ライフサイエンスコーパス: 5-HT(1B) receptor

1 mera (Chi22) that only weakly coupled to the 5-HT1B receptor.

2 agamma and Sf9 cell membranes containing the 5-HT1B receptor.

3 one of the serotonin-receptor subtypes, the 5-HT1B receptor.

4 whereas they are relatively unbiased at the 5-HT1B receptor.

5 ludes several ion channels and the serotonin 5-HT1B receptor.

6 region does not show any coupling ability to 5-HT1B receptors.

7 velopment and by signaling and expression of 5-HT1B receptors.

8 serotonin transporter, as well as 5-HT1A and 5-HT1B receptors.

9 because several neuron types in VTA express 5-HT1B receptors.

10 ween Galphai1 and the 5-hydroxytryptamine1B (5-HT1B) receptor.

11 asic, functionally active antagonists of the 5-HT(1B) receptor.

12 excitation probably through 5-HT1A (and not 5-HT1B) receptors.

13 nhanced by the neuromodulator 5-HT acting on 5-HT(1B) receptors.

14 dorsal striatum synapses induced by 5-HT via 5-HT(1B) receptors.

15 100,635, consistent with the involvement of 5-HT(1B) receptors.

16 ses GABAergic inhibition through presynaptic 5-HT1B receptors; (2) 5-HT decreases the firing of palli

17 resses GABAergic inhibition probably through 5-HT1B receptors; (2) in the external pallidal segment,

18 2+) entry, and we have now demonstrated that 5-HT(1B) receptors (5-HT(1B)Rs) liberate Gbetagamma to i

19 agonist, partial agonist, and antagonist) on 5-HT1B receptor (5-HT1BR) occupancy and the associated h

20 pendent recovery of neurotransmission during 5-HT(1B) receptor activation.

21 ogical enhancement of 5-HT release or direct 5-HT1b receptor activation may be therapeutically effica

22 ts suggest that nigral 5-HT, via presynaptic 5-HT1B receptor activation, gates the excitatory STN-->S

23 pendent of DA receptors and instead required 5-HT1B receptor activation.

24 fects of serotonin1B [5-hydroxytryptamine1B (5-HT1B)] receptor activation on cocaine reinforcement we

25 ryptamine), and L-694,247, and the selective 5-HT(1B) receptor agonist CP 93,129 produced concentrati

26 Results showed that neonatal treatment with 5-HT(1B) receptor agonist robustly impaired sexual behav

27 Systemic administration of the 5-HT(1B) receptor agonist TFMPP attenuated the inhibitor

28 Thus, stimulus trains in 5-HT(1B) receptor agonist unveil dynamic synaptic modula

29 Thus, stimulus trains in 5-HT(1B) receptor agonist unveil dynamic synaptic modula

30 n of 5-nonyloxytriptamine (NNT), a selective 5-HT(1B) receptor agonist, affects TCA organization in r

31 N-(3-Trifluoromethylphenyl)piperazine, a 5-HT(1B) receptor agonist, potently inhibited 5-HT(1A) r

32 Pentadecanoylcarnitine also had 5-HT1A and 5-HT1B receptor agonist and histamine H1 and H2 receptor

33 s inhibitory 5-HT effect was mimicked by the 5-HT1B receptor agonist CP93129 and blocked by the 5-HT1

34 the administration to wild-type mice of the 5-HT1B receptor agonist RU24969 results in a striatal in

35 models examined, whereas administration of a 5-HT1b receptor agonist selectively rescued the sociabil

36 valuated the ability of MDMA and a selective 5-HT1b receptor agonist to rescue sociability deficits i

37 e mice, CP-93,129 (1.4 mumol/kg), a specific 5-HT1B receptor agonist, had no effect in knockout mice.

38 usion of CP 93129 (20, 40, and 80 microM), a 5-HT1B receptor agonist, increased extracellular DA conc

39 uoromethyl)phenyl]-piperazine HCl (TFMPP), a 5-HT1B receptor agonist, reduced in a dose-related manne

40 rgic inputs or direct infusion of a specific 5-HT1b receptor agonist, reverses social deficits in a g

41 that intra-tegmental infusion of CP 94253, a 5-HT1B receptor agonist, significantly prolonged the eff

42 The 5-HT1B receptor agonists 5-methoxy-3-1,2,3,6-tetrahydro-

43 phenotype and have reduced responsiveness to 5-HT1B receptor agonists and reduced behavioral reaction

44 Finally, the 5-HT1B receptor agonists that blocked synaptic transmiss

45 conducted to determine whether activation of 5-HT(1B) receptors also alters photic regulation of noct

46 Overexpression of 5-HT1B receptors also shifted the dose-response curve fo

47 The rat 5-HT1B receptor (also referred to as the 5-HT1D beta rec

48 lex, such as 5-hydroxytryptamine (serotonin) 5-HT(1b) receptors and adrenergic alpha(2a) receptors.

49 drug-associated context and drug seeking via 5-HT(1B) receptors and prevent consolidation of the upda

50 two markers of serotonin neurotransmission, 5-HT(1B) receptors and serotonin reuptake sites, which a

51 H]paroxetine, selective radioligands for the 5-HT(1B) receptors and the serotonin reuptake sites, res

52 of Galphai1 increase agonist binding to the 5-HT1B receptor and receptor stimulation of GTPgammaS bi

53 Furthermore, although both 5-HT1B receptor and serotonin transporters are found in

54 n pulmonary hypertension and explain how the 5-HT1B receptor and SERT are codependent in regulating S

55 Gi1 can interact with the 5-HT1B receptor and stabilize a high affinity agonist bi

56 tatin anorectic response may be modulated by 5-HT1B receptors and that a neuronal pathway from the am

57 ffinity (Ki = 17 nM) at its species homolog, 5-HT1B receptors, and at a mutant 5-HT1D beta receptor (

58 by intra-tegmental infusion of SB 216641 (a 5-HT(1B) receptor antagonist), but not BRL 15572 (a 5-HT

59 is effect was blocked by pretreatment with a 5-HT(1B) receptor antagonist, indicating that the behavi

60 Finally, the 5-HT1B receptor antagonist NAS-181 increased the STN-tri

61 Co-infusion of the 5-HT1B receptor antagonist SB 216641 (10 microM), but no

62 in the discovery of novel, de novo designed, 5-HT(1B) receptor antagonists that lack a basic moiety a

63 microscopic immunocytochemical analysis with 5-HT1B receptor antibodies and whole-cell patch-clamp re

64 Although 5-HT(1B) receptors are believed to be expressed on nerve

65 In these neurons, 5-HT1B receptors are expressed presynaptically, and thei

66 5-HT1B receptors are inhibitory GPCRs located on the pre

67 e of abnormal stimulation of 5-HT(1A) and/or 5-HT(1B) receptors as a result of increased synaptic ava

68 tions suggest that vortioxetine binds to the 5-HT(1B) receptor at clinically relevant doses.

69 p11 increases localization of 5-HT1B receptors at the cell surface.

70 suggest that blockade and activation of VTA 5-HT1B receptors attenuates and potentiates the neuroche

71 , may cause or contribute to the increase in 5-HT(1B) receptor binding in the SCN in middle aged anim

72 5-HT(1B) receptor binding sites ([125I]cyanopindolol) we

73 The 5-HT(1B) receptor binding was significantly decreased af

74 pharmacological interventions to interrogate 5-HT1B receptor binding and function and determined bloo

75 s in serotonergic neurotransmission increase 5-HT(1B) receptors but decrease serotonin reuptake sites

76 dicate that the agonist action of NNT at the 5-HT(1B) receptor causes TCA disorganization in rat barr

77 or) inhibits Ca(2+) entry whereas another (a 5-HT(1B) receptor) competes with Ca(2+)-synaptotagmin bi

78 or) inhibits Ca(2+) entry whereas another (a 5-HT(1B) receptor) competes with Ca(2+)-synaptotagmin bi

79 usion and examined for 5-HT afferents to and 5-HT1B receptor-containing neuronal puncta and somata in

80 s in vivo and demonstrate that activation of 5-HT1B receptors contributes to the cellular responses e

81 ng sequence in Galphat either permitted full 5-HT1B receptor coupling to the chimera (Chi24) or only

82 ions within Chi22 (K300Q and L304E) restored 5-HT1B receptor coupling, and again the effects of the t

83 tagonistic drug characteristics and on local 5-HT1B receptor density.

84 In the ventral midbrain, 5-HT(1B) receptor-dependent inhibition of gamma-aminobut

85 th the structure of the 5-HT2B receptor, the 5-HT1B receptor displays a 3 angstrom outward shift at t

86 nity shift of 5-HT1A receptors compared with 5-HT1B receptors (EC50 values of 6.4 and 12.0 nM, respec

87 Simultaneous activation of 5-HT1A and 5-HT1B receptors effectively blocks L-DOPA-induced dyski

88 amic NPY, alpha-MSH, and serotonin receptor (5-HT(1B)-receptor) enhancing FI.

89 The 5-HT1A and 5-HT1B receptors exhibited both high- and low-affinity s

90 escending 5-HT neurons and to be mediated by 5-HT1B receptors expressed by AADC cells.

91 In conclusion, these studies indicate that 5-HT(1B) receptor function can be assessed using agonist

92 n (5-HT) turnover and deficient 5-HT(1A) and 5-HT(1B) receptor function in brain regions regulating e

93 These results indicate that 5-HT(1B) receptors function as autoreceptors and heteror

94 Overexpression of p11 increases 5-HT1B receptor function in cells and recapitulates cert

95 rinergic receptor-mediated inhibition of CHO/5-HT1B receptor function was blocked when 5-HT2A recepto

96 ion of 5-HT2A receptors had no effect on CHO/5-HT1B receptor function, although 5-HT2A receptor-media

97 aving synaptic properties unchanged, whereas 5-HT(1B) receptors fundamentally change properties of sy

98 Null mutant mice lacking the 5-HT1B receptor gene (5-HT1B-/-) have been developed tha

99 arch has focused on the 5-HT1A receptor, the 5-HT1B receptor has a lesser known role in modulating em

100 ing emotional behaviour and the 5-HT(1A) and 5-HT(1B) receptors have been shown to have distinct role

101 5-HT(1B)-receptor immunoreactivity decreased 13% only in

102 5-HT1B receptor immunostaining was observed associated w

103 m on the binding of [(11)C]AZ10419369 to the 5-HT(1B) receptor in the nonhuman primate brain.

104 es are warranted to evaluate the role of the 5-HT(1B) receptor in the therapeutic effects of vortioxe

105 We also inhibited 5-HT(1A) or 5-HT(1B) receptors in CA1 during conditioned place prefe

106 investigate the localisation of 5-HT(1A) and 5-HT(1B) receptors in CeA projection neurones identified

107 Due to postsynaptic 5-HT(1B) receptors in DRN terminal fields, it has not pr

108 y underscores the role played by presynaptic 5-HT(1B) receptors in mediating the effects of cocaine o

109 sent investigation to assess the function of 5-HT(1B) receptors in the modulation of synaptic transmi

110 an induce pulmonary vasoconstriction via the 5-HT1B receptor in man.

111 Here we show that serotonin 5-HT1B receptors in cholecystokinin (CCK) inhibitory int

112 as designed to assess the involvement of VTA 5-HT1B receptors in mediating the stimulatory effects of

113 Thus, increased expression of 5-HT1B receptors in NAcc efferents, probably in the term

114 viral-mediated gene transfer to overexpress 5-HT1B receptors in NAcc projections to VTA.

115 GFP injection induced elevated expression of 5-HT1B receptors in neuronal fibers in VTA and increased

116 by examining the subcellular localization of 5-HT1B receptors in the mouse SCN using electron microsc

117 For example, serotonin actions at 5-HT1B receptors in the ventral tegmental area (VTA) mod

118 als in SNr, indicating a primary role of the 5-HT1B receptors in these axon terminals.

119 that cocaine acts as an indirect agonist of 5-HT1B receptors in vivo and demonstrate that activation

120 receptor antagonist, GR127935, to antagonize 5-HT1B receptors in vivo.

121 The results suggest that activation of VTA 5-HT1B receptors increases mesolimbic DA neuron activiti

122 gic inputs that are inhibited by presynaptic 5-HT1B receptors; inhibition of excitatory synapses onto

123 s, whereas serotonin (5-HT) acting through a 5-HT1B receptor inhibits aggressive responding.

124 serotonin 1B receptor [5-hydroxytryptamine (5-HT1B) receptor] interacts with p11.

125 results thus demonstrate that stimulation of 5-HT1B receptors is required for fenfluramine-induced an

126 To test the hypothesis that stimulation of 5-HT1B receptors is required for the anorectic effect of

127 ts are in opposition to recent findings with 5-HT1B receptor knock-out mice and may have important on

128 in inhibiting light-induced phase shifts in 5-HT1B receptor knock-out mice.

129 induced phase shifts was also examined using 5-HT1B receptor knock-out mice.

130 Consequently, in projection-specific 5-HT(1B) receptor knockout mice, the fraction of individ

131 The 5-HT(1B) receptor knockout mouse was used in the present

132 nes retrogradely-labelled with CTb expressed 5-HT(1B) receptor-like immunoreactivity, whereas fewer (

133 alterations in 5-HT afferent innervation and 5-HT1B receptor localization were observed throughout th

134 clock through the activation of presynaptic 5-HT(1B) receptors located on retinal terminals in the s

135 s as a result of activation of 5-HT1A and/or 5-HT1B receptors located on presynaptic terminals.

136 he circadian system by acting at presynaptic 5-HT1B receptors located on retinal axons in the SCN.

137 ctively, and support the suggestion that VTA 5-HT(1B) receptors may be involved in part in mediating

138 he lack of 5-HT2A mediated regulation of CHO/5-HT1B receptors may be due to activation of a third pat

139 reductions found in this study suggest that 5-HT1B receptors may contribute to the etiology or expre

140 5-HT1A agonist (8-OH-DPAT), indicating that 5-HT1B receptors mediate the inhibition of EPSCs.

141 The effects of 5-HT(1B) receptor-mediated inhibition are well fit by si

142 residues within this domain are critical for 5-HT1B receptor-mediated G protein activation.

143 n SNr GABA neurons, indicating a presynaptic 5-HT1B receptor-mediated inhibition of glutamate release

144 ay be associated, at least in part, with the 5-HT1B receptor-mediated inhibition of VTA GABA release.

145 5-HT1B receptor-mediated presynaptic inhibition has been

146 ells, 5-hydroxytryptamine (5-HT)1B-like (CHO/5-HT1B) receptor-mediated inhibition of forskolin-stimul

147 ences aggressive behavior, a distinct set of 5-HT1B receptors modulates impulsive behavior during adu

148 as, with bLRs having greater 5-HT1A, but not 5-HT1B, receptor mRNA levels in the septum, hippocampus

149 We show that serotonin activates 5-HT(1B) receptors on anterior cingulate cortex inputs -

150 nterpretation that activation of presynaptic 5-HT(1B) receptors on retinal terminals in the SCN atten

151 suggests that differential expression of the 5-HT1B receptor on RGC presynaptic terminals, but not di

152 One possibility is that 5-HT1B receptors on the terminals of GABAergic projectio

153 Our results suggest that the 5-HT1B receptor participates in the regulation of ethano

154 diates 5-HT2C receptor regulation of the CHO/5-HT1B receptor pathway.

155 hiothepin >>> yohimbine, consistent with rat 5-HT(1B) receptor pharmacology.

156 ronal circuits and particularly 5-HT(1A) and 5-HT(1B) receptors play a prominent role in the regulati

157 idence suggests that 5-hydroxytriptamine-1B (5-HT1B) receptors play a role in modifying ethanol's rei

158 a transient pharmacological blockade of mNAc 5-HT(1B) receptors potentiated subsequent cocaine CPP.

159 The 5-HT(1B) receptor, present on TCAs during the first post

160 s that GABA(B) receptors alter P(r), whereas 5-HT(1B) receptors reduce evoked cleft glutamate concent

161 ion and find that serotonin (5-HT) activates 5-HT(1b) receptors resulting in a long-term depression (

162 its to membranes expressing either 5-HT1A or 5-HT1B receptors shifted the majority of the receptors t

163 h serotonin receptor 1B (5-HTR1B), modulates 5-HT1B receptor signal transduction, and is required for

164 the effect of this altered Ca(2+) signal on 5-HT(1B) receptor signaling.

165 stochemical study, using NPY, alpha-MSH, and 5-HT(1B)-receptor-specific antibodies and slides assesse

166 the behavioral consequences of mCPP-induced 5-HT(1B) receptor stimulation are unmasked in animals de

167 Together, these findings indicate that 5-HT1B receptor stimulation facilitates the reinforcing

168 odulating signaling through 5-HT4 as well as 5-HT1B receptors supports the concept that this protein

169 A(B) receptors inhibit Ca(2+) entry, whereas 5-HT(1B) receptors target SNARE complexes.

170 ity requires activation of nucleus accumbens 5-HT1B receptors, the blockade of which prevents social

171 ncrease serotonergic receptor functions (eg, 5-HT(1B) receptors), these data support the need for fur

172 ivates anterior cingulate cortex presynaptic 5-HT(1B) receptors to suppress cortical signaling throug

173 act in concert to mediate the ability of the 5-HT1B receptor to couple specifically to inhibitory G p

174 of the ability of the 5-hydroxytryptamine1B (5-HT1B) receptor to discriminate between G protein heter

175 bilities of the Galphat/Galphai1 chimeras to 5-HT1B receptors using high affinity agonist binding and

176 Functional coupling to 5-HT1B receptors was assessed by 1) [35S]GTPgammaS bindi

177 e contribution of the 5-hydroxytryptamine1B (5-HT1B) receptor, we studied the induction of the immedi

178 retrogradely-labelled neurones positive for 5-HT(1B) receptor were present in both lateral and media

179 tly into DRN using stereotaxic procedure, HA-5-HT(1B) receptors were expressed in serotonergic neuron

180 en by hunger via actions at ARH 5-HT(2C) and 5-HT(1B) receptors, whereas activation of 5-HT(DRN) to v

181 rcing effects and voluntary intake, and that 5-HT1B receptors within the ventral tegmental area (VTA)

182 dy was designed to assess the involvement of 5-HT1B receptors within the ventral tegmental area (VTA)