コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
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.
8 that blockade of hypocretin transmission at hypocretin-1 (Hcrt-1; orexin-1) receptors decreases i.v.
14 he levels of two hypothalamic neuropeptides, hypocretin-1 and melanin-concentrating hormone, measured
20 rast, the diagnostic significance of low CSF hypocretin-1 is unclear in the presence of acute CNS inf
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
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
38 gent features of neuropeptidergic functions: hypocretin and cgrp stimulated spontaneous locomotor act
40 pressure, both directly inhibit wake-active hypocretin and GABAergic cells in the lateral hypothalam
42 stimulation with the excitatory neuropeptide hypocretin and the inhibitory peptide dynorphin might ex
44 pressing the peptide neurotransmitter orexin/hypocretin are ideally situated to act as a relay betwee
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
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
58 and suggest that the absence of hypothalamic hypocretin control on mesolimbic reward centers is cruci
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
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
69 ers, with no significant differences between hypocretin-deficient and non-hypocretin-deficient patien
72 lamic neurons producing orexins (also called hypocretins) enhance innate risk-avoidance via poorly un
75 mic structure of the zebrafish and Tetraodon hypocretin genes and the complete predicted hypocretin p
79 amic neurons expressing histamine and orexin/hypocretin (hcrt) are necessary for normal regulation of
81 oss of neurons that express the neuropeptide hypocretin (Hcrt) has been implicated in narcolepsy, a d
86 etect histamine cells in human narcoleptics, hypocretin (Hcrt) receptor-2 mutant dogs, and 3 mouse na
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
91 s in mice, we show that neurons that produce hypocretin (Hcrt)/orexin in the lateral hypothalamic are
93 of orexin A (its precursor is also known as hypocretin-HCRT) and NPY, and their regulation by food i
97 tress produced a decrement in both 5-HT- and hypocretin-induced EPSCs, an effect that was correlated
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
105 n, and the hypothalamic neuropeptide orexin (hypocretin) is involved in anxiety states and arousal.
107 findings confirm recent data obtained in the hypocretin knock-out mice and suggest that the absence o
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
119 sing progress toward integrated theories for hypocretin modulation of divergent behavioral domains.
121 al a novel and important role for the orexin/hypocretin neuronal system in reward processing and addi
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
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
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
137 eported photostimulation of noradrenergic or hypocretin neurons that induces wake transitions from bo
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
144 We studied glucose inhibition of orexin/hypocretin neurons, which promote wakefulness (their los
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
157 The cell bodies of neurons expressing orexin/hypocretin neuropeptides are restricted to the lateral h
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).
166 associated with HLA-DQB1*06:02 and caused by hypocretin (orexin) deficiency, is diagnosed using the M
169 the minor allele for rs7767652, upstream of hypocretin (orexin) receptor-2 (HCRTR2), were less likel
174 1 narcolepsy, a disorder caused by a lack of hypocretin (orexin), is so strongly associated with huma
181 rstood, previous studies have implicated the hypocretin/orexin (Hcrt) and nociceptin/orphanin FQ (N/O
186 g of the presynaptic marker synaptophysin in hypocretin/orexin (HCRT) neurons to determine the dynami
189 Multiple lines of evidence indicate that hypocretin/orexin (HCRT) participates in the regulation
193 racterized mammalian sleep/wake regulator is hypocretin/orexin (Hcrt), whose loss results in the slee
200 mely melanin-concentrating hormone (MCH) and hypocretin/orexin (hcrt/orx), were not detected in LHA G
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.
206 A report on the rapid change of activity of hypocretin/orexin cells in response to contact rather th
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
218 ting hormone and proopiomelanocortin but not hypocretin/orexin neurons; pattern B, GABAergic cortical
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
227 rons in the cerebral cortex, the role of the hypocretin/orexin system in the maintenance of sleep and
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
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
239 munoreactive for serotonin (5-HT) and orexin/hypocretin (ORX), as well as a moderate density of fiber
242 anin-concentrating hormone (MCH), and orexin/hypocretins (ORX) produced in the hypothalamus mediate a
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
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-
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
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
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
276 enous opiates such as morphine inhibited the hypocretin system by direct actions on the cell body tha
278 We also identify an intrinsic role of the hypocretin system in energy expenditure that may not be
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
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
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
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
300 eurons containing orexin (ORX, also known as hypocretin), which have a crucial role in arousal, vigil