consciousness (27 of 37, 73%), abnormal wakefulness when sedation was stopped (15 of 37, 41%), c
293 prolonged cortical activation and behavioral wakefulness, whereas inhibition reduced wakefulness and
294 of SuM(Nos1/Vglut2) neurons potently drives wakefulness, whereas inhibition reduces REM sleep theta
295 etic activation of PBel(CGRP) neurons caused wakefulness, whereas optogenetic inhibition of PBel(CGRP
296 TAAR1 overexpression modestly increases wakefulness, whereas TAAR1 partial agonism increases wak
297 EEG responses in association cortices during wakefulness, which were attenuated and restricted to aud
298 esia represents a unique state that combines wakefulness with clinically relevant anesthetic concentr
299 at a period of post-training rest (eg, quiet wakefulness with eyes closed) provides a similar memory
300 gic (VTA(Vgat)) neurons generated persistent wakefulness with mania-like qualities: locomotor activit