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 produced by enterochromaffin cells is critical in mo

6 5HT(1A)R was highly purified by taking advantage of the

7 5HT(2B) was found to be preferentially expressed by anti

8 5HT-containing enteroendocrine cells are most numerous i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 Colocalization of NADPHd and 5HT within individual DR projection neurons indicates th

38 put to trigeminal structures, and ii) NO and 5HT may be simultaneously released to influence informat

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

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

41 n supports transporter protein stability and 5HT transport.

42 Triptans are 5HT(1B/1D) receptor agonists commonly prescribed for mig

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

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

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

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

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

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

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

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

51 Both 5HT-1A and alpha(1b) ADR mRNA were highly expressed thro

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

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

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

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

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

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

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

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

60 [125I]BDNF release was also modulated by 5HT(3) receptor ligands and by receptors coupled to aden

61 for heterogeneity between rostral and caudal 5HT neurons.

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

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

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

65 5HT transporter in brain regions containing 5HT projections (frontal, temporal and occipital cortex)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 rcentage of GABAergic neurons also expressed 5HT-1A or alpha(1b) ADR mRNA.

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

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

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

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

86 Following 5HT training, two antimnemonic treatments-reconsolidatio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 rter-mediated concentration of neurotoxin in 5HT neurons, may not involve 5HT receptor interaction, a

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

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

116 -DHT dose produced significant reductions in 5HT and 5HTP concentrations in all regions examined (5 m

117 e evaluated if 5,7-DHT-induced reductions in 5HT concentrations and synthesis rate in rat brain are b

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

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

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

121 f neurotoxin in 5HT neurons, may not involve 5HT receptor interaction, and does not depend on the fir

122 etes the brain of serotonin does not involve 5HT-transporter-mediated concentration of neurotoxin in

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

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

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

126 2-Me-5HT and tryptamine have been defined as partial agonists

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

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

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

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

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

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

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

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

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

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

137 described to influence DR responses, namely, 5HT-1A, alpha(1b) adrenergic (alpha(1b) ADR), and cortic

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

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

140 Likewise, non-5HT cells with diverse response profiles were identified

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

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

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

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

145 (5HT) or increase the postsynaptic action of 5HT.

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

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

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

149 The concentrations of 5HT and 5-hydroxytryptophan (5HTP, an index of 5HT synth

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

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

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

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

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

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

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

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

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

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

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

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

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

163 T and 5-hydroxytryptophan (5HTP, an index of 5HT synthesis) were measured in hypothalamus, cortex and

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 We report cell-specific regulation of 5HT biosynthesis by transient receptor potential V (TRPV

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

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

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

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

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

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

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

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

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

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

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

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

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

187 Two other 5HT reuptake blockers (chlorimipramine, alaproclate) als

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

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

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

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

192 R inhibition when administered with Fen plus 5HT.

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

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

195 on appears to be exerted through presynaptic 5HT(1B/1D) receptors in the dorsal horn to block synapti

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

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

198 sequence from the serotonin type-3 receptor (5HT(3)).

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

200 ns in all regions examined (5 microg reduced 5HT but not 5HTP), effects that were not blocked by fluo

201 velopmental defect is due in part to reduced 5HT inputs into daf-2/insulin neuroendocrine signaling.

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

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

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

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

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

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

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

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

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

215 Serotonin (5HT) is a pivotal signaling molecule that modulates beha

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

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

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

219 rge rates, depressed firing after serotonin (5HT)-1a agonist administration, and, except for the tran

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

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

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

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

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

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

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

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

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

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

230 pend on the drug's transport into serotonin (5HT) neurons via the 5HT transporter, few studies have c

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

232 Famide-like (FaRP) neuropeptides, serotonin (5HT) and dopamine expression, and ray morphology.

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

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

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

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

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

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

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

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

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

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

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

244 -hydroxy-(di-n-propylamino)tetralin (to slow 5HT neuronal firing rate) also failed to antagonize the

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

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

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

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

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

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

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

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

253 l firing rate) also failed to antagonize the 5HT depleting action of 5,7-DHT.

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

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

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

257 amine, alaproclate) also failed to block the 5HT and 5HTP depleting actions of 5,7-DHT.

258 late the expression of the gene encoding the 5HT synthesis enzyme tryptophan hydroxylase (tph-1) in t

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

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

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

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

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

264 nd does not depend on the firing rate of the 5HT neuron.

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

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

267 trimental to the anti-migraine action of the 5HT(IB/ID) receptor agonists known is triptans.

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

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

270 5HT receptor antagonist metergoline, or the 5HT(1A) agonist 8-hydroxy-(di-n-propylamino)tetralin (to

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 ansport into serotonin (5HT) neurons via the 5HT transporter, few studies have critically examined th

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

276 Pretreatment with the 5HT receptor antagonist metergoline, or the 5HT(1A) agon

277 Therefore, 5HT modulates macrophage polarization and contributes to

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

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

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

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

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

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

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

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

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

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

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

292 While 5HT decreased electrical coupling at synapses with weak

293 collagen either alone or in combination with 5HT.

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

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

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

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

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

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

300 n rat brain are blocked by pretreatment with 5HT-selective reuptake inhibitors.