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1 rt, the acute appetite-stimulating effect of orexin A.
2 reboxetine, they were by exogenously applied orexin A.
3 A-A receptor agonist) were injected prior to orexin A.
4 of food-evoked dopamine spikes by intra-VTA orexin-A.
5 the infected hypothalamic neurons contained orexin-A.
6 metabolic activity (CMRglc) than intravenous orexin-A.
8 single intracerebroventricular injection of orexin A (1 and 3 nmol) or orexin B (3 nmol), during the
12 rank order of potency orexin A > orexin B > orexin A 16-33, that it bound antagonist ligands with af
13 ng 20 h (4-24 h postinjection period) in the orexin A 3 nmol injected group whilst the frequency of i
15 ntly dropped during the first hour following orexin A administration, coinciding with orexin A-induce
19 mic (LH) orexin neurons, increases levels of orexin A and 2-arachidonoylglycerol (2-AG) in the ventra
24 dentify the specific sites of orexin action, orexin A and B were microinjected into a number of hypot
32 de that GSNs are specific target neurons for orexin A and suggest that they may mediate, at least in
36 the conduits of a negative crosstalk between orexin-A and CRF as demonstrated in transfected cells an
37 le-label immunohistochemistry confirmed that orexin-A and dynorphin-A peptides were highly colocalize
38 pounds including the native agonist peptides orexin-A and orexin-B and the potent therapeutic inhibit
40 Melanin concentrating hormone (MCH) and the orexins (A and B) have been identified as neuropeptides
41 s inhibition of the excitatory neuropeptides orexins A and B by design of orexin receptor antagonists
42 xins 1 and 2, and two neuropeptide agonists, orexins A and B, has captured the attention of the scien
45 el, MD led to increased hypothalamic CRH and orexin A, and frontal cortical orexin 1 receptors (OX1R)
50 ons, which are inhibited by low glucose, but orexin A caused smaller depolarization than on GSNs and
52 ior or superior colliculi, a large number of orexin-A-containing neuronal processes and terminal arbo
53 pressing excitatory vs. inhibitory inputs to orexin-A-containing neurons in the lateral hypothalamus
62 ucleus possessed little or no immunoreactive orexin A fibres in its core, but had fibres at its perip
63 leaflet contained a plexus of immunoreactive orexin A fibres throughout its rostro-caudal extent.
66 S score (mean+/-SD) at 4 h was higher in the orexin-A group compared to controls (57.3+/-5.8 vs. 40.7
67 frequency was similar in both groups but the orexin-A group demonstrated higher IQ values compared to
68 values remained significantly higher in the orexin-A group for the first 120 min (p=0.008) and subse
69 it was activated with rank order of potency orexin A > orexin B > orexin A 16-33, that it bound anta
72 Concentrations of CSF hypocretin-1 (formerly orexin A) have been measured in many patients with sleep
75 of this study show that MTN neurons receive orexin A hypothalamic innervation with a somatotopic arr
77 dbrain-pontine junction part of the nucleus, orexin-A-immunopositive varicosities were relatively mor
80 In the caudal pontine MTN, only scattered orexin-A-immunoreactive fibers were found, while more ro
81 lamic orexinergic input, the distribution of orexin A immunoreactivity was examined in the rat mesenc
84 s were used to determine the distribution of orexin A in the structures of the hypothalamus and thala
85 evidence for the effectiveness of intranasal orexin-A in alleviating cognitive deficits produced by l
86 Here, we show that NAc microinjection of orexin-A in medial shell amplifies the hedonic impact of
88 des corticotropin-releasing factor (CRF) and orexin-A in the ventral tegmental area (VTA) play an imp
89 lacked any electrophysiological response to orexin-A in the wake-promoting neurons of the tuberomamm
91 resistance, and in voltage-clamp recordings orexin-A induced an inward current that reversed near th
92 orexin 1 receptor antagonist (SB334867A) on orexin A-induced feeding and locomotor activity was asse
94 A antagonists failed to significantly affect orexin A-induced feeding, but muscimol significantly and
98 ent study shows that in vitro application of orexin A induces potentiation of N-methyl-D-aspartate re
101 the treatment group received 0.1 mL of 1 nM orexin-A intraventricularly, while controls received sal
103 cent studies which suggest that hypocretin 1/orexin A may be involved in modulating arousal states an
105 ities within the AccSh, we hypothesized that orexin A may partly regulate feeding behavior and locomo
106 t the hypothesis that the AccSh is a site of orexin A modulation of feeding behavior and locomotor ac
107 here was a strong trend towards an increased orexin-A mRNA expression in the rostral ventrolateral me
109 propose that enhanced inhibitory control of orexin-A neurons, and their CB1-mediated disinhibition,
116 The method was demonstrated by determining orexin A, orexin B, and a novel isoform of rat beta-endo
117 but not the smaller ingestive peptides NPY, orexin A, orexin B, CART (55-102[Met(O)(67)]), MCH, or A
120 gical signals, with Neuropeptide Y (NPY) and Orexin A (OXA) offering diagnostic information on stress
127 tial effects on performance, nasal delivered orexin-A produced a more pronounced reversal of sleep de
128 lications, co-application of dynorphin-A and orexin-A produces a sustained response that reverses dep
131 in sleep-deprived animals was accompanied by orexin-A related alterations in local cerebral glucose m
132 s behavioral studies with antagonists at the orexin A-selective receptor, OX(1), have demonstrated it
133 armacological inhibitors, we showed that, in orexin-A-stimulated cells, the AA-derived radioactivity
134 B(1) receptor antagonists on the function of orexin A suggest an interplay between these two systems
136 lly significant interactions between CRF and orexin-A that depend on oligomerization of CRF1 receptor
137 ls to the excitatory effects of both CRF and orexin-A, thus providing a mechanism by which stress ind
141 ect of intravenous administration of Hcrt-1 (orexin-A) to anaesthetized rats on glutamate and GABA re
147 , response of the OX(1) and OX(2) sensors to orexin A was slow, consistent with a multistep binding a
154 but given rAAV-orexin, detectable levels of orexin-A were evident in the CSF, indicating release of
157 These were also internalized by the peptide orexin A, which has no direct affinity for the cannabino
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