ライフサイエンスコーパス: 5HT

1 5HT and its analogues stimulated PI turnover and [Ca2+]i

2 5HT caused increased phosphorylation of extracellular si

3 5HT had inhibitory effects on Adelta and C fibre input t

4 5HT inhibited the LPS-induced release of proinflammatory

5 5HT levels increase in Mdr2(-/-) mice and in PSC human p

6 5HT produced by enterochromaffin cells is critical in mo

7 5HT(1A)R was highly purified by taking advantage of the

8 5HT(2B) was found to be preferentially expressed by anti

9 5HT-containing enteroendocrine cells are most numerous i

10 otonin 2C receptor (5-hydroxytryptamine(2C); 5HT(2C)) transcript, an RNA editing substrate in which u

11 )-DOI, 18 +/- 6; alpha-methyl-5HT, 22 +/- 3; 5HT, 40 +/- 7; 5-methoxy-dimethyl tryptamine, 64 +/- 27;

12 nce of cellular colocalization 3D5/TH or 3D5/5HT was rare.

13 surface is down-regulated when plasma 5HT ([5HT](ex)) is elevated.

14 syndrome (IBS) with diarrhoea (IBS-D) and a 5HT(4) partial agonist in IBS with constipation (IBS-C).

15 per (3)H-thymidine ((3)HTdR) demonstrated a 5HT dose-dependent increase, with no effect of Fen alone

16 Furthermore, fluoxetine, a 5HT transporter inhibitor, while having no effect alone,

17 ake and glutamate and pardoprunox which is a 5HT-1A agonist and a partial dopamine agonist.

18 ed controlled trials showed the benefit of a 5HT(3) antagonist in irritable bowel syndrome (IBS) with

19 Modulation of the TPH1/MAO-A/5HT/5HTR2A/2B/2C axis may represent a therapeutic approa

20 owing largely to the difficulty of accessing 5HT neurons for experimental manipulation.

21 hrough which a noxious stimulus can activate 5HT neurons of the NRM and in turn could trigger descend

22 pendent response to the human intruder after 5HT(2A) pharmacological antagonism, while CT/T/C individ

23 response to the human intruder threat after 5HT(2A) antagonism.

24 dergo incomplete metamorphosis) examined, AL 5HT neurons innervate the ispsilateral AL and project to

25 The evolution of AL 5HT neurons is discussed in the context of the physiolog

26 sent a transgenic route to selectively alter 5HT neuron gene expression.

27 y and examined the expression of 5HT(1A) and 5HT(2) receptors, and of the presynaptic 5HT transporter

28 f raphe 5-HT neurons, as well as 5HT(1A) and 5HT(2A) receptor hypersensitivity.

29 he five regions, as well as for 5-HT(1B) and 5HT(1D) receptors in DRG C(2), C(5) and T(5).

30 ncentrations of serotonin through 5HT-2A and 5HT-1A receptors.

31 proinflammatory cytokines, both 5HT(2B) and 5HT(7) receptors mediated the pro-M2 skewing effect of 5

32 f an anti-inflammatory state via 5HT(2B) and 5HT(7), whose identification as functionally relevant ma

33 RNA paranemic assembly of 3HT and 5HT complexes is blocked by single-base substitutions th

34 atonergic (MT1 and MT2) receptor agonist and 5HT(2C) antagonist that is an effective antidepressant i

35 Newer 5HT(3) antagonists and 5HT(4) agonists are under development.

36 dict response to both 5HT(3) antagonists and 5HT(4) agonists.

37 The release of both DA and 5HT from striatal slices of rats fed a high fat diet for

38 fusion system to assay the release of DA and 5HT from striatal slices preloaded with [(3)H]-DA or [(3

39 Studies have demonstrated defects of DA and 5HT neurotransmission in dietary fat induced obese anima

40 Selective 5-HT(2A) (DOI hydrochloride) and 5HT(7) (AS-19) agonists were administered intrathecally

41 tly expressed outward current to both NA and 5HT, but transient central and Substance P (SP)-insensit

42 Stressors release serotonin and 5HT(3) antagonists have been shown to inhibit the associ

43 Serotonin (5HT) receptor signaling and 5HT-related agents, such as the anorexogen fenfluramine

44 n supports transporter protein stability and 5HT transport.

45 grity, so that directional (basal or apical) 5HT secretion was measurable.

46 gh selectivity against interferences such as 5HT, ascorbic acid, urate, and acetaminophen; high sensi

47 sal firing of raphe 5-HT neurons, as well as 5HT(1A) and 5HT(2A) receptor hypersensitivity.

48 r hemisphere: cluster 1 and 3 showed Dip-AST/5HT immunostaining, whereas cluster 2 showed Dip-AST/Mas

49 t the 5HT reuptake transporter (SERT) and at 5HT receptors are separable mechanisms.

50 e program for future synaptic and behavioral 5HT responses, thus providing a mechanistic link for the

51 s in anxiety- and depression-like behaviors, 5HT levels, and behavioral response to antidepressant tr

52 icroscopy revealed intimate contacts between 5HT axons and NSCs (B1) or ependymal cells (E1) and thes

53 the other hand, we found that the agent bis-5HT-DTPA-Gd utilizes both mechanisms when activated.

54 e release of proinflammatory cytokines, both 5HT(2B) and 5HT(7) receptors mediated the pro-M2 skewing

55 y an apparently arbitrary retraction of both 5HT-induced and original synapses.

56 ut appear to partly predict response to both 5HT(3) antagonists and 5HT(4) agonists.

57 We conclude that a brainstem 5HT network integrates somatic and visceral inputs arisi

58 ng electrical coupling were less affected by 5HT treatment, as follows from the equations used for ca

59 is Na(+)- and Cl(-)-dependent, displaced by 5HT, and inhibited by fluoxetine, suggesting APP(+) spec

60 ic proteins during long-term facilitation by 5HT in Aplysia is delayed for several hours, suggesting

61 forms of plasticity, such as facilitation by 5HT, involve more delayed recruitment.

62 This effect was mediated by 5HT(2a) receptors which are expressed by PBel(CGRP) neur

63 for heterogeneity between rostral and caudal 5HT neurons.

64 n code that distinguishes rostral and caudal 5HT neurons.

65 ly enriched in developing rostral and caudal 5HT neurons.

66 s coding variants acting together can change 5HT transport as much as 40-fold in vitro.

67 5HT transporter in brain regions containing 5HT projections (frontal, temporal and occipital cortex)

68 Thus, we correlated 5HT(2A) binding potential (BP) and RNA gene expression i

69 Moreover, as the deficit in cortical 5HT(2A)R in Egr3(-/-) mice aligns with numerous studies

70 T-mediated outward currents and counteracted 5HT-induced hSERT currents, indicating ASP(+) possesses

71 uggesting that this channel activity couples 5HT and dopamine signaling.

72 The consequent decreased 5HT innervation of the mPFC was associated with mood and

73 B/2C antagonists or TPH1 inhibitor decreased 5HT levels as well as expression of fibrosis and inflamm

74 ns with numerous studies reporting decreased 5HT(2A)R levels in the brains of schizophrenia patients,

75 kout, we show that these molecularly defined 5HT neuron subtypes are functionally distinct.

76 e serotonergic neurons, had Ca(2+)-dependent 5HT release and selective 5HT uptake, exhibited spontane

77 wo systems, we showed that dorsal raphe (DR) 5HT neurons selectively targeted the PBel.

78 Specifically, early 5HT(1A) overexpression alters the program for future syn

79 Cells containing either 5HT or TH were found in all three sites, whereas cells c

80 Cells containing either 5HT or VAChT were found in all three sites.

81 few catecholaminergic cells expressed either 5HT-1A or alpha(1b) ADR mRNA.

82 Therefore, we propose that elevated [5HT](ex)"paralyzes" the translocation of SERT from intra

83 a demonstrate that, in response to elevated [5HT](ex), Rab4-GTP co-localizes with and binds to SERT.

84 be the purification of postmitotic embryonic 5HT neurons by flow cytometry for whole-genome microarra

85 We find that addition of exogenous 5HT to ascl1a-/- embryos at near physiological levels (m

86 t are located upstream of the Cre-expressing 5HT neurons.

87 while having no effect alone, suppressed Fen-5HT (3)HTdR inhibition when administered with Fen plus 5

88 ng the major neurotransmitters seen in fish (5HT) and mammals (ACh and adenosine).

89 en in the putative O2-sensing cells of fish (5HT) and those found in the glomus cells of mammals (ace

90 Following 5HT training, two antimnemonic treatments-reconsolidatio

91 nd, using immunohistochemistry, examined for 5HT and AVP afferent innervation/development to areas of

92 use lines, each of which provides a tool for 5HT neuron studies.

93 ive, i.e., were transneuronally labeled from 5HT neurons.

94 ition with reduced or little change in [(3)H]5HT and [(3)H]NE uptake inhibition relative to bupropion

95 ]dopamine ([(3)H]DA), [(3)H]serotonin ([(3)H]5HT), and [(3)H]norepinephrine ([(3)H]NE) uptake inhibit

96 terostatin did not alter [(3)H]-DA or [(3)H]-5HT release from striatal slices of rats adapted to high

97 n enhanced [(3)H]-DA release, but not [(3)H]-5HT release from striatal slices of rats that had been a

98 al slices preloaded with [(3)H]-DA or [(3)H]-5HT.

99 eported that stimulation of cells with high [5HT](ex) induces transamidation of a small GTPase, Rab4.

100 ce of plasma serotonin (5-hydroxytryptamine (5HT)).

101 ne hydroxylase (TH) and 5-hydroxytryptamine (5HT).

102 omaffin cell serotonin (5-hydroxytryptamine [5HT]) biosynthesis.

103 transmitter, serotonin (5-hydroxytryptamine, 5HT) regulates inflammation and tissue repair via a set

104 Serotonin (5-hydroxytryptamine; 5HT) functions in insects as a neurotransmitter, neuromo

105 Serotonin (5-hydroxytryptomine; 5HT) and serotonergic signaling pathways are important r

106 iation of SERT with Rab4-GTP depends on: (i) 5HT modification and (ii) the GTP-binding ability of Rab

107 ntly homologous to the CSD neuron, we imaged 5HT-like immunoreactivity in the brains of 40 species of

108 he insect brain) has one 5HT-immunoreactive (5HT-ir) neuron that projects into the protocerebrum, cro

109 ation animals show no significant changes in 5HT levels throughout the brain.

110 ptor expression produce permanent changes in 5HT synaptic function and associated behaviors.

111 etection of previously unobserved changes in 5HT(2C) editing in RNA samples isolated from different i

112 nal duplication animals showed a decrease in 5HT levels when compared to their wild type littermates,

113 stress blocked the CUS-induced decreases in 5HT soma within the DRif and its projections to the mPFC

114 Corresponding diversity in 5HT neuronal phenotypes is becoming apparent and is like

115 Cre recombinase is selectively expressed in 5HT neurons (ePet-Cre mice).

116 ed expression of hundreds of unique genes in 5HT neurons, thus providing an abundance of new serotone

117 ion in Hcrt, HA, and ACh neurons (but not in 5HT neurons) was consistently elevated in VEH- and ALM-t

118 s and RNA measurements showed a reduction in 5HT(2A) BP and gene expression specifically in the right

119 and binding revealed nearly 70% reduction in 5HT(2A)R expression in the prefrontal cortex of Egr3(-/-

120 enteroendocrine cells of mediators including 5HT, CCK, GLP-1, PYY and ghrelin that act on vagal affer

121 Fluoxetine exposure also increased 5HT and AVP afferent development to brain areas implicat

122 times less potent than APP(+) at inhibiting 5HT uptake and has minimal hSERT-mediated uptake.

123 g, with a critical role for the right insula 5HT(2A) in the regulation of affective responses to thre

124 Even mutants completely lacking 5HT or SERT can partially respond to fluoxetine and imip

125 timulates aggressive behavior and alters LAH 5HT and AVP development, yet only alterations in AVP aff

126 an excess of 5HT in IBS-D and abnormally low 5HT availability in IBS-C.

127 pull-down assay, the interaction between MBP-5HT(3A)-ICD constructs and RIC-3 was investigated.

128 2-Me-5HT and tryptamine have been defined as partial agonists

129 t interactions are similar for 5-HT and 2-Me-5HT but slightly different for tryptamine.

130 In contrast, 2-Me-5HT is not a genuine partial agonist since priming is no

131 The activation pattern is similar for 2-Me-5HT only at very low concentrations since profound chann

132 addition to confirming the direct medullary 5HT projection to the spinal cord we also observed large

133 VM are postsynaptic to midbrain or medullary 5HT neurons.

134 e of 38.2 mm Hg; P < 0.001) and alpha-methyl-5HT (250 microg lowered IOP 30.8% from baseline of 41.8

135 ne, 8 +/- 4; (R)-DOI, 18 +/- 6; alpha-methyl-5HT, 22 +/- 3; 5HT, 40 +/- 7; 5-methoxy-dimethyl tryptam

136 ear extremes in either oligomerization (mono-5HT-DTPA-Gd) or protein-binding in their activation mech

137 Moreover, 5HT(2A) BP in both regions was a good predictor of the s

138 genome-wide RNA-seq to deconstruct the mouse 5HT system at multiple levels of granularity-from anatom

139 ine), NATau (N-arachidonoyl taurine), and NA-5HT (N-arachidonoyl serotonin), all displaced [(3)H]TTA-

140 Newer 5HT(3) antagonists and 5HT(4) agonists are under develop

141 study the interplay between the 5HT and non-5HT systems.

142 ia feedforward connections with multiple non-5HT descending control pathways.

143 l cord we also observed large numbers of non-5HT neurons, in the medullary nucleus reticularis gigant

144 Abnormalities of 5HT-1A receptor ligands have been reported in temporal l

145 nly 5HT(7) mediated the inhibitory action of 5HT on the release of proinflammatory cytokines, both 5H

146 (5HT) or increase the postsynaptic action of 5HT.

147 the context of the physiological actions of 5HT observed in the lepidopteran AL.

148 at fight less, whereas induced activation of 5HT neurons promotes aggression.

149 enzymes for the synthesis and catabolism of 5HT, respectively.

150 Removal or doubling the concentration of 5HT in WT embryos does not significantly affect anterogr

151 a mechanism of subregion-selective death of 5HT neurons in the dorsal raphe, a defined neuroanatomic

152 pendent and subregion-specific cell death of 5HT neurons in the dorsal raphe.

153 inically relevant resource for definition of 5HT neuron subtypes and elucidation of the genetic netwo

154 ulation, rather than universal disruption of 5HT synaptic development.

155 determine if the peripheral distribution of 5HT(1B/1D/1F) receptors showed any anatomical difference

156 To examine the phylogenetic distribution of 5HT-ir neurons apparently homologous to the CSD neuron,

157 The fact that the modulatory effect of 5HT on electrical connections was negatively correlated

158 We have examined the effect of 5HT on electrical synapses possessing variable coupling

159 eptors mediated the pro-M2 skewing effect of 5HT.

160 Several studies have described an excess of 5HT in IBS-D and abnormally low 5HT availability in IBS-

161 s postnatally and examined the expression of 5HT(1A) and 5HT(2) receptors, and of the presynaptic 5HT

162 mined the specific microRNA "fingerprint" of 5HT neurons and identified a strong microRNA-target inte

163 turbation, further elucidating the impact of 5HT(2C) RNA editing on central nervous system function.

164 rium, partly because of reduced induction of 5HT production in response to butyrate and decreased sec

165 Int) mice did not increase mucosal levels of 5HT in response to S. typhimurium infection, and succumb

166 outputs independently of synaptic levels of 5HT.

167 UNEL)-positive soma and the eventual loss of 5HT neurons in the DRif and its projections to the mPFC

168 rain development, and early perturbations of 5HT receptor expression produce permanent changes in 5HT

169 al genetics, we restricted the population of 5HT neurons that can be reproducibly manipulated to iden

170 The presence of 5HT- and TH-immunoreactive cells in the aorta, pulmocuta

171 The presence of 5HT- and VAChT-immunoreactive cells in segments of the c

172 f the Tph1 gene and subsequent production of 5HT in response to bacterial infection in mice.

173 ignal-to-background ratio and reliability of 5HT release assays.

174 obial components that alter the secretion of 5HT.

175 The significance of 5HT underscores the importance of elucidating the molecu

176 ediated recombination at different stages of 5HT neuron development.

177 of tools for in vivo and in vitro studies of 5HT neurons.

178 Expression of engrailed genes in a subset of 5HT neurons in the rostral domain further distinguished

179 Therapeutic targeting of 5HT(2A) receptors during DENV infection effectively prev

180 (1)-R are strikingly different from those of 5HT-2C and EGF receptors, which demonstrate the usefulne

181 d, blinded, parallel, or crossover trials of 5HT(4) agonists, D(2) receptor antagonist, or ghrelin ag

182 inatal ETS exposure elicited upregulation of 5HT(1A) receptor expression without parallel changes in

183 ion, and enhanced phagocytosis, dependent on 5HT(2A) receptors.

184 factory centers in the insect brain) has one 5HT-immunoreactive (5HT-ir) neuron that projects into th

185 Whereas only 5HT(7) mediated the inhibitory action of 5HT on the rele

186 tein EGL-30, independent of SER-1, SER-4, or 5HT.

187 lls were unaffected directly by either NA or 5HT.

188 ds acting via some combination of DA, NE, or 5HT inhibition and/or antagonism of alpha4beta2-nAChR ca

189 than (2S,3S)-4a for inhibition of DA, NE, or 5HT uptake.

190 l principles underlying system organization, 5HT neuron subtypes, constellations of differentially ex

191 and trafficking of SERT via Rab4 in a plasma 5HT-dependent manner.

192 ating the mechanism by which elevated plasma 5HT level down-regulates the density of SERT molecules o

193 atelet surface is down-regulated when plasma 5HT ([5HT](ex)) is elevated.

194 proliferation in MVIC cultures with Fen plus 5HT exposure.

195 R inhibition when administered with Fen plus 5HT.

196 ems, perhaps by down-regulating postsynaptic 5HT 2B/2C receptors.

197 and 5HT(2) receptors, and of the presynaptic 5HT transporter in brain regions containing 5HT projecti

198 r (GR) and an increase in serotonin receptor 5HT-1a, consistent with the decreased anxiety phenotype.

199 rotonin action is the serotonin 2A receptor (5HT(2A)).

200 Instead, selective serotonin 2A receptor (5HT(2A)R) antagonists ketanserin and MDL-11939 replicate

201 on and tissue repair via a set of receptors (5HT(1-7)) whose pattern of expression varies among cell

202 s and tricyclic antidepressants may regulate 5HT outputs independently of synaptic levels of 5HT.

203 f a Pet-1 enhancer region to direct reliable 5HT neuron-specific transgene expression in the CNS.

204 ve membrane properties of midbrain reticular 5HT neurons, which heretofore have not been reported to

205 (Ep), in the presence of Serotonine-5-HT (S-5HT), Dopamine (DA), Nor-Epineprhine (Nor-Ep), Ascorbic

206 nificant variation in the amount of secreted 5HT was present among tissues derived from five differen

207 d Ca(2+)-dependent 5HT release and selective 5HT uptake, exhibited spontaneous action potentials and

208 ic targets of serotonin (5HT), the selective 5HT reuptake inhibitor (SSRI) fluoxetine (Prozac), the t

209 Serotonergic (5HT) neurons exert diverse and widespread functions in t

210 Serotonergic (5HT) neurons modulate diverse behaviors and physiology a

211 ections arising from brainstem serotonergic (5HT) neurons contribute to both facilitatory and inhibit

212 cant contribution of brainstem serotonergic (5HT) systems to the control of spinal cord "pain" transm

213 ole of microRNAs in regulating serotonergic (5HT) neuron activity.

214 We show that serotonergic (5HT) axons originating from a small group of neurons in

215 Serotonin (5HT) has long been implicated in the regulation of aggre

216 Serotonin (5HT) is a critical modulator of neural circuits that sup

217 Serotonin (5HT) is a neuroendocrine hormone synthetized in the cent

218 Serotonin (5HT) receptor signaling and 5HT-related agents, such as

219 Serotonin (5HT) systems play important roles in brain development,

220 Serotonin (5HT) triggered growth of new presynaptic varicosities, a

221 the monoamines dopamine (DA) and serotonin (5HT) and the monoamine-metabolizing enzyme monoamine oxi

222 tein subunit alpha-gustducin, and serotonin (5HT) as markers of type I, II, and III taste cells, resp

223 ), tyrosine hydroxylase (TH), and serotonin (5HT) by double immunolabelings.

224 sexta allatotropin (Mas-AT), and serotonin (5HT) raised in the same host species revealed three spat

225 ne (NE), acetylcholine (ACh), and serotonin (5HT) serve important functions in sensory perception.

226 ), tyrosine hydroxylase (TH), and serotonin (5HT) to identify putative O2-sensing cells in Rana cates

227 in catecholamine synthesis), and serotonin (5HT) to identify putative oxygen-sensing cells and to de

228 al stainings against synapsin and serotonin (5HT), we describe the overall layout as well as the fine

229 nucleus containing dopamine (DA), serotonin (5HT), gamma-aminobutyric acid (GABA) and glutamate neuro

230 ecular architecture of developing serotonin (5HT) neurons is poorly understood, yet its determination

231 ally associated with dysregulated serotonin (5HT) transmission in the medial prefrontal cortex (mPFC)

232 nic-stress-induced alterations in serotonin (5HT) neurons.

233 Monoamine serotonin (5HT) has been linked to aggression for many years across

234 to better understand the role of serotonin (5HT) in cocaine abuse and treatment, we examined the eff

235 rs found that genetic deletion of serotonin (5HT) neurons in the brainstem also prevented arousal fro

236 ons may potentiate the release of serotonin (5HT) or increase the postsynaptic action of 5HT.

237 was regulated by the activity of serotonin (5HT) type-1B receptors and correlated with altered 5HT1B

238 we dissect the genetic targets of serotonin (5HT), the selective 5HT reuptake inhibitor (SSRI) fluoxe

239 H neurones, noradrenaline (NA) or serotonin (5HT) were briefly applied in the superfusing artificial

240 subtype of EE cells that produce serotonin (5HT).

241 e regulatory processes supporting serotonin (5HT) transporter (SERT) capacity including regulated tra

242 We found that serotonin (5HT), a monoamine affected in autism, was elevated in th

243 Here, we show that serotonin (5HT), which is known to regulate gamma power, acts via 5

244 ession and the development of the serotonin (5HT) and vasopressin (AVP) neural systems modulating thi

245 holamine transporters but not the serotonin (5HT) transporter.

246 cetylcholine; ACh), dorsal raphe (serotonin; 5HT), and singly labeled Fos(+) cells in the locus coeru

247 proteins, a pattern consistent with specific 5HT receptor dysregulation, rather than universal disrup

248 editing differences in alternatively spliced 5HT(2C) variants.

249 were screened for their ability to stimulate 5HT secretion.

250 These results indicate that supraependymal 5HT axons directly interact with NSCs to regulate neurog

251 s, and in penetrance between lines targeting 5HT neurons.

252 Our results indicate that 5HT neurons influence "pain" processing at the spinal co

253 ndependent of SLC6A4 genotype, revealed that 5HT(2A) BP in the adjacent right anterior insula and ins

254 uppressive effects of SGAs, and suggest that 5HT(2A)Rs may also contribute to the sedating properties

255 aptic partners (GRASP) analyses suggest that 5HT-PLP neurons form contacts with 5HT1A receptor-expres

256 ce classifies molecular diversity across the 5HT system and discovers sertonergic subtypes, markers,

257 haracterizing molecular variation across the 5HT system is lacking, as is concomitant linkage to cell

258 We also show that dopamine antagonizes the 5HT action via the 5HT-gated ion channel MOD-1 signaling

259 t action of fluoxetine and imipramine at the 5HT reuptake transporter (SERT) and at 5HT receptors are

260 ons so as to study the interplay between the 5HT and non-5HT systems.

261 ophrenia patients, and the gene encoding the 5HT(2A)R is itself a leading schizophrenia candidate gen

262 B1 cells express the 5HT receptors 2C and 5A.

263 ility of the Gd ion and low toxicity for the 5HT-based agents, suggesting that these agents are suita

264 tracer, wheat germ agglutinin (WGA), in the 5HT neurons so as to study the interplay between the 5HT

265 The enhancement in the 5HT secretion behavior was consistent over time from a s

266 tomography was used to assess changes in the 5HT transporter and 2A receptor binding potential (BP).

267 Functional output of the 5HT system was assessed using prolactin levels.

268 d and [(35)S]GTPgammaS binding assays of the 5HT(1A) and EDG(1) GPCRs confirmed that they were proper

269 s not achieved by targeted retraction of the 5HT-induced varicosities but, rather, by an apparently a

270 , which can be released by activation of the 5HT-PLP neurons.

271 brainstem regions differentially target the 5HT neurons of the dorsal raphe (DR) and the nucleus rap

272 p spinal cord laminae V-VIII and targets the 5HT neurons of the NRM, but not of the DR.

273 lar neurons are not only postsynaptic to the 5HT neurons of the medulla, but that most are also at th

274 dopamine antagonizes the 5HT action via the 5HT-gated ion channel MOD-1 signaling, suggesting that t

275 tly boosted the number of EC cells and their 5HT secretion by up to 430 and 390%, respectively.

276 Therefore, 5HT modulates macrophage polarization and contributes to

277 networks that influence the output of these 5HT neurons.

278 ological concentrations of serotonin through 5HT-2A and 5HT-1A receptors.

279 outward current to NA and inward current to 5HT.

280 ted that these effects were primarily due to 5HT-induced modulation of membrane currents that indirec

281 minoglycan to (3)HTdR in MVIC, normalized to 5HT alone, demonstrated a significant imbalance of extra

282 , a 5HT1 receptor, abolishes the response to 5HT but has only a minor effect on the response to imipr

283 exhibit a decreased head-twitch response to 5HT(2A)R agonist 1-(2,5-dimethoxy 4-iodophenyl)-2-amino

284 to imipramine while leaving the responses to 5HT or fluoxetine intact.

285 6A4 genotyped marmosets with responsivity to 5HT(2A) antagonism during the human intruder test of anx

286 f electrical coupling could be due solely to 5HT effects on H-channel conductance.

287 ach representing at least 0.25% of the total 5HT(2C) transcripts.

288 quantify accurately the expression of twenty 5HT(2C) isoforms, each representing at least 0.25% of th

289 rotonergic input from the DR to the PBel via 5HT(2a) receptors is critical for modulating the sensiti

290 aintenance of an anti-inflammatory state via 5HT(2B) and 5HT(7), whose identification as functionally

291 nses and tissue repair, we evaluated whether 5HT modulates human macrophage polarization.

292 A third line in which 5HT neurons are marked with yellow fluorescent protein w

293 While 5HT decreased electrical coupling at synapses with weak

294 collagen either alone or in combination with 5HT.

295 However, Fen combined with 5HT increased the level of MVIC extracellular signal-rel

296 In contrast, Fen combined with 5HT inhibited the MVIC (3)HTdR response when compared wi

297 the MVIC (3)HTdR response when compared with 5HT alone.

298 ar signal-related kinase, when compared with 5HT alone.

299 minoglycan respectively, were increased with 5HT alone; however, Fen did not affect MVIC glycosaminog

300 Modification with 5HT stabilizes Rab4 in its active, GTP-bound form, Rab4-