ライフサイエンスコーパス: hypocretin

1 ent on the hypothalamic neuropeptide orexin (hypocretin).

2 attenuated the excitation of MCH neurons by hypocretin.

3 ining the neuropeptide orexin, also known as hypocretin.

4 robust direct excitation of POMC neurons by hypocretin.

5 myloid-beta, tau, total protein, YKL-40, and hypocretin.

6 neurons but showed little direct response to hypocretin.

7 beta, and not total protein, tau, YKL-40, or hypocretin.

8 modeling using the coordinates of the DQ0602-hypocretin 1-13 crystal structure.

9 Concentrations of CSF hypocretin-1 (formerly orexin A) have been measured in m

10 that blockade of hypocretin transmission at hypocretin-1 (Hcrt-1; orexin-1) receptors decreases i.v.

11 Hypocretin-1 (orexin-A) was administered to sleep-depriv

12 Orexin A/hypocretin-1 (oxA/hcrt-1) is known to be a modulator of

13 ocyte antigen typing and cerebrospinal fluid hypocretin-1 analysis are useful as adjuncts.

14 performed in all participants to measure CSF hypocretin-1 and GABA-A response.

15 he levels of two hypothalamic neuropeptides, hypocretin-1 and melanin-concentrating hormone, measured

16 Determination of CSF hypocretin-1 concentration to diagnose narcolepsy might

17 Because 98% of patients with hypocretin-1 deficiency are positive for HLA DQB1*0602,

18 Although hypocretin-1 deficiency in narcolepsy might have therape

19 Low CSF hypocretin-1 is most predictive of narcolepsy in patient

20 w/intermediate or normal cerebrospinal fluid hypocretin-1 is present in both diseases.

21 rast, the diagnostic significance of low CSF hypocretin-1 is unclear in the presence of acute CNS inf

22 nted low (</= 110 pg/mL) cerebrospinal fluid hypocretin-1 level.

23 We show that hypocretin-1 levels are maximal during positive emotion,

24 tent with a role in sleep induction, whereas hypocretin-1 levels increase at wake onset, consistent w

25 QB1*06:02 positivity (no cerebrospinal fluid hypocretin-1 results available) or narcolepsy with docum

26 nce and nuclear imaging, cerebrospinal fluid hypocretin-1, total tau, phosphorylated tau, amyloid-bet

27 hypocretin/orexin neurons is potentiated and hypocretin-1-induced action potential firing is facilita

28 signaling, MCH significantly attenuated the hypocretin-1-induced enhancement of spike frequency in h

29 Consistent with this effect, MCH attenuated hypocretin-1-induced enhancement of the frequency of min

30 el immunofluorescence of FosB/DeltaFosB with hypocretin-1.

31 o cocaine and alcohol via stimulation of the hypocretin-1/orexin-A (Hcrt-1/Ox-A) system.

32 suppress such attacks, the gene for orexin (hypocretin), a peptide lost in most human narcoleptics,

33 ficantly increased the synaptic responses to hypocretin, a measure of thalamocortical synapses, compa

34 Orexin-hypocretin, acting at its receptors, may effect changes

35 Hypocretin also enhanced excitatory inputs to POMC cells

36 Within NAc shell, orexin/hypocretin also has been reported to stimulate food inta

37 Hypocretin (also known as orexin) is a peptide neuromodu

38 gent features of neuropeptidergic functions: hypocretin and cgrp stimulated spontaneous locomotor act

39 Wake-promoting cell types include hypocretin and GABA (gamma-aminobutyric-acid)-releasing

40 pressure, both directly inhibit wake-active hypocretin and GABAergic cells in the lateral hypothalam

41 Furthermore, hypocretin and nociceptin induced modality-specific diff

42 e neurons), synergistic direct excitation by hypocretin and presynaptic attenuation of inhibition by

43 stimulation with the excitatory neuropeptide hypocretin and the inhibitory peptide dynorphin might ex

44 itonin gene-related peptide (cgrp), galanin, hypocretin, and nociceptin.

45 pressing the peptide neurotransmitter orexin/hypocretin are ideally situated to act as a relay betwee

46 Because orexins-hypocretins are neurotransmitters known to be important

47 The orexins (or hypocretins) are hypothalamic neuropeptides that have be

48 The orexins (or hypocretins) are neuropeptide transmitters made exclusiv

49 Orexin A and Orexin B (also known as hypocretins) are neuropeptides that bind two related G-c

50 Orexins (synonymous with hypocretins) are recently discovered neuropeptides made

51 Orexins (hypocretins) are two peptides (orexin A and B) produced

52 norphin might exert on cells postsynaptic to hypocretin axons, including hypocretin neurons.

53 different effects on neurons postsynaptic to hypocretin axons: direct response to only one or the oth

54 n of hypothalamic microslices that contained hypocretin cells and their axons evoked dynorphin releas

55 otine withdrawal increased the percentage of hypocretin cells expressing c-Fos in the perifornical, d

56 f-administration increased the percentage of hypocretin cells expressing FosB/DeltaFosB in the latera

57 idization, we have traced the development of hypocretin cells in zebrafish from onset of expression a

58 Hypocretin cells innervate the mediobasal hypothalamus w

59 which regulate ATP-mediated transmission in hypocretin cells of zebrafish larvae.

60 o only one or the other of the two peptides [hypocretin cells respond to dynorphin, arcuate neuropept

61 We found an increasing loss of hypocretin cells with disease progression.

62 lass of hypothalamic GI neurones, the orexin/hypocretin cells, also appear to use a non-metabolic sen

63 educed spontaneous firing of the neighboring hypocretin cells, both results consistent with reduced a

64 In addition, we show that hypocretin-containing fibers innervate the insula, Hcrt-

65 Orexin/hypocretin-containing neurons in the lateral hypothalamu

66 and suggest that the absence of hypothalamic hypocretin control on mesolimbic reward centers is cruci

67 [95% CI, 48.1%-66.3%] of 122) for narcolepsy/hypocretin deficiency (area under the curve, 0.765 [95%

68 ne optimal diagnostic cutoffs for narcolepsy/hypocretin deficiency compared with different samples: c

69 %-60.8%] of 14) for patients with narcolepsy/hypocretin deficiency vs population-based controls or al

70 Finally, 118 patients with narcolepsy/hypocretin deficiency were compared with 118 age- and se

71 ge- and sex-matched patients with narcolepsy/hypocretin deficiency were selected from 1749 patients a

72 lic encephalitis with sleepiness, cataplexy, hypocretin deficiency, and central hypothyroidism, toget

73 ss, responsible for narcolepsy-cataplexy and hypocretin deficiency, reflects a CD8+ inflammatory-medi

74 and MSLT as diagnostic tests for narcolepsy/hypocretin deficiency.

75 thin groups by final diagnosis of narcolepsy/hypocretin deficiency.

76 ers, with no significant differences between hypocretin-deficient and non-hypocretin-deficient patien

77 erences between hypocretin-deficient and non-hypocretin-deficient patients compared to controls.

78 te sleep time in adult mice, in part through hypocretin-dependent mechanisms.

79 rcuate neuropeptide Y (NPY) cells respond to hypocretin], differential desensitization causing shift

80 lamic neurons producing orexins (also called hypocretins) enhance innate risk-avoidance via poorly un

81 ouse model of narcolepsy (ataxin-ablation of hypocretin-expressing neurons).

82 ng a core 13-base pair element essential for hypocretin expression.

83 The orexin (also known as hypocretin) G protein-coupled receptors (GPCRs) respond

84 mic structure of the zebrafish and Tetraodon hypocretin genes and the complete predicted hypocretin p

85 Costimulation with dynorphin and hypocretin had three different effects on neurons postsy

86 Orexin (or hypocretin) has been implicated in mediating drug addict

87 Orexins (also called hypocretins) have been shown to be importantly involved

88 Using genetic overexpression of hypocretin (Hcrt) and optogenetic activation of hcrt-exp

89 amic neurons expressing histamine and orexin/hypocretin (hcrt) are necessary for normal regulation of

90 Hypocretin (Hcrt) cell loss is responsible for narcoleps

91 oss of neurons that express the neuropeptide hypocretin (Hcrt) has been implicated in narcolepsy, a d

92 H), melanin-concentrating hormone (MCH), and hypocretin (Hcrt) in the region of the claustrum.

93 The hypocretin (HCRT) neurons are located only in the perifo

94 epsy, which is linked to a selective loss of hypocretin (Hcrt) neurons.

95 etect histamine cells in human narcoleptics, hypocretin (Hcrt) receptor-2 mutant dogs, and 3 mouse na

96 The hypocretin (Hcrt) system is a strong candidate for media

97 n the case of neurons expressing the peptide hypocretin (HCRT), quiescent during both non-REM and REM

98 t models of sleep/wake regulation posit that Hypocretin (Hcrt)-expressing neurons in the lateral hypo

99 s in mice, we show that neurons that produce hypocretin (Hcrt)/orexin in the lateral hypothalamic are

100 Hypocretin (Hcrt, also known as orexin)-producing neuron

101 The hypocretins (Hcrts) (also called orexins) are two neurop

102 median eminence, were robustly activated by hypocretin in a dose-dependent manner.

103 We investigated the effects of hypocretins in the intravenous self-administration of th

104 tress produced a decrement in both 5-HT- and hypocretin-induced EPSCs, an effect that was correlated

105 ked reductions in 5-HT-induced EPSCs but not hypocretin-induced EPSCs.

106 failed to produce a significant decrease in hypocretin-induced EPSCs.

107 ophy might result in a blunting of 5-HT- and hypocretin-induced excitatory responses.

108 us, in contrast to previous suggestions that hypocretin inhibited POMC cells, our results demonstrate

109 hat glutamate and orexin (ORX, also known as hypocretin) inputs to the ventral tegmental area (VTA) d

110 Orexin (also known as hypocretin) is a lateral hypothalamic neuropeptide relea

111 Orexin (hypocretin) is implicated in stimulating appetite as wel

112 n, and the hypothalamic neuropeptide orexin (hypocretin) is involved in anxiety states and arousal.

113 Orexin (or hypocretin) is synthesized exclusively in dorsomedial, p

114 findings confirm recent data obtained in the hypocretin knock-out mice and suggest that the absence o

115 of forty four neurons in the rostral pons in hypocretin knock-out mice.

116 Symptomatic narcolepsy with low hypocretin level has been described in Ma antibody-assoc

117 greatly increase and decrease, respectively, hypocretin levels in normal dogs.

118 n the normal dogs, these drugs did not alter hypocretin levels in the Hcrt-r2 mutants.

119 tic humans, the narcoleptic dogs have normal hypocretin levels.

120 th a diagnosis of narcolepsy but with normal hypocretin levels.

121 as, and patients with narcolepsy with normal hypocretin levels.

122 A, suggesting that the primary mechanism for hypocretin-mediated excitation is the activation of the

123 Y (NPY), proopiomelanocortin (POMC), orexin/hypocretin, melanin-concentrating hormone (MCH), thyrotr

124 How hypocretin modulates the endocrine system remains an ope

125 Here, we examine whether hypocretin modulates the median eminence-projecting proo

126 sing progress toward integrated theories for hypocretin modulation of divergent behavioral domains.

127 A dense network of orexin/hypocretin neuronal projections contacting pericoerulear

128 al a novel and important role for the orexin/hypocretin neuronal system in reward processing and addi

129 Central orexin/hypocretin neurones are critical for sustaining consciou

130 d to overexpress the uncoupling protein 2 in hypocretin neurons (Hcrt-UCP2) have elevated hypothalami

131 Here, we show that mouse hypocretin neurons are acutely sensitive to dynorphin.

132 We found that hypocretin neurons are depressed by opiates, drugs of ab

133 by Burdakov et al. demonstrates that orexin/hypocretin neurons are inhibited by rising glucose in pa

134 t al. show that, in mice, synapses targeting hypocretin neurons become stronger when wakefulness is p

135 received direct synaptic contact from other hypocretin neurons but showed little direct response to

136 Hypocretin neurons directly innervate the PVN and the lo

137 in (CREB) is also significantly increased in hypocretin neurons in cocaine-treated animals, suggestin

138 high-frequency stimulation is facilitated in hypocretin neurons in cocaine-treated mice, suggesting t

139 gonists and antagonists on identified MCH or hypocretin neurons in green fluorescent protein-expressi

140 nt potentiation of glutamatergic synapses on hypocretin neurons in mice following a cocaine-condition

141 These results suggest that hypocretin neurons may be able to exercise a high degree

142 Orexin/hypocretin neurons of the lateral hypothalamus are widel

143 re, the potentiation of synaptic efficacy in hypocretin neurons persists during cocaine withdrawal, b

144 crospheres was used to determine whether the hypocretin neurons project directly to the paraventricul

145 Central orexin/hypocretin neurons promote wakefulness, feeding and rewa

146 Hypocretin neurons received direct synaptic contact from

147 eported photostimulation of noradrenergic or hypocretin neurons that induces wake transitions from bo

148 In summary, we show here that hypocretin neurons undergo experience-dependent synaptic

149 Activation of hypocretin neurons was analyzed by using double-label im

150 Cannabinoid actions on hypocretin neurons were abolished by ionotropic glutamat

151 g that long-lasting changes in synapses onto hypocretin neurons would probably be further potentiated

152 try centred on hypocretin-producing neurons (hypocretin neurons) is modified by drugs of abuse and ho

153 In hypocretin neurons, the reduced spike frequency induced

154 We studied glucose inhibition of orexin/hypocretin neurons, which promote wakefulness (their los

155 gulation of AMPA-type glutamate receptors on hypocretin neurons.

156 ongly suggests an autoimmune basis targeting hypocretin neurons.

157 annabinoids have opposite effects on MCH and hypocretin neurons.

158 ly by stimulation of nearby mGluR-expressing hypocretin neurons.

159 postsynaptic to hypocretin axons, including hypocretin neurons.

160 n autoimmune disorder targeting hypothalamic hypocretin neurons.

161 CD8+ inflammatory-mediated response against hypocretin neurons.

162 ting hypothalamic orexin (ORX: also known as hypocretin) neurons are highly sensitive to local change

163 The observation that loss of orexin (hypocretin) neurons causes human narcolepsy raises the p

164 site through which the orexin (also known as hypocretin) neurons drive arousal and promote the mainte

165 The orexin (hypocretin) neurons play an essential role in promoting

166 Orexin (hypocretin) neurons, located exclusively in the PeF-LH,

167 The cell bodies of neurons expressing orexin/hypocretin neuropeptides are restricted to the lateral h

168 he hypothalamic neurons producing the orexin/hypocretin neuropeptides.

169 In humans and rodents, loss of brain orexin/hypocretin (OH) neurons causes pathological sleepiness [

170 lanin-concentrating-hormone (MCH) and orexin/hypocretin (OH) neurons mediate energy accumulation and

171 neuropeptides promoting wakefulness (orexin/hypocretin; OH), or sleep (melanin-concentrating hormone

172 lamic neuropeptides, respectively called the hypocretins or orexins, which were discovered using two

173 bers of neurons that produce either orexins (hypocretins) or melanin concentrating hormone (MCH).

174 Hypocretin (orexin) and dynorphin are neuropeptides with

175 associated with HLA-DQB1*06:02 and caused by hypocretin (orexin) deficiency, is diagnosed using the M

176 Hypothalamic hypocretin (orexin) peptides mediate arousal, attention,

177 the minor allele for rs7767652, upstream of hypocretin (orexin) receptor-2 (HCRTR2), were less likel

178 Hypocretin (orexin) signaling is involved in drug addict

179 The hypocretin (orexin) system is involved in sleep/wake reg

180 Emerging evidence suggests that hypocretin (orexin) transmission may play an important r

181 Hypocretin (orexin), a neuropeptide synthesized exclusiv

182 1 narcolepsy, a disorder caused by a lack of hypocretin (orexin), is so strongly associated with huma

183 Narcolepsy is caused by the loss of hypocretin (orexin)-producing neurons in the lateral hyp

184 tic currents (EPSCs) by serotonin (5-HT) and hypocretin (orexin).

185 Hypocretin (orexin; Hcrt)-containing neurons of the hypo

186 The role of hypocretin (orexin; hcrt/orx) neurons in regulation of a

187 in receptor (LepRb) regulate the function of hypocretin/orexin (HCRT) and dopamine neurons.

188 rstood, previous studies have implicated the hypocretin/orexin (Hcrt) and nociceptin/orphanin FQ (N/O

189 Histamine and hypocretin/orexin (hcrt) are proposed to be responsible

190 lamic area (LHA), brain regions in which the hypocretin/orexin (Hcrt) cells are located.

191 Hypocretin/orexin (Hcrt) is a critical neurotransmitter

192 The hypothalamic hypocretin/orexin (Hcrt) neurons regulate sleep\wake sta

193 g of the presynaptic marker synaptophysin in hypocretin/orexin (HCRT) neurons to determine the dynami

194 ed by selective degeneration of hypothalamic hypocretin/orexin (HCRT) neurons.

195 In mammals, hypocretin/orexin (HCRT) neuropeptides are important sle

196 Multiple lines of evidence indicate that hypocretin/orexin (HCRT) participates in the regulation

197 The loss of hypothalamic hypocretin/orexin (hcrt) producing neurons causes narcol

198 The hypocretin/orexin (HCRT) system has been associated with

199 The lateral hypothalamic hypocretin/orexin (HCRT) system has been implicated in d

200 racterized mammalian sleep/wake regulator is hypocretin/orexin (Hcrt), whose loss results in the slee

201 The hypocretin/orexin (Hcrt)-containing neurones within the

202 Hypocretin/orexin (Hcrt)-producing neurons in the latera

203 The hypocretin/orexin (HCRT/ORX) excitatory neuropeptides ar

204 Hypothalamic hypocretin/orexin (hcrt/orx) neurons coordinate sleep-wa

205 Hypothalamic hypocretin/orexin (hcrt/orx) neurons promote arousal and

206 Hypothalamic hypocretin/orexin (Hcrt/Orx) neurons recently emerged as

207 mely melanin-concentrating hormone (MCH) and hypocretin/orexin (hcrt/orx), were not detected in LHA G

208 at there are reciprocal innervations between hypocretin/orexin and MCH neurons.

209 neurotensin mRNA, but they are distinct from hypocretin/orexin and melanin-concentrating hormone (MCH

210 rs, such as the well-described neuropeptides hypocretin/orexin and melanin-concentrating hormone.

211 Some neuropeptides such as hypocretin/orexin are synthesized only in single regions

212 The hypocretin/orexin arousal system plays a key role in mai

213 A report on the rapid change of activity of hypocretin/orexin cells in response to contact rather th

214 In narcolepsy caused by hypocretin/orexin deficiency, cataplexy is associated wi

215 Melanin-concentrating hormone (MCH) and hypocretin/orexin neurons in the lateral hypothalamus (L

216 entiation (LTP) of glutamatergic synapses on hypocretin/orexin neurons in the lateral hypothalamus, a

217 e, the efficacy of glutamatergic synapses on hypocretin/orexin neurons is potentiated and hypocretin-

218 naptic strength at glutamatergic synapses on hypocretin/orexin neurons was also seen when mice were s

219 vation occurs in a significant number of LHA hypocretin/orexin neurons, but not CRH or MCH neurons, i

220 We optogenetically targeted hypocretin/orexin neurons, which play a key role in arou

221 onsistent with previous reports, TRH excited hypocretin/orexin neurons.

222 ement of the frequency of miniature EPSCs in hypocretin/orexin neurons.

223 -1-induced enhancement of spike frequency in hypocretin/orexin neurons.

224 n of the extensive axonal projections of the hypocretin/orexin neurons.

225 ting hormone and proopiomelanocortin but not hypocretin/orexin neurons; pattern B, GABAergic cortical

226 The hypothalamic hypocretin/orexin neuropeptide system is able to influen

227 ed in part on this detailed description, the hypocretin/orexin neuropeptides have since been studied

228 ge body of literature today attests that the hypocretin/orexin neuropeptides play important roles in

229 LHA neurons also show increased CRH, but not hypocretin/orexin or MCH gene expression, as dehydration

230 Together these data implicate CRH but not hypocretin/orexin or MCH neurons in the LHA in the motor

231 Two groups of neurons in the LH, expressing hypocretin/orexin or melanin concentrating hormone (MCH)

232 H may exert a unique inhibitory influence on hypocretin/orexin signaling as a way to fine-tune the ou

233 rons in the cerebral cortex, the role of the hypocretin/orexin system in the maintenance of sleep and

234 The hypocretin/orexin system plays a critical role in drug a

235 wake state is dependent on the hypothalamic hypocretin/orexin system.

236 rk controlling responses evidently come from hypocretin/orexin, but not CRH or MCH, neurons in the LH

237 -opiolemelanocortin, agouti-related peptide, hypocretin/orexin, melanin-concentrating hormone, oxytoc

238 Hypocretin/orexin, produced by a group of neurons in the

239 mice expressing green fluorescent protein in hypocretin/orexin-containing neurons to examine the hypo

240 d increased the percentage of Fos-expressing hypocretin/orexin-immunoreactive neurons in these zones.

241 to examine the hypothesis that MCH modulates hypocretin/orexin-mediated effects on behavioral state a

242 ns, stronger than the actions of ghrelin and hypocretin/orexin.

243 esize melanin-concentrating hormone (MCH) or hypocretin/orexin.

244 Hypocretins/orexins are neuropeptides involved in the re

245 munoreactive for serotonin (5-HT) and orexin/hypocretin (ORX), as well as a moderate density of fiber

246 Hypothalamic orexin/hypocretin (orx/hcrt) neurons regulate energy balance, w

247 he nociceptin/orphanin FQ (N/OFQ) and orexin/hypocretin (Orx/Hcrt) systems.

248 anin-concentrating hormone (MCH), and orexin/hypocretins (ORX) produced in the hypothalamus mediate a

249 r region able to accurately mimic the native hypocretin pattern.

250 The hypocretin peptide is colocalized with an opioid peptide

251 The orexin/hypocretin peptide signaling system plays a neuromodulat

252 we specifically targeted GFP-Aequorin to the hypocretin-positive neurons of the hypothalamus.

253 ons in EPSCs evoked by 5-HT as compared with hypocretin, possibly reflecting the different pathways a

254 at could lead to the specific elimination of hypocretin producing neurons include molecular mimicry o

255 that Hap1 is abundantly expressed in orexin (hypocretin)-producing neurons (orexin neurons), which ar

256 halamic area (LHA) orexin (OX; also known as hypocretin)-producing neurons, which control feeding, ac

257 wing studies in dogs and mice, a 95% loss of hypocretin-producing cells in postmortem hypothalami fro

258 it is not clear how the circuitry centred on hypocretin-producing neurons (hypocretin neurons) is mod

259 m and hypothalamic neurons, including orexin/hypocretin-producing neurons that regulate sleep-wake st

260 hypocretin genes and the complete predicted hypocretin protein sequences from five teleosts.

261 The dual hypocretin receptor (HcrtR) antagonist almorexant (ALM)

262 5 mg/kg/day for 14 days) pretreated with the hypocretin receptor 1 (Hcrtr-1) antagonist SB334867 (5 a

263 ceptors Drd1a and Drd2 (both downregulated), hypocretin receptor 1 (Hcrtr1), kappa opioid receptor 1

264 34867 (5 and 10 mg/kg, intraperitoneal), the hypocretin receptor 2 antagonist TCSOX229 (5 and 10 mg/k

265 eep/wake regulation, and antagonists of both hypocretin receptor type 1 (HCRTR1) and/or HCRTR2 are co

266 thetic cannabinoid agonist WIN55,212-2 using hypocretin receptor-1 (Hcrtr-1) and hypocretin receptor-

267 Here, we show that orexin/hypocretin receptor-1 (ox/hcrt-1R) signaling is importan

268 Hypocretin receptor-2 (Hcrt-r2)-mutated dogs exhibit all

269 -2 using hypocretin receptor-1 (Hcrtr-1) and hypocretin receptor-2 antagonists and Hcrtr-1 knockout m

270 red with ketamine, whereas regulation of the hypocretin responses may contribute to the therapeutic b

271 iew current advances in the understanding of hypocretin's modulatory actions underlying conditions of

272 These data demonstrate that hypocretin signaling acting on Hcrtr-1 in the PVN plays

273 Narcolepsy is caused by a loss of orexin/hypocretin signaling, resulting in chronic sleepiness, f

274 is caused by a loss of orexin (also known as hypocretin) signaling, but almost nothing is known about

275 his condition is caused by a lack of orexin (hypocretin) signaling, but little is known about the neu

276 ttenuated subsequent excitatory responses to hypocretin, suggesting a long-lasting depression caused

277 st that the architecture and function of the hypocretin system are conserved in fish.

278 enous opiates such as morphine inhibited the hypocretin system by direct actions on the cell body tha

279 Dynorphin inhibits the hypocretin system by direct postsynaptic actions (hyperp

280 We also identify an intrinsic role of the hypocretin system in energy expenditure that may not be

281 The orexin/hypocretin system in the perifornical/lateral hypothalam

282 g body of evidence discerning how the orexin/hypocretin system integrates internal and external cues

283 These findings support the idea that the hypocretin system is important for behavioural changes a

284 The orexin/hypocretin system is important for reward-seeking behavi

285 One example is the recently discovered hypocretin system located in the posterior hypothalamus.

286 e data are consistent with the view that the hypocretin system may be an important direct target for

287 that a deficiency in the hypothalamic orexin/hypocretin system underlies the pathogenesis of narcolep

288 the potential interrelationship between the hypocretin system, metabolism and sleep by measuring loc

289 Disruption of the hypocretin system, such as occurs in narcolepsy, leads t

290 pa-opioid receptors enhanced activity of the hypocretin system, suggesting ongoing depression by endo

291 eceptor antagonists enhanced activity of the hypocretin system, suggesting ongoing inhibition by endo

292 of vestibular motor functions by the orexin (hypocretin) system in the perifornical/LH area through t

293 tention in the SRTT task, which is linked to hypocretin-thalamocortical responses.

294 Here we show that blockade of hypocretin transmission at hypocretin-1 (Hcrt-1; orexin-

295 These data demonstrate that insular hypocretin transmission plays a permissive role in the m

296 n the PVN during withdrawal was dependent on hypocretin transmission through Hcrtr-1 activation.

297 tates of hyperarousal that are influenced by hypocretin transmission throughout hypothalamic, extende

298 in-releasing factor, norepinephrine, orexin [hypocretin], vasopressin, dynorphin) and brain antistres

299 As dynorphin may be coreleased with hypocretin, we asked what action simultaneous stimulatio

300 eurons containing orexin (ORX, also known as hypocretin), which have a crucial role in arousal, vigil