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

3 It has high selectivity over 5-HT2A receptor.

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

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

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

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

8 good selectivity against the 5-HT2B and the 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 d expression of both HDAC2 and the serotonin 5-HT(2A) receptor.

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

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

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

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

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

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

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

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

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

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

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

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

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

25 acting at AMPA receptors and 5-HT acting at 5-HT(2A) receptors.

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

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

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

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

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

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

32 dose-related occupancy was also observed at 5-HT(2A) receptors.

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

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

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

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

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

38 ed up-regulation of frontal cortex serotonin 5-HT(2A) receptor (5-HT(2A)R) density in the adult offsp

39 elic drugs upon stimulation of the serotonin 5-HT(2A) receptor (5-HT(2A)R) in rodents.

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

41 In addition to the serotonin 5-HT(2A) receptor (5-HT(2A)R), the dopamine D(2) recepto

42 Here, we showed that the class A serotonin 5-HT(2A) receptors (5-HT(2A)Rs) affected the localizatio

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

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

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

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

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

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

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

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

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

52 e suppression of spontaneous activity, while 5-HT2A receptors act divisively on visual response gain

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

54 5-HT(2A) receptor activation by the 5-HT(2) receptor ago

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

56 Our lab has previously discovered that 5-HT(2A) receptor activation with the 5-HT(2) receptor s

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

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

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

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

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

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

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

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

65 Here we demonstrate the utility of the novel 5-HT2A receptor agonist radioligand, [(11)C]CIMBI-36, an

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

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

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

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

70 inical research into 5-Hydroxytryptamine 2A (5-HT2A) receptor agonists, such as psilocybin, show prom

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

72 y, the effects of 5-HT were mediated via the 5-HT(2A) receptor and master modulators of mitochondrial

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

74 5-HT(2A) receptors and choline acetyltransferase were lo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 The selective 5-HT2A receptor antagonist M100907 significantly attenua

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

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

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

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

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

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

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

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

101 1 antagonist, or by ketanserin, a serotonin 5-HT2A receptor antagonist.

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

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

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

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

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

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

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

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

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

111 5-HT2A receptor antagonists (including MDL-100907 and cy

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 trated in vivo binding to D(2) receptors and 5-HT(2A) receptors at steady state after 10 days of dail

127 ally and in the Western world, activation of 5-HT(2A) receptors at sub-behavioral levels may represen

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

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

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

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

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

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

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

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

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

137 5-HT(2A) receptor binding potential correlated negativel

138 0,907 in a PET imaging paradigm to assess 1) 5-HT(2A) receptor binding potential in euthymic subjects

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

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

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

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

143 5-HT(1A) and 5-HT(2A) receptor binding was significantly increased in

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

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

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

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

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

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

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

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

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

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

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

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

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

157 , expression and stimulation of human or rat 5-HT(2A) receptor by agonists such as serotonin or 2,5-d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 upt this interaction through targeting CB(1)-5-HT(2A) receptor heteromers in HEK293 cells and using a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 5-HT(2A) receptor inverse agonists thus represent a pote

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 d function in rodent cortical neurons, via a 5-HT(2A) receptor-mediated recruitment of the SIRT1-PGC-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 In vivo studies revealed that 5-HT(2A) receptor stimulation increased cortical mtDNA a

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

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

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

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

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

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

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

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

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

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

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

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

287 1A1 cell line, which expresses both IL-6 and 5-HT2A receptors, we found that IL-6 attenuates inositol

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

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

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

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

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

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

294 ine on the binding of [(11)C]Cimbi-36 to the 5-HT(2A) receptor, which has comparable sensitivity to 5

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

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

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

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

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

300 Subsequent pharmacological blockade of 5-HT(2A) receptors with ketanserin in RN-NSC-grafted rat