ライフサイエンスコーパス: 5-HT(2A) receptor

1 radiation are mediated by activation of the 5-HT2A receptor.

2 suggesting that regulation may occur at the 5-HT2A receptor.

3 zing effect of 5-HT on PVINs was mediated by 5-HT2A receptor.

4 cortical-cortical responses mediated by the 5-HT2A receptor.

5 It has high selectivity over 5-HT2A receptor.

6 good selectivity against the 5-HT2B and the 5-HT2A receptors.

7 proteins and DOI-induced desensitization of 5-HT2A receptors.

8 inhibition of a K+ current via postsynaptic 5-HT2A receptors.

9 duced up-regulation and enhanced activity of 5-HT2A receptors.

10 midal neurons, which are known to be rich in 5-HT2A receptors.

11 ring thrombosis, activates platelets via the 5-HT(2A) receptor.

12 ule was oriented toward position 5.46 of the 5-HT(2A) receptor.

13 gonist exhibiting selectivity over the human 5-HT(2A) receptor.

14 mediated heterologous desensitization of the 5-HT(2A) receptor.

15 virtual docking into a homology model of the 5-HT(2A) receptor.

16 t and highly efficacious agonists at the rat 5-HT(2A) receptor.

17 f phenethylamine ligands upon binding to the 5-HT(2A) receptor.

18 efficacy similar to that of mescaline at the 5-HT(2A) receptor.

19 agonism (EC(50)=0.62 nM) at the cloned human 5-HT(2A) receptor.

20 d efficacy equal to that of mescaline at the 5-HT(2A) receptor.

21 tent with LSD-like activity mediated via the 5-HT(2A) receptor.

22 ct is abolished by selective blockade of the 5-HT(2A) receptor.

23 ist-induced desensitization of serotonin 2A (5-HT2A) receptors.

24 is dependence accounts for its inhibition by 5-HT(2A) receptors.

25 or of inhibitory cross-talk between RTKs and 5-HT(2A) receptors.

26 ane (DOI) and on [(3)H]ketanserin binding to 5-HT(2A) receptors.

27 have elevated binding potential of cortical 5-HT(2A) receptors.

28 tic currents (sEPSCs) was mediated solely by 5-HT(2A) receptors.

29 amined derivatives also possess affinity for 5-HT(2A) receptors.

30 e and indolamine transporters, and GABAA and 5-HT(2A) receptors.

31 SERT density and concomitant upregulation of 5-HT(2A) receptors.

32 eceptor for UVB radiation, to the serotonin (5-HT(2A)) receptor.

33 as approximately 6-fold less potent at human 5-HT2A receptors ([125I]DOI) with a derived Ki value of

34 All known drugs of this class are 5-HT(2A) receptor (2AR) agonists, yet closely related 2A

35 ntified by their high affinity for serotonin 5-HT2A receptors (2AR).

36 rotonin (5-hydroxytryptamine, 5-HT), via the 5-HT(2A) receptor (5-HT(2A)R) subtype, plays a key role

37 The serotonin 5-HT2A receptor (5-HT-sub(2A)R) may play a role in reins

38 Acute treatment of wild-type platelets with 5-HT2A receptor (5-HT2AR) antagonists or SSRIs revealed

39 otoninergic system in PFC, in particular the 5-HT2A receptor (5-HT2AR) could have a role in the contr

40 havioral studies carried out in mice lacking 5-HT2A receptors (5-HT2AR) revealed a remarkable 5-HT2AR

41 ytryptamine, 5-HT) innervation and expresses 5-HT2A receptors (5-HT2ARs) and other 5-HT receptors, ra

42 We demonstrate that global disruption of 5-HT2A receptor (5HT2AR) signaling in mice reduces inhib

43 In rodents, interaction with the 5-HT(2A) receptor, a primary site of action of lysergic

44 ers of serotonin receptors, specifically the 5-HT(2A) receptor, abolish synchronous activity in the h

45 sing biases and the specific contribution of 5-HT2A receptors across different emotional domains is u

46 The 5-HT(2A) receptor activates cholinergic neurons, which p

47 5-HT(2A) receptor activation by the 5-HT(2) receptor ago

48 et of 5-HT(2A) agonists at three readouts of 5-HT(2A) receptor activation in both wild-type (WT) and

49 Here, we show that 5-HT2A receptor activation enhances NMDA transmission an

50 T2A receptors, we tested the hypothesis that 5-HT2A receptor activation is critical for gasping.

51 a pro- and antinociceptive action following 5-HT2A-receptor activation; therefore, to shed light on

52 receptors, most likely through modulation of 5-HT2A receptor activity, on spinal nociceptive transmis

53 ed light on the directional nature of spinal 5-HT2A receptor activity, we investigated the effects of

54 Evidence is provided that 5-HT(5A) and 5-HT(2A) receptor affinities probably do not covary and

55 ter activity was positively regulated by the 5-HT(2A) receptor agonist 4-bromo-3,6-dimethoxybenzocycl

56 Here we report that 5-HT(2A) receptor agonist efficacies were significantly

57 mechanical ventilation during the seizure or 5-HT2A receptor agonist pretreatment.

58 potential of peripherally acting 5-HT(1) and 5-HT(2A) receptor agonists and centrally penetrating 5-H

59 acid production, such functionally selective 5-HT(2A) receptor agonists may lack the intoxicating pro

60 high affinity and potency of a new class of 5-HT(2A) receptor agonists, N-benzyl phenethylamines.

61 of the SAR of phenethylamine-type serotonin 5-HT(2A) receptor agonists, substituted conformationally

62 of substituted tryptamine and phenethylamine 5-HT(2A) receptor agonists, we found that Ser5.43(239) i

63 threonines in the cytoplasmic domains of the 5-HT(2A) receptor and assessed the effects of these muta

64 osomal S6 kinase 2 (RSK2) phosphorylates the 5-HT(2A) receptor and attenuates 5-HT(2A) receptor signa

65 a cell type that endogenously expresses both 5-HT(2A) receptors and Cav-1.

66 5-HT(2A) receptors and choline acetyltransferase were lo

67 erpolarization current and its modulation by 5-HT(2A) receptors and point to a key role for PtdIns(4,

68 activates a serotonin system, apparently via 5-HT(2A) receptors and related intracellular pathways.

69 binds to serotonin (5-hydroxytryptamine) 2A (5-HT(2A)) receptor and that antagonists of 5-HT(2A) and

70 eight loss after RYGB and that the change in 5-HT2A receptor and 5-HT transporter binding correlated

71 In vivo cerebral 5-HT2A receptor and 5-HT transporter binding was determi

72 Additional studies demonstrated that 5-HT2A receptor and PSD-95 were co-localized in clusters

73 aining protein, directly associates with the 5-HT2A receptor and regulates 5-HT2A receptor-mediated s

74 We first demonstrated that 5-HT2A receptors and IL-6-mediated STAT3 phosphorylation

75 , a compound with affinities for sigma-2 and 5-HT2A receptors and no direct dopamine affinities, in c

76 The serotonin 2A (5-HT2A) receptor and the proinflammatory cytokine, inter

77 locybin and mescaline, require the serotonin 5-HT(2A) receptor, and induce schizophrenia-like psychos

78 gic actions of the atypical APDs, especially 5-HT(2A) receptor antagonism, are particularly important

79 al antipsychotic drugs, without the need for 5-HT(2A) receptor antagonism.

80 The selective 5-HT(2A) receptor antagonist, MDL-100907, had no effect

81 but it was inhibited by a specific serotonin 5-HT(2A) receptor antagonist, MDL11939.

82 Pretreatment with a 5-HT2A receptor antagonist and a 5-HT2C receptor agonist

83 dditionally pretreated with the preferential 5-HT2A receptor antagonist ketanserin (50 mg vs placebo)

84 ects in vivo and ex vivo were blocked by the 5-HT2A receptor antagonist ketanserin and absent in mice

85 n, we evaluated the effects of the selective 5-HT2A receptor antagonist M100907 on intravenous cocain

86 The selective 5-HT2A receptor antagonist M100907 significantly attenua

87 tion additively with eotaxin and a dual CCR3/5-HT2A receptor antagonist may be more effective in bloc

88 Also, the 5-HT2A receptor antagonist MDL 11,939 (0.0, 0.5, or 2.0

89 bursting were selectively eliminated by the 5-HT2A receptor antagonist piperidine or ketanserin.

90 Postnatal, selective 5-HT2A receptor antagonist treatment blocked PNFlx-evoke

91 s using the radioligand (123)I-5-I-R91150, a 5-HT2A receptor antagonist, as the imaging probe.

92 the effects of spinal administration of the 5-HT2A receptor antagonist, ketanserin, on the evoked re

93 a 5-HT2C receptor agonist, WAY163909, and a 5-HT2A receptor antagonist, M100907, given alone and in

94 -HT2A/C receptor antagonist, ketanserin, the 5-HT2A receptor antagonist, MDL100907, the 5-HT2C recept

95 1 antagonist, or by ketanserin, a serotonin 5-HT2A receptor antagonist.

96 um mobilization was blocked with a selective 5-HT2A receptor antagonist.

97 ective effects of LSD are fully blocked by a 5-HT2A receptor antagonist.

98 f a series of potent and selective serotonin 5-HT(2A) receptor antagonists based on a phenethylpipera

99 hat treating UV-irradiated mice with PAF and 5-HT(2A) receptor antagonists blocks skin cancer inducti

100 o measured the effect that injecting PAF and 5-HT(2A) receptor antagonists had on UV-induced skin dam

101 together, these data suggest that selective 5-HT(2A) receptor antagonists may have a role in pulmona

102 agonists and have weaker, if any, potency as 5-HT(2A) receptor antagonists.

103 er incidence in mice treated with the PAF or 5-HT(2A) receptor antagonists.

104 when the mice were injected with PAF and/or 5-HT(2A) receptor antagonists.

105 5-HT2A receptor antagonists (including MDL-100907 and cy

106 Previous studies indicate that 5-HT2A receptor antagonists attenuate the reinstatement

107 Serotonin 5-HT2A receptor antagonists have been shown to attenuate

108 onin antibodies or by treating the mice with 5-HT2A receptor antagonists.

109 ic differences among patients due to variant 5-HT(2A) receptors appear to be more important than phar

110 The molecular mechanisms by which 5-HT(2A) receptors are desensitized are unknown, and to

111 ed hypothermia is blunted and frontal cortex 5-HT(2A) receptors are increased in the Tph2 knockin mic

112 n 2A (5-HT(2A)) receptor expression and that 5-HT(2A) receptors are involved in thermoregulation.

113 Recently, it has been shown that 5-HT(2A) receptors are mostly expressed on pyramidal neu

114 y mechanism has the potential to explain how 5-HT(2A) receptors are regulated in vivo, with potential

115 The putative CaM binding regions of the 5-HT2A receptor are localized to the second intracellula

116 Importantly, central 5-HT2A receptors are also required for peripherally inje

117 triple combination and high selectivity over 5-HT2A receptors are the differentiating features which

118 series lacked high intrinsic activity at the 5-HT(2A) receptor as measured using the phosphoinositide

119 reduction of ligand binding to D1 and D2 and 5-HT2A receptors as well as loss of PDE10A enzyme in the

120 reduction of ligand binding to D1 and D2 and 5-HT2A receptors as well as loss of PDE10A enzyme in the

121 SERT and 5-HT(2A) receptor availability (binding potential, BP(ND

122 ports earlier work suggesting that increased 5-HT(2A) receptor availability characterizes a group of

123 Serotonin transporter (SERT) and 5-HT(2A) receptor availability was measured in multiple

124 Correlations were measured between SERT and 5-HT(2A) receptor availability, impulsivity and aggressi

125 res selectivity versus the highly homologous 5-HT(2A) receptor, because agonism at this receptor can

126 f note, compounds 14 and 27 exhibited potent 5-HT(2A) receptor binding affinity, high selectivity ove

127 Estrogen increases 5-HT(2A) receptor binding in human prefrontal regions.

128 No changes were found in 5-HT(2A) receptor binding in the hypothalamus or other f

129 phy (PET) study reported increased serotonin 5-HT(2A) receptor binding in unmedicated depressed patie

130 5-HT(2A) receptor binding potential correlated negativel

131 0,907 in a PET imaging paradigm to assess 1) 5-HT(2A) receptor binding potential in euthymic subjects

132 d patients demonstrated significantly higher 5-HT(2A) receptor binding potential in the frontal corte

133 The correlation of increased 5-HT(2A) receptor binding potential with increased score

134 utoradiographic analysis of 125I-LSD-labeled 5-HT(2a) receptor binding revealed no significant differ

135 Cortical 5-HT(2A) receptor binding was measured in 20 unmedicated

136 5-HT(2A) receptor binding was significantly increased af

137 5-HT(1A) and 5-HT(2A) receptor binding was significantly increased in

138 positron emission tomography measurements of 5-HT(2A) receptor binding with [(18)F]deuteroaltanserin

139 The authors investigated cortical 5-HT2A receptor binding in eight adults with Asperger's

140 Additionally, 5-HT2A receptor binding in the OFC of mid- and high-quin

141 rome had a significant reduction in cortical 5-HT2A receptor binding in the total, anterior, and post

142 rence region, was performed to calculate the 5-HT2A receptor binding indices (parameter for available

143 mportantly, we found that higher presurgical 5-HT2A receptor binding predicted greater weight loss af

144 that obese individuals have higher cerebral 5-HT2A receptor binding than lean individuals.

145 This is in opposition to other work in which 5-HT(2A) receptor blockade appeared to exacerbate thermo

146 X rat models and explore further the role of 5-HT(2A) receptor blockade.

147 that neither 5-HT2C receptor activation nor 5-HT2A receptor blockade are sufficient to produce a the

148 rs of different thickness, and the serotonin 5-HT(2A) receptor bound to pharmacologically different l

149 associated with lower SERT BP(ND) and higher 5-HT(2A) receptor BP(ND) in cortical, but not subcortica

150 ) was regionally associated with upregulated 5-HT(2A) receptor BP(ND).

151 splayed binding affinity for the recombinant 5-HT(2A) receptor, but which had poor activity when test

152 ecipitation studies revealed that the native 5-HT2A receptor, but not a mutant lacking the PDZ-bindin

153 st ketanserin, indicating that activation of 5-HT2A receptors by psilocybin profoundly modulates the

154 tection of biased agonists for the serotonin 5-HT2A receptor can guide the discovery of safer and mor

155 I-R91150 or from a decreased affinity of the 5-HT2A receptor caused by ketamine remains to be elucida

156 he top of transmembrane helix 5 of the human 5-HT(2A) receptor, comparing the wild type with S5.43(23

157 is thus probably caused by the high level of 5-HT(2A) receptor constitutive activity.

158 These data indicate that the serotonin 5-HT2A receptor contains two high affinity CaM-binding d

159 Dopamine D2 and serotonin 5-HT2A receptors contribute to modulate prefrontal corti

160 e mediodorsal thalamus (presynaptic site) of 5-HT2A receptor-deficient mice, but not in the PFC (post

161 ed significantly with a map of serotonin 2A (5-HT2A) receptor densities (the key site of action of ps

162 er's syndrome have abnormalities in cortical 5-HT2A receptor density and that this deficit may underl

163 However, cortical 5-HT2A receptor density in adults with the disorder has

164 Together, these observations suggest that 5-HT(2A) receptor-dependent signaling epigenetically aff

165 Disruption of 5-HT(2A) receptor-dependent signaling in mice was associ

166 Additionally, we find that the cortical 5-HT(2A) receptor-dependent signaling pathways are signi

167 change occurred in concert with a serotonin 5-HT(2A) receptor-dependent upregulation and increased b

168 al cortex, a trafficking event triggered via 5-HT2A-receptor-dependent downregulation of the NF-kappa

169 In contrast, the decline in the 5-HT2A receptor depolarization with increasing age was a

170 accompanied by alteration in the kinetics of 5-HT2A receptor desensitization but was associated with

171 The present study shows that 5-HT(2A) receptors do not directly stimulate cGMP format

172 efensive behavior, whereas MDL 11,939 blocks 5-HT2A receptors during social defeat to disrupt the dev

173 specifically, 11 is a potent agonist at the 5-HT2A receptor (EC50 = 28.6 nM, E(max) = 103%) that is

174 mulated calcium mobilization (EC50, 7 nM) in 5-HT2A receptor-expressing cells.

175 ggests that estrogen regulates serotonin 2A (5-HT(2A)) receptor expression and that 5-HT(2A) receptor

176 For example, changes in 5-HT(2A) receptor function in prefrontal cortex (PFC) ha

177 Further, 5-HT(2A) receptor function is enhanced in the Tph2 knock

178 ine (DOI), suggesting that IL-6 can regulate 5-HT2A receptor function.

179 ap that can be depicted as follows: 5-HT --> 5-HT(2A) receptor --> TACE --> HB-EGF shedding --> EGFR

180 The 452Tyr variant of the 5-HT(2a) receptor had reduced ability to activate phosph

181 ncreased expression and activity of cortical 5-HT2A receptors has been associated with neuropsychiatr

182 Moreover, activity at D2 and 5-HT2A receptors has proven useful for antipsychotic eff

183 le response results from a higher density of 5-HT2A receptors having the same properties as in non-pr

184 o be a functionally selective agonist at the 5-HT(2A) receptor, having 65-fold greater potency in sti

185 tual docking of these compounds into a human 5-HT(2A) receptor homology model indicated that the N-be

186 ndan-1-yl)-methanamine, was designed using a 5-HT(2A) receptor homology model.

187 Evaluation of the compound at the rat 5-HT(2A) receptor, however, revealed potent binding and

188 )C-GSK215083 also exhibited affinity for the 5-HT2A receptor; however, given the differential localiz

189 t here that RSK2 directly phosphorylates the 5-HT(2A) receptor i3 loop at the conserved residue Ser-3

190 n, and cellular proliferation induced by the 5-HT(2A) receptor in renal mesangial cells.

191 protein enriched in caveolae, complexes with 5-HT(2A) receptors in a number of cell types including C

192 o results in cortical slices, stimulation of 5-HT(2A) receptors in cells stably expressing this serot

193 addition, 2 increased 5-HT(1A) and decreased 5-HT(2A) receptors in cerebral cortex.

194 ) receptors and ((3)H)-ketanserin binding to 5-HT(2A) receptors in post-mortem tissue from the fronta

195 us, for instance, serotonergic activation of 5-HT(2A) receptors in rat aortic smooth muscle cells lea

196 However, the role of 5-HT(2A) receptors in regulating dendritic spine morphog

197 (D-AMPH) and withdrawal on the expression of 5-HT(2A) receptors in the cortex, caudate putamen, NAc a

198 Therefore, the role of 5-HT(2A) receptors in thermoregulation was assessed in t

199 ate the role of central nervous system (CNS) 5-HT(2A) receptors in TST regulation, DOI was administer

200 r with the serotonin 5-hydroxytryptamine 2A (5-HT(2A)) receptor in the mouse frontal cortex.

201 modulin (CaM) co-immunoprecipitates with the 5-HT2A receptor in NIH-3T3 fibroblasts in an agonist-dep

202 separate subjects, we evaluated the role of 5-HT2A receptors in cocaine-induced dopamine overflow in

203 Expressing 5-HT2A receptors in the mediodorsal thalamus (presynapti

204 These data suggest that 5-HT2A receptors in the NAcSh and CPu or in afferents to

205 te and enhance the activity of serotonin 2A (5-HT2A) receptors in the prefrontal cortex (PFCx).

206 anisms by which activation of serotonin(2A) (5-HT(2A)) receptors increase production of cyclic guanos

207 ing of compound 1 in a homology model of the 5-HT(2A) receptor indicated a possible binding mode in w

208 In a search for 5-HT(2A) receptor-interacting proteins, we discovered th

209 iated with the inhibition of agonist-induced 5-HT2A receptor internalization.

210 5-HT(2A) receptor inverse agonists thus represent a pote

211 The 5-HT(2A) receptor is a target of several hallucinogens,

212 In addition, the 5-HT(2A) receptor is expressed in the marginal regions i

213 Here we show that the 5-HT(2A) receptor is present in a subset of spines, in a

214 Moreover we have found that the 5-HT(2A) receptor is responsible for the hypoxia-associa

215 orn to influenza virus-infected mothers, the 5-HT(2A) receptor is upregulated and the mGlu(2) recepto

216 cular basis of the arrestin-insensitivity of 5-HT(2A) receptors is unknown but is probably caused, in

217 The 5-hydroxytryptamine 2A (5-HT(2A)) receptor is a member of the G protein-coupled

218 The 5-hydroxytryptamine 2A (5-HT(2A)) receptor is a member of the G protein-coupled

219 psychological domains and that activation of 5-HT2A receptors is central in mood regulation and emoti

220 The 5-hydroxytryptamine2A (5-HT2A) receptor is a G(q/11)-coupled serotonin receptor

221 position 5.46 is Ser242; however, in the rat 5-HT(2A) receptor, it is Ala242, suggesting that the pot

222 A) agonist-induced hypothermia and increased 5-HT(2A) receptor levels are bona fide biomarkers of chr

223 using the SERT ligand [(1)(1)C]DASB and the 5-HT(2A) receptor ligand [(1)(1)C]MDL 100907 were evalua

224 resent study was to use the highly selective 5-HT(2A) receptor ligand [(11)C]MDL 100,907 in a PET ima

225 ission computed tomography and the selective 5-HT2A receptor ligand 123I iodinated 4-amino-N-[1-[3-(4

226 siological evidence of a role of presynaptic 5-HT2A receptors located at thalamocortical synapses in

227 c (5-HT transporter, SERT) and postsynaptic (5-HT(2A) receptor) markers of 5-HT transmission in recen

228 rch suggest that antagonism of the serotonin 5-HT(2A) receptor may improve sleep maintenance insomnia

229 Specifically, activation of 5-HT2A receptors may induce a processing mode in which s

230 recent evidence suggests that activation of 5-HT2A receptors may lead to the formation of visual hal

231 marker to identify brain areas through which 5-HT2A receptors may modulate cocaine-induced behaviors.

232 tory for mitral cells (MCs) in the MOB where 5-HT2A receptors mediate a direct excitatory action.

233 The results indicate that 5-HT(2A) receptor-mediated cGMP production could be at l

234 ly stimulate cGMP formation, but rather that 5-HT(2A) receptor-mediated cGMP production is dependent

235 pe (+/+) and knockout (-/-) mice showed that 5-HT(2A) receptor-mediated phosphoinositide hydrolysis a

236 of Cav-1 in C6 glioma cells nearly abolished 5-HT(2A) receptor-mediated signal transduction as measur

237 It has been proposed that a dysregulation of 5-HT(2A) receptor-mediated signaling may contribute to t

238 Finally, we showed that CaM decreases 5-HT2A receptor-mediated [35S]GTPgammaS binding to NIH-3

239 d agonist-induced up-regulation and enhanced 5-HT2A receptor-mediated calcium release.

240 y rhythms in the cortex, likely triggered by 5-HT2A receptor-mediated excitation of deep pyramidal ce

241 The association with PSD-95 enhanced 5-HT2A receptor-mediated signal transduction, a novel ac

242 iates with the 5-HT2A receptor and regulates 5-HT2A receptor-mediated signaling and trafficking in HE

243 potentials may be a key mechanism underlying 5-HT2A receptor-mediated visual hallucinations.

244 frontal, motor and cingulate cortices, while 5-HT(2A) receptor mRNA expression in the NAc, caudal CPu

245 h withdrawal period, significantly decreased 5-HT(2A) receptor mRNA expression in the prefrontal, mot

246 ata indicate that region-specific changes in 5-HT(2A) receptor mRNA expression occur in limbic system

247 However, it is not known if alterations in 5-HT(2A) receptor mRNA expression occur in the PFC or ot

248 erse transcription-PCR (RT-PCR), PAF but not 5-HT(2A) receptor mRNA was constitutively expressed in p

249 us antagonism of dopamine D(2) and serotonin 5-HT(2A) receptors or 2) selective action at limbic cort

250 ) target primarily dopamine D2 or serotonin (5-HT2A) receptors, or both; however, these medications a

251 art, by the apparent lack of agonist-induced 5-HT(2A) receptor phosphorylation.

252 a putative role for CaM in the regulation of 5-HT2A receptor phosphorylation and desensitization.

253 These data support the concept that 5-HT(2A) receptors play a role in temperature regulation

254 Within the human 5-HT(2A) receptor, position 5.46 is Ser242; however, in

255 The 5-HT2A receptor possesses a canonical Type I PDZ-binding

256 .46 contributed to the species difference in 5-HT(2A) receptor potency observed for a pyrazinoisoindo

257 lizes the agonist-high affinity state of the 5-HT(2A) receptor (R*).

258 cal importance, our current understanding of 5-HT(2A) receptor regulation is incomplete.

259 ocess of agonist-mediated desensitization of 5-HT(2A) receptors requires the presence of two nonconse

260 results indicate that activation of central 5-HT(2A) receptors restores temperature regulation in tw

261 ore, an interaction between ketamine and the 5-HT2A receptors resulting in decreased binding of (123)

262 turally occurring variation within the human 5-HT(2A) receptor results in an amino acid substitution

263 Through the 5-hydroxytryptamine(2A) (5-HT(2A)) receptor, serotonin (5-HT) plays a role in the

264 t the 5-HT2C receptor and antagonists at the 5-HT2A receptor show promise as potential treatments for

265 (PDGFR), and ErbB4 significantly attenuates 5-HT(2A) receptor signaling in a variety of cell types i

266 rylates the 5-HT(2A) receptor and attenuates 5-HT(2A) receptor signaling.

267 onserved residue Ser-314, thereby modulating 5-HT(2A) receptor signaling.

268 ate thermoregulatory dysfunction by blocking 5-HT(2A) receptor signaling.

269 gonist-induced homologous desensitization of 5-HT2A receptor signaling as well as heterologous desens

270 The augmentation of 5-HT2A receptor signaling by PSD-95 was not accompanied

271 ivation of CB2 receptors, which up-regulates 5-HT2A receptor signaling, enhances GRK5 expression; the

272 e tested the hypothesis that IL-6 influences 5-HT2A receptor signaling, providing a potential mechani

273 Galpha11 and DOI-induced desensitization of 5-HT2A receptor signaling.

274 L-6-induced JAK-STAT activation can regulate 5-HT2A receptor signaling.

275 animal model for studying alterations of the 5-HT2A receptor status with (123)I-5-I-R91150 micro-SPEC

276 nd 5-HT(1A) blockade may result in excessive 5-HT(2A) receptor stimulation, relative to 5-HT(1A) rece

277 er disentangle the specific contributions of 5-HT2A receptors, subjects were additionally pretreated

278 determine if IL-6 specifically regulates the 5-HT2A receptor system, we measured IP production mediat

279 New studies of the 5-HT(2A) receptor, the glucocorticoid receptor, p11, mit

280 Up-regulation of KCC2 function by targeting 5-HT(2A) receptors, therefore, has therapeutic potential

281 inase 2 (RSK2) physically interacts with the 5-HT(2A) receptor third intracellular (i3) loop and modu

282 tatory responses in the MOB were mediated by 5-HT2A receptors through a direct activation.

283 tive" arrestin mutant (Arr2-R169E) can force 5-HT(2A) receptors to be regulated by arrestins.

284 al neurons, and enhances the localization of 5-HT(2A) receptors to the cell periphery.

285 thyl-5-HT), or an antagonist (ritanserin) of 5-HT(2A) receptors to the primary auditory cortex and di

286 t-independent interaction of Arr2-R169E with 5-HT(2A) receptors was inhibited by inverse agonist trea

287 last line, stably transfected with the human 5-HT2A receptor, was treated with cis-UCA.

288 1A1 cell line, which expresses both IL-6 and 5-HT2A receptors, we found that IL-6 attenuates inositol

289 -pacemakers require endogenous activation of 5-HT2A receptors, we tested the hypothesis that 5-HT2A r

290 ortical regions (by 11.1% +/- 6.0%), whereas 5-HT(2A) receptors were also modestly lower (by 8.6% +/-

291 Both 5-hydroxytryptamine(2C) (5-HT(2C)) and 5-HT(2A) receptors were coexpressed in POMC neurons.

292 ptors as well as 125I-LSD-labeled binding of 5-HT(2a) receptors were evaluated in four groups of male

293 When 5-HT(2A) receptors were expressed in human embryonic kid

294 Immunofluorescence microscopy revealed that 5-HT(2A) receptors were trapped in early endosome antige

295 Here we investigated whether 5-HT2A receptors were up-regulated during gestation and

296 ntified by their high affinity for serotonin 5-HT(2A) receptors, which is also the target of LSD-like

297 unprecedented level of signaling bias at the 5-HT2A receptor, which could help interrogate the import

298 dinated changes in the function of 5-HT7 and 5-HT2A receptors, which mediate different aspects of the

299 mer (6d; K(i) = 0.5 nM) was found to bind at 5-HT(2A) receptors with an affinity similar to that of R

300 signaling by facilitating the interaction of 5-HT(2A) receptors with Galpha(q).