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1 troencephalogram (EEG) signatures of stage 2 non-rapid eye movement sleep.
2 ment sleep and a reduction of delta power in non-rapid eye movement sleep.
3 low wave activity decreased gradually during non-rapid eye movement sleep.
4 SFAs decreased wakefulness and increased non-rapid eye movement sleep.
5 les are bursts of 11-15 Hz that occur during non-rapid eye movement sleep.
6 rapid eye movement sleep and greatly reduced non-rapid eye movement sleep.
7 ions are commonly observed during stage 2 of non-rapid eye movement sleep.
8 l during wakefulness and to a lesser extent, non-rapid eye movement sleep.
9 stability in thalamocortical networks during non-rapid eye movement sleep.
10 ) response are similar in wakefulness and in non-rapid eye movement sleep.
11 EEG slow wave activity ipsilaterally during non-rapid eye movement sleep.
12 patients) or without (7 patients) CSA during non-rapid eye movement sleep.
13 lectroencephalographic (EEG) activity during non-rapid eye movement sleep, a highly heritable trait w
14 nalysis of V1, activation enhancement during non-rapid-eye-movement sleep after training was observed
15 hown global deactivation of the brain during non rapid eye movement sleep and a regionally selective
16 hanisms, which may underlie the promotion of non-rapid eye movement sleep and have implications for t
18 motor task are reactivated during subsequent non-rapid eye movement sleep, and disrupting this neuron
19 EG) recordings are used to distinguish wake, non-rapid eye movement sleep, and rapid eye movement sle
20 EEG delta power spectrum, produced low-delta non-rapid eye movement sleep, and slightly increased wak
21 sure (PET(CO2)) was gradually reduced during non-rapid eye movement sleep by increasing tidal volume
23 almorexant were observed in wakefulness and non-rapid eye movement sleep during both dark and light
24 hereas clonazepam did the opposite, reducing non-rapid eye movement sleep EEG instability without eff
26 iggering by lights-off and redistribution of non-rapid eye movement sleep in short light-dark cycles.
29 new evidence suggests that the slow waves of non-rapid eye movement sleep may function as markers to
31 and ripples (80-200 Hz) chiefly occur during non-rapid eye movement sleep (NREM), and that ripple osc
32 ween primary brain vigilance states (waking, non-rapid eye movement sleep [NREM] and REM sleep) withi
33 ographic (EEG) delta power during subsequent non-rapid eye movement sleep (NREMS) and is associated w
34 ced EEG slow wave power ipsilaterally during non-rapid eye movement sleep (NREMS) but not during REMS
35 H infusion induced a progressive decrease in non-rapid eye movement sleep (NREMS) during the 4-week p
37 m activity of thalamocortical origin; during non-rapid eye movement sleep (NREMS), activity in the sp
38 th hormone-releasing hormone (GHRH) promotes non-rapid eye movement sleep (NREMS), in part via a well
39 AR agonist, induced significant increases in non-rapid-eye movement sleep (NREMS) lasting for 4-10 h.
40 ependent reductions in respiratory events in non-rapid-eye-movement sleep (NREMS) and rapid-eye-movem
41 injection of the immunotoxin, the amount of non-rapid-eye-movement sleep (NREMS) and rapid-eye-movem
42 ed increased slow wave activity power during non-rapid eye movement sleep over widespread, bilateral
43 contrast, frequent interictal spikes during non-rapid eye movement sleep predicted a reduced homeost
44 he electroencephalogram (delta power) during non-rapid eye movement sleep reflects homeostatic sleep
45 ained intact, males had more total sleep and non-rapid eye movement sleep than females during the act
47 the dopamine transporter (DAT) gene reduced non-rapid eye movement sleep time and increased wakefuln
48 anscranial magnetic stimulation (TMS) during non-rapid eye movement sleep to examine whether the spon
49 The characteristic change in PET,CO2 during non-rapid eye movement sleep was shown to be independent
50 f low-frequency (0.5-2.0 Hz) oscillations in non-rapid-eye-movement sleep, was significantly larger i
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