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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 beta, and not total protein, tau, YKL-40, or hypocretin.
7                        Concentrations of CSF hypocretin-1 (formerly orexin A) have been measured in m
8  that blockade of hypocretin transmission at hypocretin-1 (Hcrt-1; orexin-1) receptors decreases i.v.
9                                Low levels of hypocretin-1 (Hcrt1) in cerebrospinal fluid (CSF) are as
10                                              Hypocretin-1 (orexin-A) was administered to sleep-depriv
11                                     Orexin A/hypocretin-1 (oxA/hcrt-1) is known to be a modulator of
12 ocyte antigen typing and cerebrospinal fluid hypocretin-1 analysis are useful as adjuncts.
13 performed in all participants to measure CSF hypocretin-1 and GABA-A response.
14 he levels of two hypothalamic neuropeptides, hypocretin-1 and melanin-concentrating hormone, measured
15                         Determination of CSF hypocretin-1 concentration to diagnose narcolepsy might
16                 Because 98% of patients with hypocretin-1 deficiency are positive for HLA DQB1*0602,
17                                     Although hypocretin-1 deficiency in narcolepsy might have therape
18                                      Low CSF hypocretin-1 is most predictive of narcolepsy in patient
19 w/intermediate or normal cerebrospinal fluid hypocretin-1 is present in both diseases.
20 rast, the diagnostic significance of low CSF hypocretin-1 is unclear in the presence of acute CNS inf
21 nted low (</= 110 pg/mL) cerebrospinal fluid hypocretin-1 level.
22                                 We show that hypocretin-1 levels are maximal during positive emotion,
23 tent with a role in sleep induction, whereas hypocretin-1 levels increase at wake onset, consistent w
24 QB1*06:02 positivity (no cerebrospinal fluid hypocretin-1 results available) or narcolepsy with docum
25 nce and nuclear imaging, cerebrospinal fluid hypocretin-1, total tau, phosphorylated tau, amyloid-bet
26 hypocretin/orexin neurons is potentiated and hypocretin-1-induced action potential firing is facilita
27  signaling, MCH significantly attenuated the hypocretin-1-induced enhancement of spike frequency in h
28  Consistent with this effect, MCH attenuated hypocretin-1-induced enhancement of the frequency of min
29 el immunofluorescence of FosB/DeltaFosB with hypocretin-1.
30 o cocaine and alcohol via stimulation of the hypocretin-1/orexin-A (Hcrt-1/Ox-A) system.
31  suppress such attacks, the gene for orexin (hypocretin), a peptide lost in most human narcoleptics,
32 ficantly increased the synaptic responses to hypocretin, a measure of thalamocortical synapses, compa
33 ger atherosclerotic lesions and produce less hypocretin-a stimulatory and wake-promoting neuropeptide
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 stimulation with the excitatory neuropeptide hypocretin and the inhibitory peptide dynorphin might ex
43 itonin gene-related peptide (cgrp), galanin, hypocretin, and nociceptin.
44 pressing the peptide neurotransmitter orexin/hypocretin are ideally situated to act as a relay betwee
45                              The orexins (or hypocretins) are hypothalamic neuropeptides that have be
46         Orexin A and Orexin B (also known as hypocretins) are neuropeptides that bind two related G-c
47                     Orexins (synonymous with hypocretins) are recently discovered neuropeptides made
48                                     Orexins (hypocretins) are two peptides (orexin A and B) produced
49 norphin might exert on cells postsynaptic to hypocretin axons, including hypocretin neurons.
50 otine withdrawal increased the percentage of hypocretin cells expressing c-Fos in the perifornical, d
51 f-administration increased the percentage of hypocretin cells expressing FosB/DeltaFosB in the latera
52                                              Hypocretin cells innervate the mediobasal hypothalamus w
53  which regulate ATP-mediated transmission in hypocretin cells of zebrafish larvae.
54               We found an increasing loss of hypocretin cells with disease progression.
55 lass of hypothalamic GI neurones, the orexin/hypocretin cells, also appear to use a non-metabolic sen
56 educed spontaneous firing of the neighboring hypocretin cells, both results consistent with reduced a
57                    In addition, we show that hypocretin-containing fibers innervate the insula, Hcrt-
58 and suggest that the absence of hypothalamic hypocretin control on mesolimbic reward centers is cruci
59                                              Hypocretin controls myelopoiesis by restricting the prod
60 [95% CI, 48.1%-66.3%] of 122) for narcolepsy/hypocretin deficiency (area under the curve, 0.765 [95%
61 ne optimal diagnostic cutoffs for narcolepsy/hypocretin deficiency compared with different samples: c
62 %-60.8%] of 14) for patients with narcolepsy/hypocretin deficiency vs population-based controls or al
63        Finally, 118 patients with narcolepsy/hypocretin deficiency were compared with 118 age- and se
64 ge- and sex-matched patients with narcolepsy/hypocretin deficiency were selected from 1749 patients a
65 lic encephalitis with sleepiness, cataplexy, hypocretin deficiency, and central hypothyroidism, toget
66 ss, responsible for narcolepsy-cataplexy and hypocretin deficiency, reflects a CD8+ inflammatory-medi
67  and MSLT as diagnostic tests for narcolepsy/hypocretin deficiency.
68 thin groups by final diagnosis of narcolepsy/hypocretin deficiency.
69 ers, with no significant differences between hypocretin-deficient and non-hypocretin-deficient patien
70 erences between hypocretin-deficient and non-hypocretin-deficient patients compared to controls.
71 te sleep time in adult mice, in part through hypocretin-dependent mechanisms.
72 lamic neurons producing orexins (also called hypocretins) enhance innate risk-avoidance via poorly un
73 ouse model of narcolepsy (ataxin-ablation of hypocretin-expressing neurons).
74                    The orexin (also known as hypocretin) G protein-coupled receptors (GPCRs) respond
75 mic structure of the zebrafish and Tetraodon hypocretin genes and the complete predicted hypocretin p
76                                   Orexin (or hypocretin) has been implicated in mediating drug addict
77                         Orexins (also called hypocretins) have been shown to be importantly involved
78              Using genetic overexpression of hypocretin (Hcrt) and optogenetic activation of hcrt-exp
79 amic neurons expressing histamine and orexin/hypocretin (hcrt) are necessary for normal regulation of
80                                              Hypocretin (Hcrt) cell loss is responsible for narcoleps
81 oss of neurons that express the neuropeptide hypocretin (Hcrt) has been implicated in narcolepsy, a d
82 H), melanin-concentrating hormone (MCH), and hypocretin (Hcrt) in the region of the claustrum.
83                                          The hypocretin (HCRT) neurons are located only in the perifo
84 a chronic sleep disorder caused by a loss of hypocretin (hcrt) neurons in the hypothalamus.
85 epsy, which is linked to a selective loss of hypocretin (Hcrt) neurons.
86 etect histamine cells in human narcoleptics, hypocretin (Hcrt) receptor-2 mutant dogs, and 3 mouse na
87                                          The hypocretin (Hcrt) system is a strong candidate for media
88 n the case of neurons expressing the peptide hypocretin (HCRT), quiescent during both non-REM and REM
89 t models of sleep/wake regulation posit that Hypocretin (Hcrt)-expressing neurons in the lateral hypo
90  due to loss of neurons that uniquely supply hypocretin (HCRT).
91 s in mice, we show that neurons that produce hypocretin (Hcrt)/orexin in the lateral hypothalamic are
92                                              Hypocretin (Hcrt, also known as orexin)-producing neuron
93  of orexin A (its precursor is also known as hypocretin-HCRT) and NPY, and their regulation by food i
94                                          The hypocretins (Hcrts) (also called orexins) are two neurop
95  median eminence, were robustly activated by hypocretin in a dose-dependent manner.
96               We investigated the effects of hypocretins in the intravenous self-administration of th
97 tress produced a decrement in both 5-HT- and hypocretin-induced EPSCs, an effect that was correlated
98 ked reductions in 5-HT-induced EPSCs but not hypocretin-induced EPSCs.
99  failed to produce a significant decrease in hypocretin-induced EPSCs.
100 ophy might result in a blunting of 5-HT- and hypocretin-induced excitatory responses.
101 us, in contrast to previous suggestions that hypocretin inhibited POMC cells, our results demonstrate
102 hat glutamate and orexin (ORX, also known as hypocretin) inputs to the ventral tegmental area (VTA) d
103                        Orexin (also known as hypocretin) is a lateral hypothalamic neuropeptide relea
104                                      Orexin (hypocretin) is implicated in stimulating appetite as wel
105 n, and the hypothalamic neuropeptide orexin (hypocretin) is involved in anxiety states and arousal.
106                                   Orexin (or hypocretin) is synthesized exclusively in dorsomedial, p
107 findings confirm recent data obtained in the hypocretin knock-out mice and suggest that the absence o
108 of forty four neurons in the rostral pons in hypocretin knock-out mice.
109              Symptomatic narcolepsy with low hypocretin level has been described in Ma antibody-assoc
110 greatly increase and decrease, respectively, hypocretin levels in normal dogs.
111 n the normal dogs, these drugs did not alter hypocretin levels in the Hcrt-r2 mutants.
112 th a diagnosis of narcolepsy but with normal hypocretin levels.
113 as, and patients with narcolepsy with normal hypocretin levels.
114 tic humans, the narcoleptic dogs have normal hypocretin levels.
115 A, suggesting that the primary mechanism for hypocretin-mediated excitation is the activation of the
116  Y (NPY), proopiomelanocortin (POMC), orexin/hypocretin, melanin-concentrating hormone (MCH), thyrotr
117                                          How hypocretin modulates the endocrine system remains an ope
118                     Here, we examine whether hypocretin modulates the median eminence-projecting proo
119 sing progress toward integrated theories for hypocretin modulation of divergent behavioral domains.
120                    A dense network of orexin/hypocretin neuronal projections contacting pericoerulear
121 al a novel and important role for the orexin/hypocretin neuronal system in reward processing and addi
122                               Central orexin/hypocretin neurones are critical for sustaining consciou
123                                We found that hypocretin neurons are depressed by opiates, drugs of ab
124  by Burdakov et al. demonstrates that orexin/hypocretin neurons are inhibited by rising glucose in pa
125 t al. show that, in mice, synapses targeting hypocretin neurons become stronger when wakefulness is p
126                                              Hypocretin neurons directly innervate the PVN and the lo
127 in (CREB) is also significantly increased in hypocretin neurons in cocaine-treated animals, suggestin
128 high-frequency stimulation is facilitated in hypocretin neurons in cocaine-treated mice, suggesting t
129 gonists and antagonists on identified MCH or hypocretin neurons in green fluorescent protein-expressi
130 nt potentiation of glutamatergic synapses on hypocretin neurons in mice following a cocaine-condition
131                          Hypothalamic orexin/hypocretin neurons integrate multiple sensory cues and p
132                                       Orexin/hypocretin neurons located in the lateral hypothalamus p
133                                       Orexin/hypocretin neurons of the lateral hypothalamus are widel
134 re, the potentiation of synaptic efficacy in hypocretin neurons persists during cocaine withdrawal, b
135 crospheres was used to determine whether the hypocretin neurons project directly to the paraventricul
136                               Central orexin/hypocretin neurons promote wakefulness, feeding and rewa
137 eported photostimulation of noradrenergic or hypocretin neurons that induces wake transitions from bo
138                In summary, we show here that hypocretin neurons undergo experience-dependent synaptic
139                                Activation of hypocretin neurons was analyzed by using double-label im
140                       Cannabinoid actions on hypocretin neurons were abolished by ionotropic glutamat
141 g that long-lasting changes in synapses onto hypocretin neurons would probably be further potentiated
142 try centred on hypocretin-producing neurons (hypocretin neurons) is modified by drugs of abuse and ho
143                                           In hypocretin neurons, the reduced spike frequency induced
144      We studied glucose inhibition of orexin/hypocretin neurons, which promote wakefulness (their los
145 n autoimmune disorder targeting hypothalamic hypocretin neurons.
146  CD8+ inflammatory-mediated response against hypocretin neurons.
147 gulation of AMPA-type glutamate receptors on hypocretin neurons.
148 ongly suggests an autoimmune basis targeting hypocretin neurons.
149 annabinoids have opposite effects on MCH and hypocretin neurons.
150 ly by stimulation of nearby mGluR-expressing hypocretin neurons.
151  postsynaptic to hypocretin axons, including hypocretin neurons.
152 ting hypothalamic orexin (ORX: also known as hypocretin) neurons are highly sensitive to local change
153 site through which the orexin (also known as hypocretin) neurons drive arousal and promote the mainte
154 loss or dysfunction of orexin (also known as hypocretin) neurons of the lateral hypothalamus.
155                                  The orexin (hypocretin) neurons play an essential role in promoting
156                                      Orexin (hypocretin) neurons, located exclusively in the PeF-LH,
157 The cell bodies of neurons expressing orexin/hypocretin neuropeptides are restricted to the lateral h
158 he hypothalamic neurons producing the orexin/hypocretin neuropeptides.
159                                      Whereas hypocretin-null and haematopoietic hypocretin-receptor-n
160  In humans and rodents, loss of brain orexin/hypocretin (OH) neurons causes pathological sleepiness [
161 lanin-concentrating-hormone (MCH) and orexin/hypocretin (OH) neurons mediate energy accumulation and
162  neuropeptides promoting wakefulness (orexin/hypocretin; OH), or sleep (melanin-concentrating hormone
163 lamic neuropeptides, respectively called the hypocretins or orexins, which were discovered using two
164 bers of neurons that produce either orexins (hypocretins) or melanin concentrating hormone (MCH).
165                                              Hypocretin (orexin) and dynorphin are neuropeptides with
166 associated with HLA-DQB1*06:02 and caused by hypocretin (orexin) deficiency, is diagnosed using the M
167                                 Hypothalamic hypocretin (orexin) peptides mediate arousal, attention,
168 demonstrated antagonistic activities against hypocretin (orexin) receptor 2.
169  the minor allele for rs7767652, upstream of hypocretin (orexin) receptor-2 (HCRTR2), were less likel
170                                              Hypocretin (orexin) signaling is involved in drug addict
171                                          The hypocretin (orexin) system is involved in sleep/wake reg
172              Emerging evidence suggests that hypocretin (orexin) transmission may play an important r
173                                              Hypocretin (orexin), a neuropeptide synthesized exclusiv
174 1 narcolepsy, a disorder caused by a lack of hypocretin (orexin), is so strongly associated with huma
175          Narcolepsy is caused by the loss of hypocretin (orexin)-producing neurons in the lateral hyp
176 tic currents (EPSCs) by serotonin (5-HT) and hypocretin (orexin).
177                                              Hypocretin (orexin; Hcrt)-containing neurons of the hypo
178                                  The role of hypocretin (orexin; hcrt/orx) neurons in regulation of a
179 in receptor (LepRb) regulate the function of hypocretin/orexin (HCRT) and dopamine neurons.
180                                              Hypocretin/orexin (HCRT) and melanin concentrating hormo
181 rstood, previous studies have implicated the hypocretin/orexin (Hcrt) and nociceptin/orphanin FQ (N/O
182                                Histamine and hypocretin/orexin (hcrt) are proposed to be responsible
183 lamic area (LHA), brain regions in which the hypocretin/orexin (Hcrt) cells are located.
184                                              Hypocretin/orexin (Hcrt) is a critical neurotransmitter
185                             The hypothalamic hypocretin/orexin (Hcrt) neurons regulate sleep\wake sta
186 g of the presynaptic marker synaptophysin in hypocretin/orexin (HCRT) neurons to determine the dynami
187 ed by selective degeneration of hypothalamic hypocretin/orexin (HCRT) neurons.
188                                  In mammals, hypocretin/orexin (HCRT) neuropeptides are important sle
189     Multiple lines of evidence indicate that hypocretin/orexin (HCRT) participates in the regulation
190                     The loss of hypothalamic hypocretin/orexin (hcrt) producing neurons causes narcol
191                                          The hypocretin/orexin (HCRT) system has been associated with
192                     The lateral hypothalamic hypocretin/orexin (HCRT) system has been implicated in d
193 racterized mammalian sleep/wake regulator is hypocretin/orexin (Hcrt), whose loss results in the slee
194                                          The hypocretin/orexin (Hcrt)-containing neurones within the
195                                              Hypocretin/orexin (Hcrt)-producing neurons in the latera
196                                          The hypocretin/orexin (HCRT/ORX) excitatory neuropeptides ar
197                                 Hypothalamic hypocretin/orexin (hcrt/orx) neurons coordinate sleep-wa
198                                 Hypothalamic hypocretin/orexin (hcrt/orx) neurons promote arousal and
199                                 Hypothalamic hypocretin/orexin (Hcrt/Orx) neurons recently emerged as
200 mely melanin-concentrating hormone (MCH) and hypocretin/orexin (hcrt/orx), were not detected in LHA G
201 at there are reciprocal innervations between hypocretin/orexin and MCH neurons.
202 neurotensin mRNA, but they are distinct from hypocretin/orexin and melanin-concentrating hormone (MCH
203 rs, such as the well-described neuropeptides hypocretin/orexin and melanin-concentrating hormone.
204                   Some neuropeptides such as hypocretin/orexin are synthesized only in single regions
205                                          The hypocretin/orexin arousal system plays a key role in mai
206  A report on the rapid change of activity of hypocretin/orexin cells in response to contact rather th
207                      In narcolepsy caused by hypocretin/orexin deficiency, cataplexy is associated wi
208      Melanin-concentrating hormone (MCH) and hypocretin/orexin neurons in the lateral hypothalamus (L
209 entiation (LTP) of glutamatergic synapses on hypocretin/orexin neurons in the lateral hypothalamus, a
210 e, the efficacy of glutamatergic synapses on hypocretin/orexin neurons is potentiated and hypocretin-
211 naptic strength at glutamatergic synapses on hypocretin/orexin neurons was also seen when mice were s
212 vation occurs in a significant number of LHA hypocretin/orexin neurons, but not CRH or MCH neurons, i
213                  We optogenetically targeted hypocretin/orexin neurons, which play a key role in arou
214 onsistent with previous reports, TRH excited hypocretin/orexin neurons.
215 ement of the frequency of miniature EPSCs in hypocretin/orexin neurons.
216 -1-induced enhancement of spike frequency in hypocretin/orexin neurons.
217 n of the extensive axonal projections of the hypocretin/orexin neurons.
218 ting hormone and proopiomelanocortin but not hypocretin/orexin neurons; pattern B, GABAergic cortical
219                             The hypothalamic hypocretin/orexin neuropeptide system is able to influen
220 ed in part on this detailed description, the hypocretin/orexin neuropeptides have since been studied
221 ge body of literature today attests that the hypocretin/orexin neuropeptides play important roles in
222 LHA neurons also show increased CRH, but not hypocretin/orexin or MCH gene expression, as dehydration
223    Together these data implicate CRH but not hypocretin/orexin or MCH neurons in the LHA in the motor
224  Two groups of neurons in the LH, expressing hypocretin/orexin or melanin concentrating hormone (MCH)
225 H may exert a unique inhibitory influence on hypocretin/orexin signaling as a way to fine-tune the ou
226                           Dysfunction of the hypocretin/orexin system has been implicated as the unde
227 rons in the cerebral cortex, the role of the hypocretin/orexin system in the maintenance of sleep and
228                                          The hypocretin/orexin system plays a critical role in drug a
229  wake state is dependent on the hypothalamic hypocretin/orexin system.
230 rk controlling responses evidently come from hypocretin/orexin, but not CRH or MCH, neurons in the LH
231 -opiolemelanocortin, agouti-related peptide, hypocretin/orexin, melanin-concentrating hormone, oxytoc
232 ivation of stress neuromodulators, including hypocretin/orexin, norepinephrine, corticotropin-releasi
233                                              Hypocretin/orexin, produced by a group of neurons in the
234 mice expressing green fluorescent protein in hypocretin/orexin-containing neurons to examine the hypo
235 d increased the percentage of Fos-expressing hypocretin/orexin-immunoreactive neurons in these zones.
236 to examine the hypothesis that MCH modulates hypocretin/orexin-mediated effects on behavioral state a
237 ns, stronger than the actions of ghrelin and hypocretin/orexin.
238 esize melanin-concentrating hormone (MCH) or hypocretin/orexin.
239 munoreactive for serotonin (5-HT) and orexin/hypocretin (ORX), as well as a moderate density of fiber
240                          Hypothalamic orexin/hypocretin (orx/hcrt) neurons regulate energy balance, w
241 he nociceptin/orphanin FQ (N/OFQ) and orexin/hypocretin (Orx/Hcrt) systems.
242 anin-concentrating hormone (MCH), and orexin/hypocretins (ORX) produced in the hypothalamus mediate a
243 r region able to accurately mimic the native hypocretin pattern.
244                                   The orexin/hypocretin peptide signaling system plays a neuromodulat
245 we specifically targeted GFP-Aequorin to the hypocretin-positive neurons of the hypothalamus.
246 ons in EPSCs evoked by 5-HT as compared with hypocretin, possibly reflecting the different pathways a
247 at could lead to the specific elimination of hypocretin producing neurons include molecular mimicry o
248 that Hap1 is abundantly expressed in orexin (hypocretin)-producing neurons (orexin neurons), which ar
249 neurons to lateral hypothalamic area orexin (hypocretin)-producing neurons that project to the latero
250 halamic area (LHA) orexin (OX; also known as hypocretin)-producing neurons, which control feeding, ac
251 wing studies in dogs and mice, a 95% loss of hypocretin-producing cells in postmortem hypothalami fro
252 it is not clear how the circuitry centred on hypocretin-producing neurons (hypocretin neurons) is mod
253 m and hypothalamic neurons, including orexin/hypocretin-producing neurons that regulate sleep-wake st
254  hypocretin genes and the complete predicted hypocretin protein sequences from five teleosts.
255                                     The dual hypocretin receptor (HcrtR) antagonist almorexant (ALM)
256 5 mg/kg/day for 14 days) pretreated with the hypocretin receptor 1 (Hcrtr-1) antagonist SB334867 (5 a
257 ceptors Drd1a and Drd2 (both downregulated), hypocretin receptor 1 (Hcrtr1), kappa opioid receptor 1
258 34867 (5 and 10 mg/kg, intraperitoneal), the hypocretin receptor 2 antagonist TCSOX229 (5 and 10 mg/k
259 eep/wake regulation, and antagonists of both hypocretin receptor type 1 (HCRTR1) and/or HCRTR2 are co
260 thetic cannabinoid agonist WIN55,212-2 using hypocretin receptor-1 (Hcrtr-1) and hypocretin receptor-
261                    Here, we show that orexin/hypocretin receptor-1 (ox/hcrt-1R) signaling is importan
262                                              Hypocretin receptor-2 (Hcrt-r2)-mutated dogs exhibit all
263 -2 using hypocretin receptor-1 (Hcrtr-1) and hypocretin receptor-2 antagonists and Hcrtr-1 knockout m
264 sis by restricting the production of CSF1 by hypocretin-receptor-expressing pre-neutrophils in the bo
265   Whereas hypocretin-null and haematopoietic hypocretin-receptor-null mice develop monocytosis and ac
266 red with ketamine, whereas regulation of the hypocretin responses may contribute to the therapeutic b
267 iew current advances in the understanding of hypocretin's modulatory actions underlying conditions of
268                  These data demonstrate that hypocretin signaling acting on Hcrtr-1 in the PVN plays
269     Narcolepsy is caused by a loss of orexin/hypocretin signaling, resulting in chronic sleepiness, f
270 is caused by a loss of orexin (also known as hypocretin) signaling, but almost nothing is known about
271 his condition is caused by a lack of orexin (hypocretin) signaling, but little is known about the neu
272 the neurons producing orexins (also known as hypocretins) sparked great advances in the field.
273 ttenuated subsequent excitatory responses to hypocretin, suggesting a long-lasting depression caused
274 ith either haematopoietic CSF1 deficiency or hypocretin supplementation have reduced numbers of circu
275 st that the architecture and function of the hypocretin system are conserved in fish.
276 enous opiates such as morphine inhibited the hypocretin system by direct actions on the cell body tha
277                       Dynorphin inhibits the hypocretin system by direct postsynaptic actions (hyperp
278    We also identify an intrinsic role of the hypocretin system in energy expenditure that may not be
279                                   The orexin/hypocretin system in the perifornical/lateral hypothalam
280 g body of evidence discerning how the orexin/hypocretin system integrates internal and external cues
281     These findings support the idea that the hypocretin system is important for behavioural changes a
282                                   The orexin/hypocretin system is important for reward-seeking behavi
283       One example is the recently discovered hypocretin system located in the posterior hypothalamus.
284 e data are consistent with the view that the hypocretin system may be an important direct target for
285 that a deficiency in the hypothalamic orexin/hypocretin system underlies the pathogenesis of narcolep
286  the potential interrelationship between the hypocretin system, metabolism and sleep by measuring loc
287                            Disruption of the hypocretin system, such as occurs in narcolepsy, leads t
288 pa-opioid receptors enhanced activity of the hypocretin system, suggesting ongoing depression by endo
289 eceptor antagonists enhanced activity of the hypocretin system, suggesting ongoing inhibition by endo
290 of vestibular motor functions by the orexin (hypocretin) system in the perifornical/LH area through t
291                                  The orexin (hypocretin) system is important for reward-driven motiva
292 tention in the SRTT task, which is linked to hypocretin-thalamocortical responses.
293                Here we show that blockade of hypocretin transmission at hypocretin-1 (Hcrt-1; orexin-
294          These data demonstrate that insular hypocretin transmission plays a permissive role in the m
295 n the PVN during withdrawal was dependent on hypocretin transmission through Hcrtr-1 activation.
296 tates of hyperarousal that are influenced by hypocretin transmission throughout hypothalamic, extende
297 releasing factor, dynorphin, norepinephrine, hypocretin, vasopressin, glucocorticoids, and neuroimmun
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

 
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