ライフサイエンスコーパス: NK(3) receptor

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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 86, and SR 142801 demonstrated that only the NK3 receptor antagonist SR 142801 inhibited the SP-induc

17 rats, intraperitoneal administration of the NK3-receptor antagonist SR 142,801 reduced, whereas the

18 Treatment with the neurokinin (NK)(1) and NK(3) receptor antagonists attenuated the responses, whe

19 tor antagonist SR48968 (3 mg kg(-1)), by the NK(3) receptor antagonists SR142801 (3 mg kg(-1)) and SB

20 e have screened compound databases for novel NK(3) receptor antagonists using a virtual screening pro

21 coapplication of L-732,138 and SB222200 (an NK3 receptor antagonists), showing that both NK1 and NK3

22 ects were sensitive to NK1-, but not NK2- or NK3-receptor antagonists.

23 However, activation of both nigral NK1 and NK3 receptors appears to be required for increased locom

24 y domains that are present in the NK1 and/or NK3 receptors are compromised in these chimeric receptor

25 These results suggest that peripheral NK3 receptors are involved in the mediation of both visc

26 eir ability to inhibit ligand binding to the NK(3) receptor as well as to inhibit senktide-induced ca

27 similar to DABK, was inhibited by NK(1) and NK(3) receptor blockade.

28 press sodium appetite; (c) the activation of NK3 receptors decreases the oral excitatory influence of

29 cted NK1-/- mice with antagonists to NK2 and NK3 receptors, either singly or in combination.

30 hanging exon sequences between human NK1 and NK3 receptor genes.

31 The role of neurokinin (NK) B and NK3 receptors in visceral pain and gastrointestinal diso

32 Our data indicate that activation of NK(3) receptors induces the expression of FLI within cir

33 established recently that the neurokinin-3 (NK3) receptor is the predominant neurokinin receptor fou

34 th potencies in the nM range and antagonized NK(3) receptor-mediated increases in intracellular calci

35 In contrast to the high abundance of NK3 receptor mRNA within dopamine (DA) cells of the rat

36 he rat midbrain, neurokinin-1 (NK1), but not NK3, receptor mRNA was localized to human midbrain DA ce

37 These results show that activation of NK3 receptors reduces the intake of NaCl and of a neutra

38 Also, central NK3 receptors seem to play a role in the modulation of v

39 nd selectivity over the tachykinin NK(2) and NK(3) receptor subtypes.

40 with their affinities for the parent NK1 and NK3 receptors, we are proposing that certain inhibitory

41 ptor antagonists), showing that both NK1 and NK3 receptors were involved.

42 These findings indicate that NK1, but not NK3, receptors within the SN may be tonically stimulated

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