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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.
7                                              Orexin A (0, 100, 500, and 1000 pmol, in 0.5 microl arti
8  single intracerebroventricular injection of orexin A (1 and 3 nmol) or orexin B (3 nmol), during the
9                                              Orexin A (1 micromol/l) caused a 500% increase (P < 0.01
10                           Fourth ventricular orexin-A (1 nmol) activated Fos expression in the raphe
11                             Nanoinjection of orexin-A (12 pmol) into the rostral raphe pallidus (rRPa
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
14                    Central administration of orexin-A acutely suppressed cataplectic behavioral arres
15 ntly dropped during the first hour following orexin A administration, coinciding with orexin A-induce
16 ve behavior and autonomic functions of local orexin-A administration in nonanesthetized rats.
17                                              Orexin-A administration to the fourth ventricle induced
18                                              Orexin A altered the intrinsic neuronal properties of GS
19 mic (LH) orexin neurons, increases levels of orexin A and 2-arachidonoylglycerol (2-AG) in the ventra
20                 The neuromodulatory peptides orexin A and B are important central nervous system regu
21                            The neuropeptides orexin A and B are synthesised by perifornical and later
22                                              Orexin A and B fibers were visible across the brain, wit
23                                              Orexin A and B neurons were located in a single populati
24 dentify the specific sites of orexin action, orexin A and B were microinjected into a number of hypot
25      Orexins (hypocretins) are two peptides (orexin A and B) produced from the pre-pro-orexin precurs
26                                              Orexin A and B, a recently identified pair of neuropepti
27            It is concluded that the peptides orexin A and B, acting on orexin receptors, which are GT
28 e-controlling neuropeptides such as ghrelin, orexin A and neuropeptide Y is also discussed.
29                                              Orexin A and Orexin B (also known as hypocretins) are ne
30                                              Orexin A and orexin B stimulate feeding when administere
31                                              Orexin A and orexin B were microinjected into the perifo
32 de that GSNs are specific target neurons for orexin A and suggest that they may mediate, at least in
33                                              Orexin-A and -B are brain-gut peptides that stimulate fo
34                  It has long been known that orexin-A and -B excite basal forebrain cholinergic neuro
35                       These peptides, termed orexin-A and -B, have no significant structural similari
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
39                                              Orexin-A and orexin-B are neuropeptides originally ident
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
43             Hypocretins 1 and 2 (also called orexins A and B, respectively) are hypothalamic neuropep
44      The hypothalamic peptides hypocretin-1 (orexin A) and hypocretin-2 (Hcrt-2; orexin B) are import
45 el, MD led to increased hypothalamic CRH and orexin A, and frontal cortical orexin 1 receptors (OX1R)
46 letely blocked by prior administration of an orexin A antagonist.
47        prepro-orexin mRNA and immunoreactive orexin-A are localized in neurons within and around the
48                                              Orexin A augmented feeding in the 0-1 h and 1-2 h post-i
49  greatly reduced the binding and function of orexin A but not antagonist ligands.
50 ons, which are inhibited by low glucose, but orexin A caused smaller depolarization than on GSNs and
51 using both calcium mobilization and [(125)I]-orexin-A competition binding.
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
54 active neurons were not colocalized with the orexin-A-containing neurons.
55 mplex promotes a long-term disruption of the orexin-A-CRF negative crosstalk.
56                          Results showed that orexin-A delivered via the intravenous and nasal routes
57             We find that, as with yohimbine, orexin A depression of excitatory transmission in BNST i
58         While the effects of dynorphin-A and orexin-A desensitize over multiple applications, co-appl
59     The responses both to dynorphin-A and to orexin-A desensitize, but co-application of dynorphin-A
60                                              Orexin-A elicits arousal EEG during anesthetic burst-sup
61  of the hypothalamus as an area important to orexin A feeding regulation.
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.
64                      Immunoreactive varicose orexin A fibres were found throughout the hypothalamus.
65 and all were found to contain immunoreactive orexin A fibres.
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 &gt; orexin B > orexin A 16-33, that it bound anta
70                                              Orexin A (&gt;/=500 pmol) stimulated feeding in the PFH and
71                                              Orexin-A had no effect on the resting discharge of affer
72 Concentrations of CSF hypocretin-1 (formerly orexin A) have been measured in many patients with sleep
73  alcohol via stimulation of the hypocretin-1/orexin-A (Hcrt-1/Ox-A) system.
74                                              Orexin A/hypocretin-1 (oxA/hcrt-1) is known to be a modu
75  of this study show that MTN neurons receive orexin A hypothalamic innervation with a somatotopic arr
76 esencephalic trigeminal nucleus (MTN), using orexin A immunohistochemistry.
77 dbrain-pontine junction part of the nucleus, orexin-A-immunopositive varicosities were relatively mor
78                              The presence of orexin A-immunoreactive fibres in the neural architectur
79 tween TRH-immunoreactive nerve terminals and orexin-A-immunoreactive cell bodies.
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
82                                              Orexin-A-immunostained nerve fibers and terminals were f
83 cadian system suggests an important role for orexin A in circadian timekeeping processes.
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
87                                  The role of orexin-A in recovery of arousal after CA deserves furthe
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
90                                 Injection of orexin-A increased vital signs to baseline levels.
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
93                                              Orexin A-induced feeding was significantly attenuated by
94 A antagonists failed to significantly affect orexin A-induced feeding, but muscimol significantly and
95 significantly and dose dependently inhibited orexin A-induced feeding.
96 ing orexin A administration, coinciding with orexin A-induced feeding.
97                                              Orexin A-induced locomotor activity was not affected by
98 ent study shows that in vitro application of orexin A induces potentiation of N-methyl-D-aspartate re
99  neurons express OX-R1 and OX-R2 and whether orexin-A inhibits responses to CCK.
100       We examined whether microinjections of orexin-A into the VP hotspot enhance the hedonic impact
101  the treatment group received 0.1 mL of 1 nM orexin-A intraventricularly, while controls received sal
102                                              Orexin A is a neuropeptide located exclusively in neuron
103 cent studies which suggest that hypocretin 1/orexin A may be involved in modulating arousal states an
104           Together, these data indicate that orexin A may influence food intake by decreasing GABAerg
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
108         To test this hypothesis, we measured orexin-A mRNA expression in the rostral ventrolateral me
109  propose that enhanced inhibitory control of orexin-A neurons, and their CB1-mediated disinhibition,
110                                  Hypocretin (orexin), a neuropeptide synthesized exclusively in the p
111                                              Orexin A or B (10-1000 nM) directly and reversibly depol
112                               Superfusion of orexin A or B (10-300 nM) caused a slow depolarization i
113 he diaphragm, were immunopositive for either orexin-A or MCH.
114                          Bath application of orexin-A or orexin-B (30-300 nM) produced a slow depolar
115 the patch solution significantly reduced the orexin A- or B-induced depolarizations.
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
118 behavior had lower hippocampal expression of Orexin A (OrxA).
119                         POMC neurons receive orexin-A (OX-A)-expressing inputs and express both OX-A
120 gical signals, with Neuropeptide Y (NPY) and Orexin A (OXA) offering diagnostic information on stress
121  many NPY cells in the grass rat IGL exhibit orexin-A (OXA) fiber appositions.
122                                              Orexin-A (OXA) increases food intake in rodents, and fas
123              Moreover, administration of the orexin A peptide directly into the ventral tegmental are
124       In dopaminergic neurons of VTA slices, orexin A presynaptically inhibits GABAergic transmission
125 whereas at -70 mV the excitatory response to orexin-A prevails.
126 whereas at -70 mV the excitatory response to orexin-A prevails.
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
129 itize, but co-application of dynorphin-A and orexin-A produces a sustained response.
130              These findings demonstrate that orexin A receptive sites for stimulation of food intake
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
135 e highest dose (10 microg/kg) of intravenous orexin-A tested.
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
138                                  Addition of orexin A to individual cells expressing an OX(1) sensor
139                     Moreover, the ability of orexin A to internalize the CB(1) receptor was also bloc
140            The higher potency of the agonist orexin A to regulate the CB(1)-OX(1) heteromer compared
141 ect of intravenous administration of Hcrt-1 (orexin-A) to anaesthetized rats on glutamate and GABA re
142                In rats resuscitated from CA, orexin-A transiently increased arousal and EEG entropy w
143                             The synthesis of orexin A undergoes diurnal variation in certain areas of
144                               This effect of orexin A was concentration-dependent and blocked by OX(1
145                                              Orexin A was found to enhance food intake when injected
146                              The response to orexin A was significantly reduced in the presence of th
147 , response of the OX(1) and OX(2) sensors to orexin A was slow, consistent with a multistep binding a
148                                  Remarkably, orexin A was substantially more potent in producing inte
149 and1 microL of saline with or without 3 nmol orexin-A was infused.
150 he fraction of infected cells that contained orexin-A was lower.
151            The improvement in performance by orexin-A was specific to trials classified as high versu
152                                Hypocretin-1 (orexin-A) was administered to sleep-deprived (30-36 h) r
153                     Cells immunoreactive for orexin A were noted in the lateral hypothalamic area.
154  but given rAAV-orexin, detectable levels of orexin-A were evident in the CSF, indicating release of
155             Two methods of administration of orexin-A were tested, intravenous injections (2.5-10.0 m
156                                              Orexin A, which depolarizes thalamocortical neurons loca
157  These were also internalized by the peptide orexin A, which has no direct affinity for the cannabino
158                         We hypothesized that orexin-A would improve arousal and EEG entropy after CA.

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