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1 ide > NKA > SP, indicating involvement of an NK3 receptor.
2 ve agonists and antagonists of NK1, NK2, and NK3 receptors.
3 netrating antagonists of either NK1, NK2, or NK3 receptors.
4 cium responses in cells expressing the human NK(3) receptor.
5    Preferential binding of NKB to endogenous NK(3) receptors affects a variety of biological and phys
6 entricular (icv) injections of the selective NK(3) receptor agonist (succinyl-[Asp(6), N-Me-Phe(8)] s
7 vel compounds were identified that inhibited NK(3) receptor agonist binding, with potencies in the nM
8 st, an NK2 receptor agonist (GR64349), or an NK3 receptor agonist (Pro7-NKB), would induce vomiting a
9 ance P (SENK; 25, 100, 200 ng), a tachykinin NK3 receptor agonist, and [Sar9, Met(O2)11]-substance P
10 f central injection of senktide, a selective NK3 receptor agonist, would alter serum LH in ovariectom
11 tration of alterations in LH secretion by an NK3 receptor agonist.
12 s required for injections of a neurokinin-3 (NK3) receptor agonist (senktide) to suppress intake or w
13 r antagonist SR 142,801 reduced, whereas the NK3-receptor agonist senktide increased, both the rectoc
14 ]neurokinin A or senktide, selective NK2 and NK3 receptor agonists, respectively (100 nM; n = 3 for e
15 receptor agonists, nor the selective NK2- or NK3-receptor agonists, caused a significant dose-depende
16                                              NK3 receptor antagonism has emerged as a novel therapeut
17 86, and SR 142801 demonstrated that only the NK3 receptor antagonist SR 142801 inhibited the SP-induc
18  rats, intraperitoneal administration of the NK3-receptor antagonist SR 142,801 reduced, whereas the
19    Treatment with the neurokinin (NK)(1) and NK(3) receptor antagonists attenuated the responses, whe
20 tor antagonist SR48968 (3 mg kg(-1)), by the NK(3) receptor antagonists SR142801 (3 mg kg(-1)) and SB
21 e have screened compound databases for novel NK(3) receptor antagonists using a virtual screening pro
22  coapplication of L-732,138 and SB222200 (an NK3 receptor antagonists), showing that both NK1 and NK3
23 ects were sensitive to NK1-, but not NK2- or NK3-receptor antagonists.
24   However, activation of both nigral NK1 and NK3 receptors appears to be required for increased locom
25 y domains that are present in the NK1 and/or NK3 receptors are compromised in these chimeric receptor
26        These results suggest that peripheral NK3 receptors are involved in the mediation of both visc
27 eir ability to inhibit ligand binding to the NK(3) receptor as well as to inhibit senktide-induced ca
28  similar to DABK, was inhibited by NK(1) and NK(3) receptor blockade.
29 press sodium appetite; (c) the activation of NK3 receptors decreases the oral excitatory influence of
30 cted NK1-/- mice with antagonists to NK2 and NK3 receptors, either singly or in combination.
31 hanging exon sequences between human NK1 and NK3 receptor genes.
32            The role of neurokinin (NK) B and NK3 receptors in visceral pain and gastrointestinal diso
33         Our data indicate that activation of NK(3) receptors induces the expression of FLI within cir
34  established recently that the neurokinin-3 (NK3) receptor is the predominant neurokinin receptor fou
35 th potencies in the nM range and antagonized NK(3) receptor-mediated increases in intracellular calci
36         In contrast to the high abundance of NK3 receptor mRNA within dopamine (DA) cells of the rat
37 he rat midbrain, neurokinin-1 (NK1), but not NK3, receptor mRNA was localized to human midbrain DA ce
38                                Activation of NK3 receptors (NK3Rs) facilitates the excitability of pr
39        These results show that activation of NK3 receptors reduces the intake of NaCl and of a neutra
40                                Also, central NK3 receptors seem to play a role in the modulation of v
41 nd selectivity over the tachykinin NK(2) and NK(3) receptor subtypes.
42 with their affinities for the parent NK1 and NK3 receptors, we are proposing that certain inhibitory
43 ptor antagonists), showing that both NK1 and NK3 receptors were involved.
44    These findings indicate that NK1, but not NK3, receptors within the SN may be tonically stimulated