ライフサイエンスコーパス: 5-HT2C receptor

1 the 1S,2R isomer had highest affinity at the 5-HT2C receptor.

2 ines for the 5-HT2A receptor but not for the 5-HT2C receptor.

3 EAS motoneurons were immunopositive for the 5-HT2C receptor.

4 oligands at cloned human 5-HT2A, 5-HT2B, and 5-HT2C receptors.

5 approximately equal efficacy to serotonin in 5-HT2C receptors.

6 n NIH 3T3 cells expressing the rat 5-HT2A or 5-HT2C receptors.

7 expressing cloned human 5-HT2A, 5-HT2B, and 5-HT2C receptors.

8 expressing cloned human 5-HT2A, 5-HT2B, and 5-HT2C receptors.

9 ce and a reliance on serotonergic 5-HT2A and 5-HT2C receptors.

10 gen binding protein was used to label native 5-HT2C receptors.

11 and 5-HT-stimulated endocytosis of wild-type 5-HT2C receptors.

12 ediate their input through the activation of 5-HT2C receptors.

13 han seen with serotonin 5-hydroxytryptamine (5-HT2C) receptor.

14 monstrate that mice with genetically ablated 5-HT2C receptors (2CKO mice) display deficits in executi

15 motoneurons that were immunoreactive for the 5-HT2C receptor (5-HT2C-IR) were targeted for specific e

16 nent serotonin receptors in the brain is the 5-HT2C receptor (5-HT2C-R).

17 The serotonin (5-hydroxytryptamine, 5-HT) 5-HT2C receptor (5-HT2CR) within the medial prefrontal c

18 te 4775-nt cDNA encoding the human serotonin 5-HT2c receptor (5-HT2cR), a G-protein-coupled receptor,

19 ng the dopamine D2 receptor (DA D2R) and the 5-HT2c receptor (5-HT2cR), and an immediate early gene a

20 DRN) projections to the BNST, via actions at 5-HT2C receptors (5-HT2CRs), engage a CRF(BNST) inhibito

21 coding the serotonin 5-hydroxytryptamine 2C (5-HT2C) receptor (5-HT2CR) undergo adenosine-to-inosine

22 onists at the human serotonin2A (5-HT2A) and 5-HT2C receptors activate differentially two signal tran

23 al multiphoton calcium imaging revealed that 5-HT2C receptor activation amplified odor-evoked activit

24 These results suggest that neither 5-HT2C receptor activation nor 5-HT2A receptor blockade

25 tional G proteins compared with constitutive 5-HT2C receptor activation.

26 om our laboratory demonstrating constitutive 5-HT2C receptor activity, we examined the contribution o

27 acological blockade and constitutive loss of 5-HT2C receptor activity.

28 herefore extended our previous work with the 5-HT2C receptor agonist 1-(m-chlorophenyl)-piperazine hy

29 ment with a 5-HT2A receptor antagonist and a 5-HT2C receptor agonist attenuated the MDMA-induced incr

30 Infusions of the moderately selective 5-HT2C receptor agonist RO 60-0175 had no effects on fee

31 Thus, we examined the effects of a 5-HT2C receptor agonist, WAY163909, and a 5-HT2A recepto

32 Compound (+)-22a was identified as a potent 5-HT2C receptor agonist, with good selectivity against t

33 ffer leads to the development of a selective 5-HT2C receptor agonist.

34 stemic treatment with a 5-hydroxytryptamine (5-HT2C) receptor agonist and mimicked by systemic treatm

35 cord injury results in different effects by 5-HT2C receptor agonists and antagonists.

36 In addition, administration of 5-HT2C receptor agonists does not induce activity-depend

37 ries of compounds that are potent, selective 5-HT2C receptor agonists is described herein as we conti

38 For example, administration of 5-HT2C receptor agonists suppresses locomotor activity i

39 24-h exposure to inverse agonists acting at 5-HT2C receptors also selectively enhanced IP accumulati

40 Agonists at the 5-HT2C receptor and antagonists at the 5-HT2A receptor s

41 improved ligands with better potency at the 5-HT2C receptor and excellent selectivity against the 5-

42 antibody that recognizes 5-HT1B, 5-HT2A, and 5-HT2C receptors and an antibody against S100beta, a Sch

43 -fold) binding selectivity for 5-HT2A versus 5-HT2C receptors and, hence, might serve as a useful tem

44 ed serotonin signaling through serotonin 2C (5-HT2C) receptors and amplified by decreased serotonergi

45 ines studied, mesulergine (selective for the 5-HT2C receptor) and d-lysergic acid diethylamide (selec

46 to chronic SSRI treatment, whereas local SNr 5-HT2C receptor antagonism or optogenetic activation of

47 Lastly, we find that 5-HT2C receptor antagonism potentiates the antidepressan

48 we show novel and highly discrete effects of 5-HT2C receptor antagonism that suggest manipulation of

49 tivity that can also be reversed by systemic 5-HT2C receptor antagonism.

50 can be reversed by systemic or SNr-localized 5-HT2C receptor antagonism.

51 ckground strain mice in response to either a 5-HT2C receptor antagonist (SB242084) or a GABAB recepto

52 st and mimicked by systemic treatment with a 5-HT2C receptor antagonist in intact animals.

53 orophenylethyl)]-4-piperidine methanol), the 5-HT2C receptor antagonist SB-242084 (6-chloro-5-methyl-

54 y rats was reversed by administration of the 5-HT2C receptor antagonist SB-242084.

55 The specific 5-HT2C receptor antagonist SB242084 also led to enhanced

56 the 5-CSRTT, wild-type mice treated with the 5-HT2C receptor antagonist SB242084 exhibited diminished

57 ked anxiety and depressive behavior, whereas 5-HT2C receptor antagonist treatment prevented anxiety b

58 4-piperidine-methanol (MDL 100,907), and the 5-HT2C receptor antagonist, 5-methyl-1-(3-pyridylcarbamo

59 The 5-HT2C receptor antagonist, but not the 5-HT2A receptor

60 ither the 5-HT2A receptor antagonist nor the 5-HT2C receptor antagonist, injected alone, altered the

61 e 5-HT2A receptor antagonist, MDL100907, the 5-HT2C receptor antagonist, SB242084, or the 5-HT1A rece

62 weight-supported stepping with SB 206,553, a 5-HT2C receptor antagonist.

63 retreatment with a selective 5-HT2A, but not 5-HT2C, receptor antagonist.

64 vior, highlighting the potential benefits of 5-HT2C receptor antagonists for both reduction of motor

65 thermore, treatment with chemically distinct 5-HT2C receptor antagonists resulted in a time-dependent

66 Thus, agonist occupation of the 5-HT2C receptor apparently activates different or additi

67 port that null mutant mice lacking serotonin 5-HT2C receptors are extremely susceptible to AGSs.

68 ese results provide additional evidence that 5-HT2C receptors are suitable drug targets with fewer si

69 Serotonin 5-HT2C receptors are widely expressed throughout the hip

70 Finally, 5-HT3, but not 5-HT2C receptors, are required for the anorectic effects

71 hinese hamster ovary cells stably expressing 5-HT2C receptors as biodetectors to monitor 5-HT release

72 Relative to 5-HT2C receptor binding, WAY-161503 was approximately 6-

73 inhibited by activation of transfected human 5-HT2C receptors but not 5-HT2A receptors.

74 had no effect on ligand binding to wild-type 5-HT2C receptors, but inhibited basal and 5-HT-stimulate

75 l for decoding the oligomer status of native 5-HT2C receptors by molecular brightness analysis.

76 starved NIH-3T3 fibroblasts transfected with 5-HT2C receptor cDNA.

77 The data suggest that drugs acting on the 5-HT2C receptor could selectively affect discrete neuron

78 WAY-161503 was a full agonist in stimulating 5-HT2C-receptor-coupled [3H]inositol phosphate (IP) form

79 nes, whereas the interchange mutation of the 5-HT2C receptor did not affect indoleamine affinity.

80 5-HT2C receptors displayed a diffusion coefficient of 5

81 Although heterodimerization with 5-HT2C receptors does not alter 5-HT2C Galphaq-dependent

82 used to follow CFP- and YFP-tagged serotonin 5-HT2C receptors during biosynthesis in the endoplasmic

83 Our data suggest that mCPP activates 5-HT2C receptors during testing to enhance the display o

84 an explanation for the dissociation between 5-HT2C receptor editing phenotypes and behavioral stress

85 to demonstrate the homodimeric structure of 5-HT2C receptors endogenously expressed in their native

86 ealed molecular brightness values for native 5-HT2C receptors equivalent to the molecular brightness

87 s of PNU-69176E were observed with the human 5-HT2C receptor expressed in several mammalian cell line

88 dependent on the ratio of CFP- to YFP-tagged 5-HT2C receptors expressed in each region and was indepe

89 nist activation of the 5-hydroxytryptamineC (5-HT2C) receptor expressed in NIH-3T3 fibroblasts result

90 ipase A2-coupled arachidonic acid release in 5-HT2C receptor expressing cells albeit with lower poten

91 In contrast, chemogenetic inhibition of VTA 5-HT2C receptor expressing neurons had no effect on the

92 Activation of VTA 5-HT2C receptor expressing neurons significantly reduced

93 E) line to clarify the function of subset of 5-HT2C receptor expressing VTA neurons in the modulation

94 trated that serotonin 5-hydroxytryptamine2C (5-HT2C) receptors form homodimers.

95 inactive 5-HT2C receptors inhibit wild-type 5-HT2C receptor function by forming nonfunctional hetero

96 ptor antagonism that suggest manipulation of 5-HT2C receptor function may be of use in correcting mal

97 ne to inosine editing of mRNA from the human 5-HT2C receptor gene (HTR2C) occurs at five exonic posit

98 ce with a targeted mutation of the serotonin 5-HT2C receptor gene consume more food despite normal re

99 f hippocampal function, mice with a targeted 5-HT2C-receptor gene mutation were examined.

100 orm of the serotonin 5-hydroxytryptamine 2C (5-HT2C) receptor, global analysis of construct quantal b

101 The human 5-hydroxytryptamine-2C (5-HT2C) receptor has been the target of potential anxiol

102 demonstrate formation of functional MT2 and 5-HT2C receptor heteromers both in transfected cells and

103 In oocytes co-expressing both hPTHR and 5-HT2C receptors, homologous desensitization was seen, b

104 At the 5-HT2C receptor, however, affinities were considerably h

105 At the cloned human 5-HT2B and 5-HT2C receptors, however, 3a had about twice the affini

106 ice during task performance, indicating that 5-HT2C receptors impact dopamine homeostasis during a vi

107 genous expression of an inactive form of the 5-HT2C receptor in the locus ceruleus is associated with

108 Expression of wild-type 5-HT2C receptors in an S138R-expressing stable cell line

109 Native 5-HT2C receptors in choroid plexus epithelial cells were

110 , alcoholics may have reduced sensitivity of 5-HT2C receptors in comparison with healthy subjects.

111 into the ARC, and specific antagonism of the 5-HT2C receptors in the ARC diminished the leptin anorec

112 their selectivity toward 5-HT2A, 5-HT2B, and 5-HT2C receptors in the calcium flux assay with the ulti

113 our findings demonstrate opposing roles for 5-HT2C receptors in the effects of SSRIs on motor functi

114 sm that retains basic response properties of 5-HT2C receptors in the face of changing synaptic input

115 ence for denervation-induced upregulation of 5-HT2C receptors in the injured spinal cord.

116 These findings strongly implicate 5-HT2C receptors in the serotonergic suppression of DA-m

117 hat SSRIs impair motor function by acting on 5-HT2C receptors in the substantia nigra pars reticulata

118 agenesis of Ser138 to Arg (S138R) produced a 5-HT2C receptor incapable of binding ligand or stimulati

119 Therefore, inactive 5-HT2C receptors inhibit wild-type 5-HT2C receptor funct

120 nance energy transfer studies confirmed that 5-HT2C receptors interact with either 5-HT2A or 5-HT2B r

121 ia physical association of melatonin MT2 and 5-HT2C receptors into functional heteromers.

122 cortical pre-mRNA encoding the serotonin 2C (5-HT2C) receptor is altered by adenosine-to-inosine edit

123 te that the 5-HT2A, but surprisingly not the 5-HT2C, receptor is critical for weight loss, anorexia,

124 (+)-19, which showed an EC50 of 24 nM at the 5-HT2C receptor, is fully selective over the 5-HT2B rece

125 The non-edited human 5-HT2C receptor isoform INI activates phospholipase D vi

126 chain only for tryptamines that bind to the 5-HT2C receptor isoform.

127 Although spiperone also binds at 5-HT2C receptors, it is one of the very few agents that

128 Wild-type and 5-HT2C receptor-/- (KO) mice and normal Sprague-Dawley r

129 5-HT2C receptor ligands modulated [3H]thymidine incorpor

130 Three classes of 5-HT2C receptor ligands were distinguished in transfecte

131 r formation is a naturally occurring step in 5-HT2C receptor maturation and processing.

132 ctive 5-HT2 receptor agonists, targeting the 5-HT2C receptor may have clinical relevance for the trea

133 Recent evidence suggests that 5-HT2C receptors may be a promising target for schizophr

134 tent with their rank order to decrease basal 5-HT2C receptor-mediated phosphoinositide hydrolysis.

135 5-HT2C receptor mRNA expression was always restricted to

136 he substantia nigra revealed coexpression of 5-HT2C receptor mRNA with glutamic acid decarboxylase bu

137 expressed detectable levels of 5-HT2a and/or 5-HT2c receptor mRNA with half of the cells expressing b

138 i.p.) reduced the intake of high fat diet in 5-HT2C receptor mutant mice (saline 4.54 +/- 0.47 kcal v

139 5-HT2C receptor mutants exhibited abnormal performance i

140 d compound was most potent, with a Ki at the 5-HT2C receptor of 1.9 nM.

141 e the localization of 5-hydroxytryptamine2C (5-HT2C) receptors on the motoneurons innervating the ext

142 do[4,5-d]azepines that are potent, selective 5-HT2C receptor partial agonists is described.

143 5-HT2A receptor polymorphism 102-T/C and the 5-HT2C receptor polymorphism Cys23Ser.

144 Serotonin 2C (5-HT2C) receptor pre-mRNA is a substrate for RNA editing

145 /arachidonic acid signaling cascade mediates 5-HT2C receptor regulation of the CHO/5-HT1B receptor pa

146 Agonism of the 5-HT2C receptor represents one of the most well-studied

147 These results suggest that the activation of 5-HT2C receptors selectively inhibits morphine-induced D

148 control processes and suggest that impaired 5-HT2C receptor signaling during development may predisp

149 series of reversals, indicating that intact 5-HT2C receptor signaling is required to accurately resp

150 represents a novel mechanism for regulating 5-HT2C receptor signaling to pathways linked to actin cy

151 findings suggest that constitutively active 5-HT2C receptors stimulate cell division in transfected

152 ist-labeled cloned human 5-HT2A, 5-HT2B, and 5-HT2C receptor subtypes.

153 gnal transduction cascades of the 5-HT2A and 5-HT2C receptor subtypes.

154 gher affinity of 5-HT and tryptamine for the 5-HT2C receptor than for the 5-HT2A receptors is not due

155 utilizes an active site mutant D134A (D3.32) 5-HT2C receptor to identify atypical agonist structures.

156 r was created and coexpressed with wild-type 5-HT2C receptors to determine whether dimerization regul

157 To assess the contribution of 5-HT2C receptors to the serotonergic regulation of hippo

158 The human serotonin 5-HT2C receptor undergoes adenosineto-inosine RNA editin

159 ding mode of this series of compounds to the 5-HT2C receptor was also investigated in a modeling stud

160 r the human 5-hydroxytryptamine (5-HT)2A and 5-HT2C receptors was investigated with the use of recipr

161 nitoring of FRET between CFP- and YFP-tagged 5-HT2C receptors was performed by acceptor photobleachin

162 A line of mutant mice devoid of 5-HT2C receptors was used to examine the contribution of

163 Heterodimerization of S138R with wild-type 5-HT2C receptors was visualized in living cells using co

164 pping after SCI is through activation of the 5-HT2C receptor, we performed the following experiments.

165 Here, we show that activation of serotonin 5-HT2C receptors, which engage Erk1/2 pathway via a beta

166 esulergine) radioligand binding to the human 5-HT2C receptor with derived Ki values of 3.3 +/- 0.9 an

167 on the role of functional selectivity at the 5-HT2C receptor with respect to antipsychotic activity.

168 Activation of 5-HT2C receptors with 5-HT or (+/-)-1-(2,5-dimethoxy-4-i