ライフサイエンスコーパス: NK(1) receptor

1 ut, paradoxically, not in mice that lack the NK1 receptor.

2 eptors with the most potent affinity for the NK1 receptor.

3 ysiological roles previously assigned to the NK1 receptor.

4 iated by activation of the G-protein coupled NK1 receptor.

5 o desensitization and resensitization of the NK1 receptor.

6 of action of novel antidepressants acting at NK1 receptors.

7 es also occasionally were immunoreactive for NK1 receptors.

8 Ps, but not of IPSPs, involves activation of NK1 receptors.

9 r reflex bradycardia which is independent of NK1 receptors.

10 were not mediated entirely by its action at NK1 receptors.

11 RP67580 were due to an action of the drug at NK1 receptors.

12 and a facilitatory role for gastrointestinal NK1 receptors.

13 chloride conductance in MSNs, acting through NK1 receptors.

14 eptors and excellent antagonist activity for NK1 receptors.

15 activities at delta/mu opioid receptors and NK1 receptors.

16 s are inhibited, but not stimulated, through NK1 receptors.

17 (PKC) mediates stimulation of CaV2.3 through NK1 receptors.

18 P (SSP-SAP) selectively killed neurons with NK1 receptors.

19 e spinal cord that express the neurokinin-1 (NK1) receptor.

20 oma cell line UC11 that expresses endogenous NK(1) receptor.

21 showed high potency and selectivity for the NK(1) receptor.

22 ugate to target NTS neurons with neurokinin (NK1) receptors.

23 ly active antagonists at rat, but not human, NK(1) receptors.

24 odies directed against NMDA, non-NMDA or SP (NK1) receptors; 2) that glutamate injected into the tail

25 NK1 receptor but negligible affinity for rat NK1 receptors, 3a, was discovered by directed screening.

26 and activity because blockade of tachykinin NK1 receptors (66.3+/-13.7% inhibition, n=6; P<0.001), a

27 n and inflammation through the neurokinin-1 (NK1) receptor, a G protein-coupled receptor.

28 We also report that NK1 receptors accelerate the inactivation kinetics of Ca

29 The results suggest that NK1 receptor activation in the DR excites a population o

30 nce P, indicating that they were mediated by NK1 receptor activation.

31 ), which has previously been proposed as the NK1 receptor active form.

32 Comparisons of the NK(1) receptor affinity for the various conformational f

33 SP responses were mimicked by the NK1 receptor agonist [Sar9,Met(O(2))11]-substance P (SSP

34 ed that emesis produced by SP or a selective NK1 receptor agonist is sensitive to brain penetrating a

35 GR73632) or non-penetrating (e.g. SarMet-SP) NK1 receptor agonist, an NK2 receptor agonist (GR64349),

36 2)11]-substance P (Sar Met; 100, 200 ng), an NK1 receptor agonist, on normal (gastric fistula closed)

37 Neither the selective, non-penetrating NK1 receptor agonists, nor the selective NK2- or NK3-rec

38 wever, only a few (16/144; 11%) neurons with NK1 receptor also contained enkephalin immunoreactivity

39 ch between sites of SP release and available NK1 receptors, although receptive neurons may contain re

40 ive rage neurons are excited in two ways: by NK(1) receptors and by an ascending input from the PAG.

41 sis infusions of substance P desensitize the NK(1) receptors and that substance P-induced vasodilatat

42 antisera against the NK1 receptor or of the NK1 receptor and either 1) SP or 2) the vesicular acetyl

43 oximately 80% of projection neurons with the NK1 receptor and in 25-45% of those without it.

44 ges in the CNS, such as up-regulation of the NK1 receptor and substance P, lead to antiopioid effects

45 , differences in desensitization between the NK1 receptor and the NK2 receptor may be related to diff

46 mediated by the G-protein-coupled neurokinin NK1 receptor and the tyrosine kinase-linked platelet-der

47 eptive neurons: Acting predominantly through NK1 receptors and G(i/o) proteins, SP stimulates increas

48 t higher concentrations; the latter involves NK1 receptors and presumably results from release of sub

49 sence of peripheral axons immunolabelled for NK1 receptors and the demonstration that exogenous perip

50 he major endogenous ligand for neurokinin 1 (NK1) receptors and, together with acetylcholine, has an

51 ugh two distinct pathways: via activation of NK(1) receptors, and via a novel neurokinin receptor-ind

52 Two asymmetric syntheses of the NK(1) receptor antagonist 1-[2-(R)-{1-(R)-[3,5-bis(trifl

53 ereoselective synthesis of the orally active NK(1) receptor antagonist Aprepitant is described.

54 mpounds, and suggests that the high affinity NK(1) receptor antagonist L-760735 may prove to be usefu

55 oride 3 is a high affinity, orally active, h-NK(1) receptor antagonist with a long central duration o

56 resent study, the high affinity substance P (NK(1)) receptor antagonist L-760735 (3 mg/kg) significan

57 etrant, hydroisoindoline-based neurokinin-1 (NK(1)) receptor antagonist with a long central duration

58 tagonist, dexamethasone, and a neurokinin 1 (NK(1)) receptor antagonist.

59 ion by determining the effect of a selective NK1 receptor antagonist (RP67580) on the nociceptive fle

60 ceptor antagonist alone (27%) but not by the NK1 receptor antagonist alone.

61 The topical application of SP or its NK1 receptor antagonist has no significant effect on the

62 In another set of experiments, the specific NK1 receptor antagonist L-703,606 (5 microg) was microin

63 ation of NK1R-LI was blocked by the specific NK1 receptor antagonist WIN 62577 (1 microm) and by tetr

64 usly identified as a potent, brain-penetrant NK1 receptor antagonist with a long duration of action a

65 ld be offered a three-drug combination of an NK1 receptor antagonist, a 5-HT3 receptor antagonist, an

66 The tachykinin NK1 receptor antagonist, GR205171 (100 micrograms/kg i.v

67 The centrally penetrant NK1 receptor antagonist, GR205171 (100 micrograms/kg i.v

68 on was unaffected by the peripherally acting NK1 receptor antagonist, GR82334 (0.2 mg/kg i.v.) or CGR

69 ved an i.p. injection of either the specific NK1 receptor antagonist, L-760,735 (5 mg/kg), or saline

70 xhibited antinociception to a low dose of an NK1 receptor antagonist.

71 significantly attenuated by a neurokinin-1 (NK1) receptor antagonist (SR140333, 3 muM).

72 The neurokinin type 1 (NK1) receptor antagonist CP-99,994 (5 microM) blocked th

73 or non-peptidergic (L703, 606) neurokinin 1 (NK1) receptor antagonist in one masseter muscle 15 min p

74 d following the infusion of the substance P (NK1) receptor antagonist, CP96.345 (in doses of 0.05, 0.

75 The NK1-receptor antagonist MK-869 (L-754,030) has demonstra

76 l combination of netupitant (a neurokinin 1 [NK1] receptor antagonist) and palonosetron (a 5-hydroxyt

77 rinic M3 receptor antagonists and tachykinin NK1 receptor antagonists inhibit neurogenic secretion.

78 -substance P (SSP), and fully blocked by the NK1 receptor antagonists L-732,138, or extracellular zin

79 ecursor 1 (Tac1) gene or coadministration of NK1 receptor antagonists produces long-lasting hyperalge

80 In the presence of opioid, GABA(A), and NK1 receptor antagonists, antidromic stimulation of a po

81 n and the antiemetic potential of tachykinin NK1 receptor antagonists.

82 clinical studies suggest that neurokinin 1 (NK1) receptor antagonists have efficacy in the treatment

83 that were localized in the dorsal DR, where NK1 receptors are most dense.

84 These findings suggest that, in the NAc, NK1 receptors are recycled through endosomal compartment

85 1a (AT1a), vasopressin V2, and neurokinin 1 (NK1) receptors are seven-transmembrane receptors (7TMRs)

86 partially dependent on cells expressing the NK1 receptor as ablating these cells at the time of inju

87 an African trypanosomiasis by modulating the NK1 receptor as well as the parasite.

88 f spinally-projecting neurons and identifies NK1 receptors as potential targets for therapeutic modul

89 Ablation of peripheral NK1 receptors attenuated the ability of GR73632 to induc

90 hesus showed that this compound provides 90% NK(1) receptor blockade in rhesus brain at a plasma leve

91 sponse was abolished by a neurokinin type 1 (NK1) receptor blocker (CP-99,994, 5 microM) but this had

92 h had sub-micromolar affinity for the rabbit NK1 receptor but negligible affinity for rat NK1 recepto

93 acellular solution, the Ca2+ response of the NK1 receptor, but not the NK2 receptor, rapidly desensit

94 4) whether selective ablation of peripheral NK1 receptors can affect emesis produced by GR73632.

95 hese results indicate that SP acting through NK1 receptors can have direct neuromodulatory effects on

96 These results indicate that SP, via an NK1 receptor, can induce a Ca(2+)-dependent outward pota

97 n unopposed by NA, substance P acting at the NK1 receptor causes chronic thermal hyperalgesia, and th

98 Because the promoter region of the NK1 receptor contains a cAMP response element (CRE), we

99 These data suggest NK(1) receptors contribute to active vasodilatation and

100 Although neurokinin 1 (NK1) receptors contribute to hyperalgesia, and their exp

101 antagonists to the substance P receptor (the NK1 receptor) could achieve the same effect as NA replac

102 The NK1 receptor couples to both G(s) and G(q/11), resides o

103 e to active vasodilatation and that combined NK(1) receptor desensitization and NO synthase inhibitio

104 dditionally, these data provide evidence for NK1 receptor desensitization as there was no observable

105 This suggests that the NK1 receptor desensitizes by phosphorylation and resensi

106 sis via the activation of central tachykinin NK1 receptors during the delayed phase of vomiting produ

107 vity in the amygdaloid complex, induction of NK(1) receptor endocytosis in the amygdala following imm

108 the number of dendritic processes undergoing NK(1) receptor endocytosis in the basolateral amygdala t

109 ntify the effect of immobilisation stress on NK(1) receptor endocytosis morphology, a marker of local

110 re, we examined modulation of CaV2.3 through NK1 receptors expressed in human embryonic kidney 293 ce

111 This attenuation is mediated via NK1 receptors expressed on GABAergic interneurones withi

112 Lamina I neurokinin 1 (NK1) receptor expressing (NK1R(+)) dorsal horn neurons,

113 Lamina I and III neurokinin 1 (NK1) receptor expressing (NK1R+) dorsal horn neurons, ma

114 Behavioral analysis of the NK1 receptor gene knock-out (NK1-/-) mouse indicated tha

115 activate in regulating the expression of the NK1 receptor gene.

116 We find that NK1 receptors generate complex modulation of CaV2.3.

117 This suggests that substance P and the NK1 receptor have roles in the maintenance of articular

118 neurokinin 1 (NK1) receptor with a chimeric NK1 receptor having beta-arrestin1 fused to the receptor

119 PAG neurons that had NK1 receptor immunolabeling were interdigitated with and

120 Most contacts on NK1 receptor-immunoreactive cells were associated with s

121 ences among different morphological types of NK1 receptor-immunoreactive neuron.

122 NK1 receptor-immunoreactive projection cells received a

123 in monkey relatively few pyramidal cells are NK1 receptor-immunoreactive.

124 The distribution of NK(1) receptor immunoreactivity in the amygdaloid comple

125 t mice, indicating an essential role for the NK(1) receptor in mediating NKB-induced skin oedema.

126 Overall, the findings indicate that NK(1) receptors in the medial hypothalamus facilitate de

127 The results indicate that NK(1) receptors in the PAG potentiate defensive rage and

128 -channel-like potassium currents through the NK1 receptor in a G protein-independent but tyrosine kin

129 d in chondrocyte mechanotransduction via the NK1 receptor in an autocrine and paracrine manner.

130 In contrast, neuronal profiles with NK1 receptor in both the PAG and the DRN often contained

131 fect of disrupting the gene encoding for the NK1 receptor in mice on the clinical and neuroinflammato

132 PPT mRNA, substance P, and the corresponding NK1 receptor in vivo and in vitro.

133 rst time, affirm a cardinal role for central NK1 receptors in SP-induced vomiting, and a facilitatory

134 ignaling molecule that induces expression of NK1 receptors in spinal neurons.

135 ured Abeta afferents is unlikely to activate NK1 receptors in the dorsal horn or contribute to neurop

136 3632 (2.5 mg/kg, i.p.)-induced activation of NK1 receptors increases Fos-measured neuronal activity i

137 P signaling by a chemical antagonist to the NK1 receptor inhibited chondrocyte responses to mechanic

138 ptide substance P (SP) acting via tachykinin NK1 receptor inhibition of GABA(A) currents.

139 nity cross-linking demonstrated a direct HGF/NK1-receptor interaction.

140 addition, we did not detect any Abeta-evoked NK1 receptor internalization in neurons from laminas I,

141 We also looked for evidence of neurokinin 1 (NK1) receptor internalization in the dorsal horn after e

142 We conclude that presence or absence of the NK1 receptor is a better indicator of function than morp

143 The present study demonstrates that the NK1 receptor is essential for the full development of no

144 In animal models, the NK1 receptor is required for opioids to produce their re

145 aracterized receptor for these peptides, the NK1 receptor, is present on platelets.

146 T 343), a highly potent ligand for the human NK1 receptor (Ki = 0.16 nM).

147 xtravasation produced by NKB in the lungs of NK(1) receptor knockout mice was unaffected by treatment

148 d (125)I-albumin in wild-type and tachykinin NK(1) receptor knockout mice.

149 In both the NAc shell and core, NK1 receptor labeling was localized mainly to somatic an

150 Inhibition of the NK1 receptor may therefore provide benefit in patients v

151 ation concerning R-type calcium channels and NK1 receptors may help in understanding nociception, syn

152 Altogether, our results indicate that NK1 receptors modulate CaV2.3 using three different sign

153 he circadian system may, by interacting with NK1 receptors, modulate photic responses of the SCN pace

154 Within the human midbrain, the abundance of NK1 receptor mRNA differed significantly among the disti

155 e in binding was preceded by an elevation in NK1 receptor mRNA.

156 In contrast, lamina I neurons lacking NK1 receptor (NK1R-) received polysynaptic A fiber input

157 eralgesia and increased expression of spinal NK1 receptors (NK1Rs).

158 At the NK1 receptor of substance P (SP), the free hydroxyl at C

159 w site of action for substance P in the NTS (NK1 receptors on the central terminals of sensory fibres

160 fection leads to a selective upregulation of NK1 receptors on the vasculature.

161 projection neurons express the neurokinin 1 (NK1) receptor, on which substance P acts, and most cells

162 localization either of antisera against the NK1 receptor or of the NK1 receptor and either 1) SP or

163 an either enhance (e.g. 5-HT3, CCK1, VR1 and NK1 receptors) or reduce (e.g. ghrelin, leptin, k-opioid

164 Inhibition or deficiency of the NK1 receptor, or SP agonist activity, resulted in substa

165 Blocking the NK1 receptor pharmacologically reproduced, in an enantio

166 amined in gerbils, a species with human-like NK(1) receptor pharmacology.

167 Our data suggest that the NK1 receptor-positive projection neurons in lamina I are

168 Almost all neurokinin 1 (NK1) receptor-positive neurons in lamina I (a major sour

169 esults show that two distinct regions of the NK1 receptor possess multiple determinants for SP bindin

170 icrom dose of substance P to desensitize the NK(1) receptors prior to whole-body heating.

171 ine and tachykinins acting on muscarinic and NK1 receptors, respectively.

172 chemical shift assignments for the mammalian NK1 receptor-selective agonists alpha-neurokinin (NKA) a

173 ta-neurokinin (NKB) as well as the mammalian NK1 receptor-selective antagonists [d-Pro2,d-Phe7,d-Trp9

174 2) evaluate the role of cells expressing the NK1 receptor, shown to be involved in central sensitizat

175 Thus, i.m. SP mediates an unconventional NK1 receptor signal pathway to inhibit acid activation i

176 ciated with a lack of NA is due to increased NK1-receptor stimulation.

177 vidence that MORs are on the same neurons as NK1 receptors, suggesting that MOR ligands directly modu

178 Some lamina I neurons expressing the NK1 receptor, the receptor for substance P, are also cob

179 gate the regulation of the DR-5-HT system by NK1 receptors, the effects of substance P (an NK1 agonis

180 r stores through its preferred neurokinin 1 (NK1) receptor, thus inducing NO production via activatio

181 e the potential involvement of neurokinin-1 (NK(1)) receptors to active vasodilatation.

182 d peptide (CGRP) regulates the expression of NK1 receptors via a pathway involving activation of the

183 ssues by Western blots, and the mRNA for the NK1 receptor was also found in cochlear tissues of postn

184 The NK1 receptor was detected on SGNs by immunocytochemistry

185 e agonist-dependent ERK1/2 activation by the NK1 receptor was independent of protein kinase A (PKA) o

186 principal receptor for SP, the neurokinin 1 (NK1) receptor, was examined with respect to other neurot

187 hat 48-65% of cell bodies and dendrites with NK1 receptor were dually immunolabeled for glutamate.

188 In the DRN, dendrites containing NK1 receptor were selectively distributed in the dorsome

189 horn where both the opioid receptors and the NK1 receptors were found to be expressed, to show an enh

190 ectivity and as antagonist for neurokinin-1 (NK1) receptors were designed and synthesized for potenti

191 The first sub-nanomolar ligand for the human NK1 receptor which arose from this series, 4af, combined

192 encodes another high affinity ligand of the NK1 receptor which may play an important role in mediati

193 stive of an internalization of neurokinin-1 (NK1) receptors, which are highly specific to substance P

194 and for in vivo quantification of tachykinin NK(1) receptors with PET.

195 ntration-dependently in CHO cells expressing NK1 receptors with a maximal 12-fold increase in inosito

196 Blockade of NK1 receptors with CP 96345 significantly attenuated RAR

197 /2 activation by the wild-type neurokinin 1 (NK1) receptor with a chimeric NK1 receptor having beta-a

198 tive dendrites (n = 534 dendrites) contained NK1 receptors without VAchT, 29% contained both products