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1 activation and loss of postural muscle tone (atonia).
2 ment sleep with dominant theta waves without atonia.
3 he dissociation of theta activity and muscle atonia.
4  are regulated and in turn produce REM sleep atonia.
5 ccompanied by rapid eye movements and muscle atonia.
6 d sufficient for generating REM sleep muscle atonia.
7 sleep), yet also in promoting PS with muscle atonia.
8 iting brainstem regions that suppress muscle atonia.
9 rough which positive emotions trigger muscle atonia.
10 nts of the medullary circuitry mediating REM atonia.
11 pocampal EEG, rapid eye movements and muscle atonia.
12 rticipates in rapid eye movement (REM) sleep atonia.
13  seen during mesopontine stimulation-induced atonia.
14 tion similar to waking accompanied by muscle atonia.
15 ese IPSPs appeared exclusively during muscle atonia.
16 ons before and after carbachol-induced motor atonia.
17  neurons reduces sleep and impairs REM sleep atonia.
18  infancy occurs against a backdrop of muscle atonia, a result that is consistent with the view that A
19 he relationship between MT and nuchal muscle atonia, a widely recognized component of REM sleep.
20 ivated electroencephalogram (EEG) and muscle atonia, accompanied by vivid dreams.
21 ative rapid eye movement (REM) sleep without atonia analysis in the submentalis and anterior tibialis
22 f consciousness) and to the spinal cord (for atonia and antinociception).
23 produces an REM sleep-like state with muscle atonia and cortical activation, both of which are cardin
24 pathology that can progressively afflict REM atonia and midbrain dopaminergic centers.
25                     Brief episodes of muscle atonia and postural collapse resembling cataplexy were a
26  and mechanisms underlying REM sleep without atonia and RBD based on data in cat and rat are presente
27  lesions eliminate REM sleep skeletal muscle atonia and release elaborate behavior.
28 g the inhibitory population abolished muscle atonia and sympathetic hypoactivity during rapid eye mov
29 demonstrating independent pathways mediating atonia and the EEG components of REM provide a basis for
30 ry sources to determine their effects on REM atonia and using transgenic mice to identify the neurotr
31  to be recorded during the carbachol-induced atonia, and eight of these also during the subsequent re
32  that elevated submentalis REM sleep without atonia appears to be a potentially useful biomarker for
33 5% CI 1.5-10.7; p=0.0015), REM sleep without atonia at visit 1 (2.2, 1.2-4.2; p=0.043), and presence
34 rks in rodents are responsible for REM motor atonia by retrogradely tracing inputs to the spinal vent
35 e many common features, including the muscle atonia, cataplexy is a distinct state in mice.
36 al, cellular and synaptic basis of REM sleep atonia control is a critical step for treating many slee
37 teristic curves determined REM sleep without atonia cutoffs distinguishing synucleinopathies from tau
38                               The absence of atonia during rapid eye movement (REM) sleep and dream-e
39    The descending signal for postural muscle atonia during REM sleep is thought to originate from glu
40 erized by the loss of normal skeletal muscle atonia during REM sleep with prominent motor activity ac
41 t, in turn, probably serve to promote muscle atonia during REM sleep.
42  a failure of the circuitry regulating motor atonia during REM sleep.
43 medial medulla and spinal cord and regulates atonia during REM sleep.
44 to the medulla and spinal cord and regulates atonia during REM sleep.
45 ude that the inhibitory system that mediates atonia during the state of active sleep can be activated
46 litatory mechanism contributes to the muscle atonia elicited in the decerebrate animal and in the int
47       All but one were suppressed during the atonia in parallel to the suppression of XII, phrenic an
48 ecifically elevated during REM sleep without atonia in patients with PD, but not in dystonia.
49 ventral medulla do not result in loss of REM atonia in rats.
50 duction in REM sleep, and loss of normal REM atonia in some individuals may partially protect against
51 d the mechanisms of carbachol-induced muscle atonia in the alpha-chloralose-anesthetized animal.
52 e (indicative of wakefulness) and periods of atonia (indicative of sleep).
53 intrusion of rapid eye movement sleep muscle atonia into wakefulness.
54 gical features of REM are normal except that atonia is absent and elaborate behaviors may be exhibite
55 s (HR = 1.69), constipation (HR = 1.67), REM atonia loss (HR = 1.54), and age (HR = 1.54).
56 eep positively correlated with the extent of atonia loss, with beta elevation preceding the activatio
57 s state in fetal sheep is neck nuchal muscle atonia (NA).
58 btained in unanesthetized cats during muscle atonia occurring during natural active sleep.
59 ning the neural circuits responsible for the atonia of active sleep.
60 f spinal motoneurons necessary for the motor atonia of rapid-eye movement (REM) sleep in cats.
61  in association with loss of skeletal muscle atonia of REM sleep.
62  a motor suppression similar to the postural atonia of REM sleep.
63 stration of rapid eye movement sleep without atonia on polysomnography.
64 ctivity was correlated with bilateral muscle atonia or blockage of locomotion.
65  PS with cortical activation, PS with muscle atonia, or W with muscle tone.
66                          At all ages, muscle atonia preceded MT and persisted until awake behaviors o
67 ucleus and assess their behaviour during the atonia produced by microinjections of a cholinergic agon
68 observed in rapid eye movement sleep without atonia (REM-A), created in cats by bilateral pontine les
69 y give rise to the phenomenon of REM without atonia (REM-A), in which the electrophysiological featur
70 vity that occur during the carbachol-induced atonia suggest that a similar withdrawal of serotonergic
71 M resulted in an intermittent loss of muscle atonia, taking the form of exaggerated phasic muscle twi
72              Following the recovery from the atonia, the firing rates of the eight cells increased to
73                   Following the induction of atonia, the membrane potential activity was dominated by
74 n membrane properties in adult cats in which atonia was produced by the injection of carbachol into t
75 ry patterns during RBD and REM sleep without atonia were analysed and compared with another age-match
76 the above drugs produced cataplexy or muscle atonia when perfused into either the ventral tegmental a
77 urred predominantly during periods of muscle atonia (with or without concurrent myoclonic twitching),