ライフサイエンスコーパス: cataplexy

1 periods and by sudden losses of muscle tone (cataplexy).

2 In addition, lesions of the amygdala reduce cataplexy.

3 d that these cells promote emotion-triggered cataplexy.

4 e, were not correlated with their effects on cataplexy.

5 fragmented non-rapid eye movement sleep, and cataplexy.

6 rt) producing neurons causes narcolepsy with cataplexy.

7 h restless legs syndrome and narcolepsy with cataplexy.

8 ional role in initiating but not maintaining cataplexy.

9 for HLA allele DQB1*0602, most of whom have cataplexy.

10 nderlies the pathogenesis of narcolepsy with cataplexy.

11 -expressing PF neurones may cause narcolepsy/cataplexy.

12 5.9% (males) and 1.1% (females), all without cataplexy.

13 p-related phenomena into wakefulness such as cataplexy.

14 tone in waking and its loss in REM sleep and cataplexy.

15 critical component of the pathophysiology of cataplexy.

16 tive in waking and increased activity during cataplexy.

17 -off neurones did not cease discharge during cataplexy.

18 f the locus coeruleus cease discharge during cataplexy.

19 alized motor inhibition during REM sleep and cataplexy.

20 ocretin-containing cells in human narcolepsy-cataplexy.

21 ions, and episodes of motor paralysis called cataplexy.

22 hen used at doses that completely suppressed cataplexy.

23 cterized by excessive daytime sleepiness and cataplexy.

24 e structure produced a moderate reduction in cataplexy.

25 e, SKF 38393 and SCH 23390 had no effects on cataplexy.

26 determine its functional role in controlling cataplexy.

27 ion of these neurons reduces reward-promoted cataplexy.

28 the entrance into rather than the exit from cataplexy.

29 own about the neural mechanisms that mediate cataplexy.

30 crucial element in the neural mechanisms of cataplexy.

31 ntral nucleus of the amygdala (CeA) promotes cataplexy.

32 mber of cataplexy episodes and time spent in cataplexy.

33 tion characterized by chronic sleepiness and cataplexy.

34 NREM and REM sleep in dogs without inducing cataplexy.

35 behaviour disorder (RBD) and narcolepsy with cataplexy.

36 cterized by excessive daytime sleepiness and cataplexy.

37 consistently associated with emotion-induced cataplexy.

38 g stimuli and contains neurons active during cataplexy.

39 cterized by excessive daytime sleepiness and cataplexy.

40 isms through which positive emotions trigger cataplexy.

41 neity among patients with narcolepsy without cataplexy.

42 d it contains neurons that are active during cataplexy.

43 site through which positive emotions trigger cataplexy.

44 but substantially reduced the triggering of cataplexy.

45 by chocolate but did not affect spontaneous cataplexy.

46 iness, fragmentation of nighttime sleep, and cataplexy.

47 I), or the lateral hypothalamus (LH) blocked cataplexy.

48 t with evidence that strong emotions trigger cataplexy.

49 eir receptors, is associated with narcolepsy/cataplexy, a disorder characterized by an increased pres

50 cterized by excessive daytime sleepiness and cataplexy, a loss of muscle tone triggered by emotional

51 Narcolepsy-cataplexy, a neurological disorder associated with the a

52 Human narcolepsy-cataplexy, a sleep disorder associated with a centrally

53 Cataplexy, a sudden unexpected muscle paralysis, is a de

54 Cataplexy, a symptom associated with narcolepsy, is a wa

55 Cataplexy, a symptom associated with narcolepsy, represe

56 703, CG3509, and TA0910 on daytime sleep and cataplexy, a symptom of abnormal REM sleep, were assesse

57 We measured sleep/wake behavior and cataplexy after injection of saline or the hM3/hM4 ligan

58 During laughter (without cataplexy) an increased hemodynamic response occurred in

59 ds, especially chocolate, markedly increased cataplexy and activated neurons in the medial prefrontal

60 hows that amygdala neurons are active during cataplexy and cataplexy is reduced by lesions of the amy

61 lepsy such as preserved consciousness during cataplexy and fragmented nighttime sleep.

62 aspects of rapid eye movement sleep such as cataplexy and hallucinations.

63 phalitic process, responsible for narcolepsy-cataplexy and hypocretin deficiency, reflects a CD8+ inf

64 psy is associated with excessive somnolence, cataplexy and increased propensity for rapid eye movemen

65 % of the patients, sometimes with narcolepsy-cataplexy and low CSF hypocretin.

66 Thus, although cataplexy and REM sleep share many common features, incl

67 stations mimicking human narcolepsy, such as cataplexy and sleep attacks.

68 y important part of the circuitry underlying cataplexy and suggest that increased amygdala activity i

69 othalamus that contain neurons active during cataplexy and that innervate brainstem regions known to

70 with those obtained in idiopathic narcolepsy-cataplexy and with normal control brains.

71 nolence syndromes (excluding narcolepsy with cataplexy) and evidence for abnormal cerebrospinal fluid

72 aracterized by excessive daytime sleepiness, cataplexy, and other pathological manifestations of the

73 It is characterized by daytime sleepiness, cataplexy, and striking transitions from wakefulness int

74 d respond to drugs that increase or decrease cataplexy as do narcoleptic humans; yet, unlike narcolep

75 gest a high prevalence of narcolepsy without cataplexy, as defined by the International Classificatio

76 cell groups, histamine neurons are active in cataplexy at a level similar to or greater than that in

77 show that GABA cell activation only promotes cataplexy attacks associated with emotionally rewarding

78 s triggered a 253% increase in the number of cataplexy attacks without affecting their duration, sugg

79 these cells are not required for initiating cataplexy attacks.

80 the entire CeA produces a marked increase in cataplexy attacks.

81 t the amygdala is functionally important for cataplexy because the amygdala has a role in processing

82 t be most useful in ambulatory patients with cataplexy but with a normal multiple sleep latency test

83 (chocolate or running wheels) also increased cataplexy, but CNO produced no further increase.

84 at emotionally rewarding stimuli may trigger cataplexy by activating GABA cells in the CeA.SIGNIFICAN

85 to emotional stimuli could directly trigger cataplexy by inhibiting brainstem regions that suppress

86 rgic drugs, despite the strong modulation of cataplexy by these drugs.

87 The Hcrt-r2 mutation causes drug-induced cataplexy by virtue of its long-term effect on the funct

88 tin was examined in 38 successive narcolepsy-cataplexy cases [36 human leukocyte antigen (HLA)-DQB1*0

89 Narcolepsy with cataplexy, characterized by sleepiness and rapid onset i

90 All of these neurons were less active during cataplexy compared with REM sleep.

91 cit/hyperactivity disorder, bulimia nervosa, cataplexy, dysthymic disorder, fibromyalgia, generalized

92 one cannot be maintained and narcolepsy with cataplexy ensues.

93 e because, in their absence, narcolepsy with cataplexy ensues.

94 as mediated through a reduction in number of cataplexy episodes and time spent in cataplexy.

95 y is characterized by chronic sleepiness and cataplexy, episodes of profound muscle weakness that are

96 Lesions also reduced the cataplexy events triggered by conditions associated with

97 Humans prone to cataplexy experience sudden losses of postural muscle to

98 urred in 16 patients, and of these 10 showed cataplexy for a total of 77 events (mean duration = 4.4

99 l subjects and 420 narcoleptic subjects with cataplexy, from three ethnic groups, were HLA typed, and

100 normal transitions to paradoxical sleep, and cataplexy, hallmarks of narcolepsy.

101 s in the CeA.SIGNIFICANCE STATEMENT Although cataplexy has been closely linked to positive emotions f

102 uprapontine mechanisms associated with human cataplexy have not been clarified.

103 aracterized by excessive daytime sleepiness, cataplexy, hypnagonic hallucinations, sleep paralysis, a

104 r diencephalic encephalitis with sleepiness, cataplexy, hypocretin deficiency, and central hypothyroi

105 h of the above listed drugs had no effect on cataplexy in any of the other brain regions examined.

106 1600 microg/kg, i.v.), significantly reduced cataplexy in canine narcolepsy.

107 motivated behaviors and typically preceding cataplexy in Hcrt(ko/ko) mice.

108 nteraction and anger, behaviours that induce cataplexy in human narcoleptics.

109 fficient and necessary for the production of cataplexy in mice, and they likely are a key part of the

110 tor conditions similar to those that trigger cataplexy in narcoleptic animals.

111 igated the effects of monoaminergic drugs on cataplexy in narcoleptic canines when perfused locally v

112 se, while raclopride produced a decrease, in cataplexy in narcoleptic canines.

113 ar mechanism may be operative in spontaneous cataplexy in narcoleptic dogs as well as in narcoleptic

114 el by these drugs do not produce episodes of cataplexy in normal dogs.

115 xic lesions of the amygdala markedly reduced cataplexy in orexin knock-out mice, a model of narcoleps

116 tration for the treatment of narcolepsy with cataplexy in patients aged more than 16 years.SUMMARY: A

117 hM3, CNO approximately doubled the amount of cataplexy in the first 3 h after dosing under baseline c

118 Cataplexy in the narcoleptic canine may be modulated by

119 We find that drugs that reduce or increase cataplexy in the narcoleptic dogs, greatly increase and

120 In mice expressing hM4, CNO reduced cataplexy in the presence of chocolate or running wheels

121 eered chloride channel substantially reduced cataplexy induced by chocolate but did not affect sponta

122 bic reward centers is crucial in determining cataplexy induced by emotions.

123 ble for the human diseases of narcolepsy and cataplexy; inhibition of orexin receptors is an effectiv

124 ommon features, including the muscle atonia, cataplexy is a distinct state in mice.

125 Cataplexy is a hallmark of narcolepsy characterized by t

126 Narcolepsy-cataplexy is a neurological disorder associated with the

127 Narcolepsy with cataplexy is a rare and severe sleep disorder caused by

128 supports the hypothesis that narcolepsy with cataplexy is an autoimmune disease.

129 epsy caused by hypocretin/orexin deficiency, cataplexy is associated with a marked increase in neural

130 e diagnosis of narcolepsy without documented cataplexy is based on the observation of two or more sle

131 Narcolepsy with cataplexy is caused by a loss of orexin (also known as h

132 In humans and canines with narcolepsy, cataplexy is considered to be a separate and distinct be

133 ons trigger cataplexy.SIGNIFICANCE STATEMENT Cataplexy is one of the major symptoms of narcolepsy, bu

134 dala neurons are active during cataplexy and cataplexy is reduced by lesions of the amygdala.

135 We found that cataplexy is substantially increased by selective activa

136 One of the most striking aspects of cataplexy is that it is often triggered by strong, gener

137 Idiopathic narcolepsy with cataplexy is thought to be an autoimmune disorder target

138 OX2R(-/-) mice are only mildly affected with cataplexy-like attacks of REM sleep, whereas orexin(-/-)

139 ) of mice lacking orexin receptors inhibited cataplexy-like episodes and pathological fragmentation o

140 The suppression of cataplexy-like episodes correlated with the number of se

141 ed sleepiness, hypnagogic hallucinations and cataplexy-like symptoms, suggesting a narcolepsy-like ph

142 These findings show that cataplexy may be regulated by D2/D3 dopaminergic recepto

143 and MSLT, including 25 with narcolepsy with cataplexy (N+C), 41 with narcolepsy without cataplexy (N

144 cataplexy (N+C), 41 with narcolepsy without cataplexy (N-C), 21 with idiopathic hypersomnia with lon

145 In prior work, we reported that, during cataplexy, noradrenergic neurons cease discharge, and se

146 Our results indicate that the CeA promotes cataplexy onset and that emotionally rewarding stimuli m

147 ing and good response to stimulants, without cataplexy or any indication of abnormal REM (rapid eye m

148 ol animals, none of the above drugs produced cataplexy or muscle atonia when perfused into either the

149 ere, we demonstrate rescue of the narcolepsy-cataplexy phenotype of orexin neuron-ablated mice by gen

150 is was defined as narcolepsy associated with cataplexy plus HLA-DQB1*06:02 positivity (no cerebrospin

151 nism through which positive emotions trigger cataplexy.SIGNIFICANCE STATEMENT Cataplexy is one of the

152 normal manifestations of REM sleep including cataplexy, sleep paralysis, and hypnagogic hallucination

153 is characterized by excessive sleepiness and cataplexy, sudden episodes of muscle weakness during wak

154 y is characterized by chronic sleepiness and cataplexy-sudden muscle paralysis triggered by strong, p

155 nhibition of GABA CeA cells does not prevent cataplexy, suggesting these cells are not required for i

156 and serotonergic cell discharge profiles in cataplexy suggests different roles for these cell groups

157 During cataplexy, suprapontine BOLD signal increase was present

158 f REM sleep control unique to the narcolepsy-cataplexy syndrome emerges from loss of signaling throug

159 sing these hallucinations include narcolepsy-cataplexy syndrome, peduncular hallucinosis, treated idi

160 omnographic recordings and the food elicited cataplexy test (FECT), respectively.

161 plexy was quantified using the Food-Elicited Cataplexy Test and analyzed by electroencephalogram, ele

162 Both TAAR1 compounds also mitigated cataplexy, the pathognomonic symptom of this disorder, i

163 GABA cells in the amygdala as regulators of cataplexy triggered by positive emotions and identifies

164 The comparison of cataplexy versus laugh episodes revealed the involvement

165 Although cataplexy was identified >130 years ago, its neural mech

166 Cataplexy was marked by brief losses of mylohyoid muscle

167 No evidence of cataplexy was observed.

168 Cataplexy was quantified using the Food-Elicited Cataple

169 In 10 children, cataplexy was the presenting symptom.

170 scle atonia and postural collapse resembling cataplexy were also noted while rats maintained the elec

171 n of fun and amusement (laughter) and of (2) cataplexy were analyzed and compared.

172 e, locomotor activity, body temperature, and cataplexy were assessed in two mouse narcolepsy models.

173 Cataplexy, which is a sudden loss of muscle tone during

174 Remarkably, narcolepsy with or without cataplexy with low/intermediate or normal cerebrospinal

175 f histamine neurons in human narcolepsy with cataplexy, with no overlap between narcoleptics and cont

176 l area produced a dose-dependent increase in cataplexy without significantly reducing basal muscle to