ライフサイエンスコーパス: cataplexy

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

2 site through which positive emotions trigger cataplexy.

3 but substantially reduced the triggering of cataplexy.

4 by chocolate but did not affect spontaneous cataplexy.

5 GABAergic neurons' real-time dynamic during cataplexy.

6 iness, fragmentation of nighttime sleep, and cataplexy.

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

8 t with evidence that strong emotions trigger cataplexy.

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

10 ABAergic neurons may trigger emotion-induced cataplexy.

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

12 rt) producing neurons causes narcolepsy with cataplexy.

13 h restless legs syndrome and narcolepsy with cataplexy.

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

15 nderlies the pathogenesis of narcolepsy with cataplexy.

16 -expressing PF neurones may cause narcolepsy/cataplexy.

17 5.9% (males) and 1.1% (females), all without cataplexy.

18 p-related phenomena into wakefulness such as cataplexy.

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

20 critical component of the pathophysiology of cataplexy.

21 tive in waking and increased activity during cataplexy.

22 -off neurones did not cease discharge during cataplexy.

23 f the locus coeruleus cease discharge during cataplexy.

24 alized motor inhibition during REM sleep and cataplexy.

25 ocretin-containing cells in human narcolepsy-cataplexy.

26 ions, and episodes of motor paralysis called cataplexy.

27 hen used at doses that completely suppressed cataplexy.

28 In addition, lesions of the amygdala reduce cataplexy.

29 cterized by excessive daytime sleepiness and cataplexy.

30 e structure produced a moderate reduction in cataplexy.

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

32 d that these cells promote emotion-triggered cataplexy.

33 acid receptor agonist) reduces both EDS and cataplexy.

34 ntenance of wakefulness but did not suppress cataplexy.

35 determine its functional role in controlling cataplexy.

36 rized by poor maintenance of wakefulness and cataplexy.

37 cells in a mouse model of narcolepsy reduces cataplexy.

38 g stimuli and contains neurons active during cataplexy.

39 ional role in initiating but not maintaining cataplexy.

40 d as the underlying cause of narcolepsy with cataplexy.

41 ion of these neurons reduces reward-promoted cataplexy.

42 the entrance into rather than the exit from cataplexy.

43 own about the neural mechanisms that mediate cataplexy.

44 crucial element in the neural mechanisms of cataplexy.

45 ations that promote wakefulness and suppress cataplexy.

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

47 mber of cataplexy episodes and time spent in cataplexy.

48 tion characterized by chronic sleepiness and cataplexy.

49 NREM and REM sleep in dogs without inducing cataplexy.

50 behaviour disorder (RBD) and narcolepsy with cataplexy.

51 cterized by excessive daytime sleepiness and cataplexy.

52 ly synchronized during predator odor-induced cataplexy.

53 consistently associated with emotion-induced cataplexy.

54 cterized by excessive daytime sleepiness and cataplexy.

55 isms through which positive emotions trigger cataplexy.

56 neity among patients with narcolepsy without cataplexy.

57 d it contains neurons that are active during cataplexy.

58 cluding the involuntary loss of muscle tone (cataplexy).(1) Here, we show that the South Asian fish s

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

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

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

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

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

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

65 Cataplexy, a symptom associated with narcolepsy, represe

66 703, CG3509, and TA0910 on daytime sleep and cataplexy, a symptom of abnormal REM sleep, were assesse

67 cterized by excessive daytime sleepiness and cataplexy, accompanied by sleep-wake symptoms, such as h

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

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

70 ic attack, hemorrhagic stroke, narcolepsy or cataplexy, anaphylaxis, acute myocardial infarction, myo

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

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

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

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

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

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

77 % of the patients, sometimes with narcolepsy-cataplexy and low CSF hypocretin.

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

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

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

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

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

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

84 is characterized by excessive sleepiness and cataplexy, and is linked to a loss of orexin-producing n

85 producing neurons results in narcolepsy with cataplexy, and orexin agonists have been shown to increa

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

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

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

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

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

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

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

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

94 these cells are not required for initiating cataplexy attacks.

95 rily aims to increase wakefulness and reduce cataplexy attacks.

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

97 ued their intense activities into succeeding cataplexy bouts.

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

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

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

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

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

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

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

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

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

107 ological therapies for treating both EDS and cataplexy, discusses concerns specific to children and r

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

109 e disorder (excessive daytime sleepiness and cataplexy), effects on cognitive symptoms are not charac

110 one cannot be maintained and narcolepsy with cataplexy ensues.

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

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

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

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

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

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

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

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

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

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

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

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

123 compounds stabilized wakefulness and reduced cataplexy in a mouse model of NT1.

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

125 1600 microg/kg, i.v.), significantly reduced cataplexy in canine narcolepsy.

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

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

128 s) causes the sleep disorder narcolepsy with cataplexy in humans and in animal models.

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

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

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

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

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

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

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

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

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

138 Cataplexy in the narcoleptic canine may be modulated by

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

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

141 ent (REM) sleep in mice and rats and reduces cataplexy in two mouse models of narcolepsy.

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

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

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

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

146 Cataplexy is a hallmark of narcolepsy characterized by t

147 Narcolepsy-cataplexy is a neurological disorder associated with the

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

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

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

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

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

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

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

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

156 We found that cataplexy is substantially increased by selective activa

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

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

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

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

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

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

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

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

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

166 rized by excessive daytime sleepiness (EDS), cataplexy, nighttime sleep disturbances, and REM-sleep-r

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

168 tral nucleus of the amygdala (CeA) triggered cataplexy of sleep disorder narcolepsy.

169 ed in cataplexy were identified: spontaneous cataplexy-ON and predator odor-induced cataplexy-ON neur

170 neous cataplexy-ON and predator odor-induced cataplexy-ON neurons.

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

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

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

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

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

176 gnaling in the vlPAG/LPT region can suppress cataplexy, providing key insights into how orexins regul

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

178 aytime sleepiness and can be associated with cataplexy, sleep paralysis and sleep-related hallucinati

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

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

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

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

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

184 During cataplexy, suprapontine BOLD signal increase was present

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

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

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

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

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

190 ncluding poor maintenance of wakefulness and cataplexy; these symptoms were substantially improved by

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

192 The comparison of cataplexy versus laugh episodes revealed the involvement

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

194 Cataplexy was marked by brief losses of mylohyoid muscle

195 No evidence of cataplexy was observed.

196 Cataplexy was quantified using the Food-Elicited Cataple

197 In 10 children, cataplexy was the presenting symptom.

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

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

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

201 stinct GABAergic neuronal groups involved in cataplexy were identified: spontaneous cataplexy-ON and

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

203 fective in treating both hypersomnolence and cataplexy while generally being well tolerated at prescr

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

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

206 ine tegmentum (vlPAG/LPT), OX-201 suppressed cataplexy without improving maintenance of wakefulness.

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