ライフサイエンスコーパス: 5-HT(2C) receptor

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

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

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

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

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

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

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

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

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

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

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

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

13 obesity in mutant mice lacking the serotonin 5-HT(2C) receptor.

14 ed following pharmacological blockade of the 5-HT(2C) receptor.

15 says for affinity at 5-HT(1A), 5-HT(2A), and 5-HT(2C) receptors.

16 y than their S-antipodes at the 5-HT(2A) and 5-HT(2C) receptors.

17 was not detected for the extensively edited 5-HT(2C) receptors.

18 suggesting involvement of both 5-HT(2A) and 5-HT(2C) receptors.

19 mine binds weakly to 5-HT(2A), 5-HT(2B), and 5-HT(2C) receptors.

20 e than 20-fold selectivity for 5-HT(2A) over 5-HT(2C) receptors.

21 he DRN via 5-HT(2A) and, to a lesser extent, 5-HT(2C) receptors.

22 ith DeltaPDZ receptors relative to wild-type 5-HT(2C) receptors.

23 be potent agonists of the human 5-HT(2A) and 5-HT(2C) receptors.

24 ffinity for the closely related 5-HT(2B) and 5-HT(2C) receptors.

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

26 However, binding to 5-HT(2C) receptors ([3H]mesulgergine) in DiO rats was no

27 droxytryptamine; 5-HT) signaling through the 5-HT(2C) receptor (5-HT(2C)R) is essential in normal phy

28 inding studies have shown that the serotonin 5-HT(2C) receptor (5-HT(2C)R) is widely expressed throug

29 he treatment of psychiatric disorders is the 5-HT(2C) receptor (5-HT(2C)R).

30 in [5-hydroxytryptamine (5-HT)] 5-HT(2A) and 5-HT(2C) receptors (5-HT(2A)Rs and 5-HT(2C)Rs), which in

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

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

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

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

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

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

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

38 een shown to have agonist-like properties at 5-HT(2C) receptors, a follow-up experiment was performed

39 mediated by stimulation of serotonergic 2C (5-HT(2C)) receptors, a serotonergic receptor subtype pre

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

41 n both systems, serotonin stimulation of the 5-HT(2C) receptor activates phospholipase D in addition

42 active Galpha(q) subunits mediate endogenous 5-HT(2C) receptor activation of PLCbeta and that Gbetaga

43 eracting with active Galpha(q), also blocked 5-HT(2C) receptor activation.

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

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

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

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

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

49 Microinjections of the 5-HT(2C) receptor agonist (+/-)-DOI hydrochloride into t

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

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

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

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

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

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

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

57 e presence of tetrodotoxin, were mimicked by 5-HT(2C) receptor agonists and reversed by 5-HT(2C) anta

58 mpounds, several were potent and efficacious 5-HT(2C) receptor agonists with selectivity over both 5-

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

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

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

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

63 24-h exposure to inverse agonists acting at 5-HT2C receptors also selectively enhanced IP accumulati

64 s striatal LTSIs acting through postsynaptic 5-HT(2C) receptors and increasing an M type current.

65 ine exhibited high affinity for 5-HT(2B) and 5-HT(2C) receptors and more moderate affinity for 5-HT(2

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

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

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

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

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

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

72 5-HT(2C) receptor antagonism appears to contribute to th

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

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

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

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

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

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

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

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

81 4-piperidine-methanol (MDL 100,907), and the 5-HT2C receptor antagonist, 5-methyl-1-(3-pyridylcarbamo

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

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

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

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

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

87 nner, which was antagonized by the selective 5-HT(2C) receptor antagonists 8-[5-(2,4-dimethoxy-5-(4-t

88 These effects of 5-HT1B and 5-HT(2C) receptor antagonists likely reflected blockade

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

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

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

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

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

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

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

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

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

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

99 e present the entire sequence of a zebrafish 5-HT(2C) receptor cDNA including the 3' untranslated reg

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

101 SCI also evoked an increase in 5-HT(2C) receptor cluster number and intensity, suggesti

102 ies are inverse agonists at the human cloned 5-HT(2C) receptor, completely abolishing basal activity

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

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

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

106 fluorescence-tagged 5-hydroxytryptamine 2C (5-HT(2C)) receptors diffusing within the plasma membrane

107 5-HT2C receptors displayed a diffusion coefficient of 5

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

109 Expression of the 5-HT(2C) receptor during ontogeny was found as early as

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

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

112 Methods used to date to quantify 5-HT(2C) receptor editing are labor-intensive, expensive

113 ormation regarding the relative abundance of 5-HT(2C) receptor editing variants.

114 el, ultra high-throughput method to quantify 5-HT(2C) receptor editing, compare it to a more conventi

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

116 the intracellular signaling mechanism of the 5-HT(2C) receptor endogenously expressed in choroid plex

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

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

119 The results of this study suggest that 5-HT(2C) receptors exist as constitutive homodimers on t

120 hysical techniques were used to determine if 5-HT(2C) receptors exist as homodimers on the plasma mem

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

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

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

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

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

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

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

128 binding affinity, high selectivity over the 5-HT(2C) receptor, favorable CNS partitioning, and good

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

130 Therefore, it is concluded that 5-HT(2C) receptors freely diffusing within the plasma me

131 uggest the use of zebrafish for the study of 5-HT(2C) receptor function in behavior, development and

132 timulation are unmasked in animals devoid of 5-HT(2C) receptor function.

133 ofoundly modulates metabotropic 5-HT(2A) and 5-HT(2C) receptor function.

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

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

136 These studies revealed that the nonedited 5-HT(2C) receptor functionally couples to G(q) and G(13)

137 -nucleotide change (rs6318, Cys23Ser) in the 5-HT(2C) receptor gene (HTR2C) has been associated with

138 hese results indicate that a mutation of the 5-HT(2C) receptor gene (htr2c) increases LA, which contr

139 The results characterize the zebrafish 5-HT(2C) receptor gene and gene expression pattern for t

140 hism of the promoter region of the serotonin 5-HT(2C) receptor gene is associated with antipsychotic-

141 The cloned 5-HT(2C) receptor gene is located on chromosome 7, is ap

142 y in mice bearing a targeted mutation of the 5-HT(2C) receptor gene.

143 thologs and clearly identifies the gene as a 5-HT(2C) receptor gene.

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

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

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

147 The similarities to mammalian 5-HT(2C) receptor genes suggest the use of zebrafish for

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

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

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

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

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

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

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

155 ls, and preclinical findings have implicated 5-HT(2C) receptors in motivated behaviors and psychotrop

156 o determine the roles played by 5-HT(1A) and 5-HT(2C) receptors in the medial hypothalamus on the exp

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

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

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

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

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

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

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

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

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

166 mice by previous pharmacological blockade of 5-HT(2C) receptors, indicating that the mutant phenotype

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

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

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

170 and biological activity of a novel series of 5-HT(2C) receptor inverse agonists are reported.

171 ut not all, atypical APDs are also effective 5-HT(2C) receptor inverse agonists or neutral antagonist

172 The 5-HT(2C) receptor is one of 14 different serotonin (5-HT

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

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

175 (+)-19, which showed an EC50 of 24 nM at the 5-HT2C receptor, is fully selective over the 5-HT2B rece

176 We examined the ability of the nonedited 5-HT(2C) receptor isoform (INI) and two extensively edit

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

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

179 he tissue-specific expression of seven major 5-HT(2C) receptor isoforms encoded by eleven distinct RN

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

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

182 the plasma membrane of live cells expressing 5-HT(2C) receptors labeled with cyan (donor) and yellow

183 RET) was assessed in HEK293 cells expressing 5-HT(2C) receptors labeled with Renilla luciferase and y

184 of DeltaPDZ receptors recovered to wild-type 5-HT(2C) receptor levels.

185 5-HT2C receptor ligands modulated [3H]thymidine incorpor

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

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

188 Galpha(q) signaling pathways of the mER and 5-HT(2C) receptors may converge to enhance synaptic effi

189 nduced [Ca(2+)](i) release imply that edited 5-HT(2C) receptors may produce distinct physiological re

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

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

192 Because 5-HT(2C) receptors mediate many of the effects of seroto

193 Serotonin 2C (5-HT(2C)) receptors mediate the inhibitory effects of se

194 responses, there was no gender difference in 5-HT(2C) receptor-mediated effects.

195 receptor-mediated activation of cAMP but not 5-HT(2C) receptor-mediated phosphatidylinositide hydroly

196 r-G(q) protein interacting domain, disrupted 5-HT(2C) receptor-mediated phosphatidylinositide hydroly

197 agamma subunits were ineffective at blocking 5-HT(2C) receptor-mediated phosphoinositol turnover.

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

199 f immunoreactive bands the predicted size of 5-HT(2C) receptor monomers and homodimers that were dete

200 5-HT2C receptor mRNA expression was always restricted to

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

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

203 unal muscle, whereas 5-HT(1A), 5-HT(1D), and 5-HT(2C) receptor mRNAs were not.

204 igated determinants of energy expenditure in 5-HT(2C) receptor mutant mice.

205 of locomotor activity (LA) were observed in 5-HT(2C) receptor mutant mice.

206 sequent development of late-onset obesity in 5-HT(2C) receptor mutant mice.

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

208 5-HT2C receptor mutants exhibited abnormal performance i

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

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

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

212 hat desensitization occurs in the absence of 5-HT(2C) receptor phosphorylation and suggest that recep

213 5-HT2A receptor polymorphism 102-T/C and the 5-HT2C receptor polymorphism Cys23Ser.

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

215 uced no anxiogenic behaviors suggesting that 5-HT(2C) receptors primarily within the BLA are responsi

216 and is 54% identical to the human and mouse 5-HT(2C) receptor protein sequences.

217 FCS and PCH analysis of fluorescence-tagged 5-HT(2C) receptors provided molecular brightness values

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

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

220 tion at Ser(459) enhances resensitization of 5-HT(2C) receptor responses.

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

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

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

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

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

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

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

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

229 Phosphorylation of mutant 5-HT(2C) receptors that lack the carboxyl-terminal PDZ r

230 ediate their effects through 5-HT(2A) and/or 5-HT(2C) receptors, the isoxazoles 3d and 4d constitute

231 a large excess of untagged, non-fluorescent 5-HT(2C) receptors, the molecular brightness was reduced

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

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

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

235 at least 300-fold higher than the levels of 5-HT(2C) receptor transcript, which were barely detectab

236 RNA encoding the human 5-HT(2C) receptor undergoes adenosine-to-inosine RNA edi

237 The human serotonin 5-HT(2C) receptor undergoes RNA editing that creates mul

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

239 In the present study, an inactive 5-HT(2C) receptor was created and coexpressed with wild-

240 The 5-HT(2C) receptor was Galpha(q)-coupled to PLC activatio

241 rodimer between the GHS-R1a receptor and the 5-HT(2C) receptor was identified.

242 and large intestine), but that encoding the 5-HT(2C) receptor was not.

243 N- and C-terminal halves of YFP attached to 5-HT(2C) receptors was observed in endoplasmic reticulum

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

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

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

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

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

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

250 When GFP-tagged 5-HT(2C) receptors were co-expressed with a large excess

251 Phosphorylation-deficient serotonin 5-HT(2C) receptors were generated to determine whether p

252 umerous transcripts, including the mammalian 5-HT(2C) receptor, which can be edited at five distinct

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

254 d an essential requirement for activation of 5-HT(2C) receptors while 5-HT(1A/1B), 5-HT(7) and 5-HT(2

255 nt of cells expressing DeltaPDZ or wild-type 5-HT(2C) receptors with 100 nm serotonin elicited initia

256 ells stably expressing DeltaPDZ or wild-type 5-HT(2C) receptors with serotonin produced identical max

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

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

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

260 began to examine the effects of stimulating 5-HT(2C) receptors within the basolateral (BLA) or centr

261 These results suggest that activation of 5-HT(2C) receptors within the BLA influences the activit