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1 ealed that MCF-7 cells express high-affinity NPY receptor.
2 that is only visible after inhibition of Y1 NPY receptors.
3 at [D-Trp32]NPY(1-36) produced activation of NPY receptors.
4 sensitive binding sites, presumably Y2 or Y5 NPY receptors.
5 utamate release by activation of presynaptic NPY receptors.
6 s of the Gi-coupled micro opioid, GABA-B and NPY receptors.
7 discordance with the abundant expression of NPY receptors, a group of inhibitory Gi protein coupled
8 er, our data suggest that the Y1 and Y2 type NPY receptors act both presynaptically and postsynaptica
10 the first time to quantitatively detect the NPY-receptor activation directly without a secondary or
12 y, we could show that the impedimetric based NPY-receptor activation monitoring is not restricted to
13 ther, our novel impedance spectroscopy based NPY-receptor activation monitoring system offers the opp
15 trast to other identified ARC cells in which NPY receptor agonists were reported to generate excitato
17 the three previously described Y1, Y2 and Y3 NPY receptors and the Y4 pancreatic polypeptide- (PP-) p
18 n different cell lines that natively express NPY-receptors and proof the specificity of the observed
19 ng, immunoreactivity (IR) mapping of NPY and NPY receptors, and electrophysiological recordings from
21 arlier study showed that the neuropeptide Y (NPY) receptor antagonist PYX-2 blocks the enhancement of
23 injection of saline (200 nl) or the putative NPY receptor antagonists [D-Trp32]NPY(1-36) (3.3 microgr
27 ersal of injury-induced tactile allodynia by NPY receptor antagonists would have significant implicat
31 key role in stimulating feeding, thus making NPY receptors attractive appetite suppressant drug targe
32 n (NPY-SAP) bilaterally into the Arc to kill NPY receptor-bearing neurons or via neonatal monosodium
33 neous release of glutamate and activation of NPY receptors, because both the extended response to NPY
34 tients and aim to determine whether specific NPY receptor blockers can prevent arrhythmia and attenua
36 of dopamine release by sigma receptors or by NPY receptors, but this population is not identical to t
38 volved in neuronal remodeling and present in NPY receptor containing neurons within the BLA, blocked
39 icroM BIBP3226 demonstrated that the reduced NPY receptor density was due to reductions in Y2 or Y5 r
40 ivation, suggesting that sigma receptors and NPY receptors do not represent a common population in ra
41 that at least two functional populations of NPY receptors exist in the SCN, distinguishable on the b
45 netic elements involved in the regulation of NPY receptor expression, we have cloned and characterize
51 receptor NPFR1, a mammalian neuropeptide Y (NPY) receptor homolog, centrally regulates the response
52 challenge with small molecule antagonists of NPY receptors implicated in mediating the feeding effect
54 ve changes in the density of neuropeptide Y (NPY) receptors in the obese Zucker rat which has an incr
59 functional level of NPR-1, a neuropeptide Y (NPY) receptor-like protein, can account for natural vari
63 ine, muscarinic, metabotropic glutamate, and NPY receptors on excitatory synapses and GABA(B) and opi
67 matic analysis of expression patterns of all NPY receptors (Rs), Y1R, Y2R, Y4R, and Y5R in lingual ep
70 report the cloning by expression of a novel NPY receptor subtype from a rat hypothalamus cDNA librar
71 e studies complete the mapping of the cloned NPY receptor subtypes in human and mouse and, together w
72 was used to examine for regional changes in NPY receptor subtypes in obese versus lean Zucker rats.
73 , and examined the contributions of specific NPY receptor subtypes to these neural and behavioral eff
77 Taken together, these data establish spinal NPY receptor systems as an endogenous braking mechanism
81 creened for binding affinity at two discrete NPY receptor types using human neuroblastoma cell membra
82 ed or completely absent, suggesting that the NPY receptor was activated in the absence of elevated in
86 ial neurons that express the neuropeptide Y (NPY) receptor Y1 (Y1R neurons) is increased following in
88 ully blocked by antagonists for any specific NPY receptors (Y1, Y2, or Y5), while proliferation was b
89 s completely prevented by antagonists of the NPY receptors (Y1R+Y2R+Y5R), indicating that it was medi
90 acterized the human gene encoding the type 2 NPY receptor (Y2 receptor, HGMW-approved symbol NPY2R).2