ライフサイエンスコーパス: 5-HT(3) receptor

1 ory responses through ligand-gated channels (5-HT3 receptors).

2 loop and the critical role of Pro 8* in the 5-HT3 receptor.

3 ding preferentially to the open state of the 5-HT3 receptor.

4 em acts by causing open-channel block of the 5-HT3 receptor.

5 sis (CoMFA) is applied to antagonists of the 5-HT3 receptor.

6 of agonists to the desensitized form of the 5-HT3 receptor.

7 r is the best-characterized heteropentameric 5-HT3 receptor.

8 neuronal activation in the DVC by activating 5-HT3 receptors.

9 Extrinsic nerves are activated by 5-HT3 receptors.

10 ction is not clear and may involve hindbrain 5-HT3 receptors.

11 e nerve responses apparently by blocking the 5-HT3 receptors.

12 ze a 5-HT-containing pathway which activates 5-HT3 receptors.

13 holecystokinin A receptors and serotonin via 5-HT3 receptors.

14 s high-affinity CCK-A receptors also express 5-HT3 receptors.

15 nly high- or low-affinity CCK-A receptors or 5-HT3 receptors.

16 may also be responsive to serotonin through 5-HT3 receptors.

17 nd 31 units, respectively, by activating the 5-HT3 receptors.

18 and is an antagonist of serotonin 5-HT2 and 5-HT3 receptors.

19 receptor subunit (5-HT3A) yields functional 5-HT3 receptors.

20 ediated by 5-HT in the colonic mucosa and by 5-HT3 receptors.

21 alterations in the neuronal distribution of 5-HT3 receptors.

22 se and differential expression of 5-HT1A and 5-HT3 receptors.

23 ch activates an inhibitory pathway involving 5-HT3 receptors.

24 One of these is the ionotropic 5-HT(3) receptor.

25 nt determinant of agonist recognition at the 5-HT(3) receptor.

26 ient kinetic investigations of the serotonin 5-HT(3) receptor.

27 ed the highest affinity (pK(i) > 10) for the 5-HT(3) receptor.

28 at expression of gLTD involves activation of 5-HT(3) receptor.

29 f 5-HT receptors, including the 5-HT type-3 (5-HT3) receptors.

30 that was in part mediated by 5-HT acting via 5-HT(3) receptors.

31 smission via a facilitatory action at spinal 5-HT(3) receptors.

32 ic afferent endings via both 5-HT(3) and non-5-HT(3) receptors.

33 me superfamily, including GABA(A), nACh, and 5-HT(3) receptors.

34 y prevented by functional blockade of spinal 5-HT(3) receptors.

35 s multimodal subunit-dependent antagonism of 5-HT(3) receptors.

36 gonist, is a potent competitive inhibitor of 5-HT(3) receptors.

37 actions on 5-HT-evoked currents mediated by 5-HT(3) receptors.

38 d at 20 degrees or when an antagonist of the 5-HT3 receptor, [3H]granisetron, was used as the radioli

39 onses elicited by systemic injections of the 5-HT(3) receptor (5-HT(3)R) agonists such as phenylbigua

40 The molecular makeup of the serotonin 5-HT(3) receptor (5-HT(3)R) channel was investigated in

41 The serotonin 5-HT(3) receptor (5-HT(3)R) is a member of the cys-loop

42 The serotonin 5-HT(3) receptor (5-HT(3)R) is a member of the Cys-loop

43 sal enterochromaffin cells and activation of 5-HT(3) receptors (5-HT(3)Rs) on neurons in the gut wall

44 ass of negative allosteric modulators of the 5-HT(3) receptors (5-HT(3)Rs).

45 The 5-HT3 receptor (5-HT3R) antagonist Alosetron (Alos) redu

46 permeability seen in native and recombinant 5-HT3 receptor (5-HT3R) channels, we reported previously

47 The kinetics of desensitization of the 5-HT3 receptor (5-HT3R)-gated ion channel were investiga

48 spinal dorsal horn via activation of spinal 5-HT3 receptors (5-HT3Rs).

49 ave the capacity to synthesize two different 5-HT3 receptors, 5-HT3A+/3B- and 5-HT3A+/3B+ receptors.

50 of the 5-HT3A receptor subunit rendered the 5-HT3 receptor 70-fold more sensitive to serotonin and p

51 st channel conductance displayed by neuronal 5-HT3 receptors (9-17 pS).

52 The 5-HT(3) receptor, a pentameric ligand-gated ion channel

53 e activity of this compound class verses the 5-HT(3) receptor, a structural homologue of the alpha7 n

54 ond messenger pathways, or to the ionotropic 5-HT3 receptor, a non-selective cation channel that medi

55 bout PKC modulation of the serotonin type 3 (5-HT3) receptor, a ligand-gated membrane ion channel tha

56 nthesize at least two structurally different 5-HT(3) receptors: a heteromeric 5-HT(3A/3B) receptor an

57 I cells activates gustatory nerve fibers via 5-HT3 receptors, accounting for a significant proportion

58 m, these results suggest that stimulation of 5-HT3 receptors activates an intracellular signalling ca

59 ate in the inhibition of aggression, whereas 5-HT3 receptor activation facilitates aggression, the au

60 This excitatory response to 5-HT3 receptor activation may be partly a direct postsyn

61 tamine (5-HT)1A receptors and facilitated by 5-HT3 receptor activation.

62 response was regulated by serotonin Type 3 (5-HT(3)) receptor activity and correlated with altered 5

63 of descending serotonergic pathways or tonic 5-HT3 receptor activity in maintaining hypersensitivity

64 Likewise, posterior IC administration of the 5-HT(3) receptor agonist m-chlorophenylbiguanide (mCPBG)

65 ptor by intrathecal injection of a selective 5-HT(3) receptor agonist, SR57227, induced spinal glial

66 icrog kg(-1)) and PBG (100 microg kg(-1)), a 5-HT(3) receptor agonist, stimulated nine ischaemically

67 T(3B) with 5-HT(3A) modified the duration of 5-HT(3) receptor agonist-induced responses, linearized t

68 Pretreatment of ganglia with the 5-HT3 receptor agonist 1-m-(chlorophenyl) biguanide (m-C

69 ione (DNQX) on the excitatory actions of the 5-HT3 receptor agonist 1-phenylbiguanide (PBG) were stud

70 Only the 5-HT3 receptor agonist altered the quality of the lordos

71 A 5-HT3 receptor agonist CPBG (1 microM), mimicked the unm

72 that phenyldiguanide (later recognized as a 5-HT3 receptor agonist) stimulated the firing of C-fibre

73 This initial response was mimicked by the 5-HT3 receptor agonist, 2-methyl-5-HT, whereas 5-methoxy

74 sed with the 5-HT1A receptor agonist and the 5-HT3 receptor agonist, m-chlorophenyl-biguanide (mCPBG;

75 The 5-HT3 receptor agonist, m-chlorophenylbiguanide (mCPBG),

76 retic application of PBG, a highly selective 5-HT3 receptor agonist, significantly increased activity

77 2-methylserotonin (100 microg kg-1, i.a.), a 5-HT3 receptor agonist, stimulated eleven of twelve affe

78 In contrast, 5-HT(3) receptor agonists increased sEPSCs on a minority

79 5-HT(3) receptor agonists increased the firing rate of T

80 5-HT(3) receptor agonists increased the frequency, but n

81 These findings suggest that tachyphylaxis to 5-HT(3) receptor agonists may be due to the desensitizat

82 r antagonist ondansetron and mimicked by the 5-HT(3) receptor agonists SR5227 and mCPBG.

83 5-HT(3) receptor agonists stimulate intestinal motility,

84 milar before and after the injections of the 5-HT(3) receptor agonists.

85 pressure and cardiac output elicited by the 5-HT(3)-receptor agonists, phenylbiguanide (100 microg/k

86 data are consistent with the hypothesis that 5-HT3 receptor agonists activate DVMN neurones partly by

87 urrent by low concentrations of bath-applied 5-HT3 receptor agonists is compatible with the cyclic mo

88 The effects of 5-HT3 receptor agonists on cortical circuit response pro

89 The effect was mimicked by two other 5-HT3 receptor agonists, 2-methyl-5-HT and m-chloropheny

90 by white matter stimulation were reduced by 5-HT3 receptor agonists, whereas the frequency of sponta

91 With the exception of the 5-HT3 receptor, all of the cloned serotonin receptors be

92 ude that colonic sensory neurones expressing 5-HT(3) receptors also functionally express the receptor

93 Functional down-regulation of 5-HT(3) receptors also occurs in the post-infected anima

94 Neuronal 5-HT3 receptors also display a permeability to calcium i

95 genetic or pharmacological disruption of the 5-HT(3) receptor, an excitatory serotonin-gated ion chan

96 n the basis of its ability to inactivate the 5-HT3 receptor, an excitatory serotonin-gated ion channe

97 mechanisms underlying the activation of the 5-HT(3) receptor and its contribution to facilitation of

98 sion of the functional 5-HT3A subunit of the 5-HT3 receptor and the central CB1 cannabinoid receptor

99 erents, mainly through direct stimulation of 5-HT3 receptors and that the action of 5-HT on these aff

100 allosteric regulation of agonist binding to 5-HT3 receptors and the first example of a ligandgated i

101 ether gustatory afferents express functional 5-HT3 receptors and, if so, whether these receptors play

102 notropic glycine receptor, GABA(A) receptor, 5-HT(3) receptor, and nAChR subunits contain a pair of h

103 face at both homomeric and heteromeric human 5-HT(3) receptors, and explain why the competitive pharm

104 e receptors, GABA(A) receptors, serotonin-3 (5-HT(3)) receptors, and glutamate-gated chloride ion cha

105 -application of 5-HT (300 microM), acting at 5-HT3 receptors, and ACh (3 mM) or ATP (1 mM) were addit

106 of disgust and taste avoidance by selective 5-HT(3) receptor antagonism/agonism in the posterior (gr

107 sponses to 2-methyl-5-HT were blocked by the 5-HT(3) receptor antagonist alosetron (2 x 10(-7) M), wh

108 etic risk radiation therapy should receive a 5-HT(3) receptor antagonist before each fraction and for

109 The 5-HT(3) receptor antagonist granisetron (1 microM) and t

110 Treatment of ganglia with the 5-HT(3) receptor antagonist MDL 72222 (0.5 microM) durin

111 Pretreatment of ganglia with the 5-HT(3) receptor antagonist ondansetron (0.4 microm) alo

112 TS-TH-EGFP neurons, an effect blocked by the 5-HT(3) receptor antagonist ondansetron and mimicked by

113 to treat morphine dependence, also exhibited 5-HT(3) receptor antagonist properties.

114 response to acetylcholine was blocked by the 5-HT(3) receptor antagonist renzapride with a similar IC

115 Pretreatment of ganglia with the 5-HT(3) receptor antagonist tropisetron (0.5 microM) com

116 or any highly emetic agents should receive a 5-HT(3) receptor antagonist, dexamethasone, and a neurok

117 etron (300 microg kg(-1), I.V.), a selective 5-HT(3) receptor antagonist, eliminated the afferent's r

118 Intracranial administration of the 5-HT(3) receptor antagonist, ondansetron (OND), to the p

119 The 5-HT(3) receptor antagonist, ondansetron, has been shown

120 tion and predict therapeutic response to the 5-HT(3) receptor antagonist, ondansetron.

121 Aprepitant, a 5-HT3 receptor antagonist (5HT3-RA), and dexamethasone a

122 Similar pretreatment with the 5-HT3 receptor antagonist 3-tropanyl-3,5-dichlorobenzoat

123 kg-1, i.v.), or treatment with the selective 5-HT3 receptor antagonist alosetron (30 microg kg-1, i.v

124 Although tropisetron is a 5-HT3 receptor antagonist and an alpha7nAChR partial ago

125 1) receptor antagonist in conjunction with a 5-HT3 receptor antagonist and corticosteroid in patients

126 Rolapitant in combination with a 5-HT3 receptor antagonist and dexamethasone is well tole

127 Rolapitant in combination with a 5-HT3 receptor antagonist and dexamethasone is well-tole

128 isetron; 500 ng), or were coinfused with the 5-HT3 receptor antagonist and the 5-HT2A/2C receptor ago

129 o 3.8 +/- 1.1 spikes s(-1)) by the selective 5-HT3 receptor antagonist granisetron.

130 coefficient = 1.8) that were blocked by the 5-HT3 receptor antagonist ondansetron (IC50 = 103 pM) an

131 led to do so in Tph1(-/-) colon; and (9) the 5-HT3 receptor antagonist ondansetron, which reduced CMM

132 ivity effect of intrathecal injection of the 5-HT3 receptor antagonist ondansetron.

133 otetralin (DPAT; 0.1 mg/kg and 0.3 mg/kg) or 5-HT3 receptor antagonist tropisetron (0.3 mg/kg) treatm

134 d Fos-LI in the DVC of ondansetron (1 mg/kg; 5-HT3 receptor antagonist) and vehicle-treated rats foll

135 Rats were infused with the 5-HT3 receptor antagonist, 3-tropanyl-indole-3 carbonyla

136 A combination of aprepitant, a 5-HT3 receptor antagonist, and dexamethasone is recommen

137 combination of an NK1 receptor antagonist, a 5-HT3 receptor antagonist, and dexamethasone.

138 ICS205-930 (1 microM), a 5-HT3 receptor antagonist, completely blocked the 5-HT-i

139 -HT response was completely abolished by the 5-HT3 receptor antagonist, granisetron (0.5 mg kg-1).

140 njection of tropisetron (200 microg kg-1), a 5-HT3 receptor antagonist, significantly attenuated the

141 fusions with 100 ng, 250 ng or 500 ng of the 5-HT3 receptor antagonist, tropisetron.

142 and 5-HT4 receptor antagonists, but not by a 5-HT3 receptor antagonist.

143 was less affected by VMN infusions with the 5-HT3 receptor antagonist.

144 urthermore, this mutation also converted the 5-HT3 receptor antagonist/very weak partial agonist, apo

145 rolapitant, in combination with a serotonin (5-HT3) receptor antagonist and dexamethasone, for the pr

146 f ondansetron, a selective serotonin type-3 (5-HT3) receptor antagonist, attenuates cholecystokinin (

147 rotonin and this effect was blocked with the 5-HT3-receptor antagonist ondansetron.

148 ) and palonosetron (a 5-hydroxytryptamine-3 [5-HT3] receptor antagonist) for the prevention of acute

149 5-HT(3) receptor antagonists have proved effective in su

150 5-HT(3) receptor antagonists reduce symptoms of IBS clin

151 ative efficacy of the 5-hydroxytryptamine-3 (5-HT(3)) receptor antagonists.

152 wide dynamic range neurons are inhibited by 5-HT3 receptor antagonists in rats following spinal nerv

153 whisking frequencies, and selective 5-HT2 or 5-HT3 receptor antagonists suppress this rhythmic firing

154 Unilateral infusion of selective 5-HT2 or 5-HT3 receptor antagonists suppresses ipsilateral whiski

155 by DPPIV inhibition or by cholecystokinin or 5-HT3 receptor antagonists, but was inhibited by atropin

156 nged efficacy, and acts synergistically with 5-HT3 receptor antagonists.

157 The 5-HT3 receptor "antagonists' (+)-tubocurarine and quipaz

158 Given that both GABA(A) and 5-HT(3) receptors are involved in the generation of DRRs

159 Probably the most studied modulators of 5-HT(3) receptors are the high affinity competitive 'set

160 5-Hydroxytryptamine type 3 (5-HT(3)) receptors are cation-selective Cys loop recepto

161 oline (nACh) and 5-hydroxytryptamine type 3 (5-HT(3)) receptors are cation-selective ion channels of

162 5-Hydroxytryptamine type 3 (5-HT(3)) receptors are ligand-gated ion channels that pl

163 The 5-HT3 receptors are serotonin-gated ion channels that ph

164 5-hydroxytryptamine type 3 (5-HT3) receptors are cation-selective transmitter-gated

165 5-hydroxytryptamine type 3 (5-HT3) receptors are members of the Cys-loop receptor su

166 Serotonin type 3 (5-HT3) receptors are members of the pentameric Cys-loop

167 t likely to be due to a direct action on the 5-HT3 receptor as it could be recorded using intracellul

168 be the role of two residues in loop A of the 5-HT3 receptor: Asn128 and Glu129.

169 gle-channel conductance of human recombinant 5-HT3 receptors assembled as homomers of 5-HT3A subunits

170 ptors at a concentration up to 100 mum or on 5-HT(3) receptors at a concentration up to 10 mum.

171 ain targets but that allosterically modulate 5-HT(3) receptors at clinically relevant concentrations.

172 reas was prepared and tested for 5-HT(4) and 5-HT(3) receptor binding, 5-HT(4) receptor agonism in th

173 us, the data support a modified model of the 5-HT3 receptor binding site and show that loop A plays a

174 143, Tyr153, and Tyr234), which dominate the 5-HT3 receptor binding site.

175 We report that recombinantly expressed 5-HT3 receptor binding sites are reduced by chronic expo

176 sisted for 8 weeks PI and was susceptible to 5-HT(3) receptor blockade.

177 hese physiologic data, the effects of spinal 5-HT3 receptor blockade on behavioral hypersensitivity a

178 Second, we examined the effects of hindbrain 5-HT3 receptor blockade on suppression of intake by syst

179 The efficacy of a new 5-HT3 receptor blocking drug in the treatment of the dia

180 In the present study, activation of spinal 5-HT(3) receptor by intrathecal injection of a selective

181 O-CNB-5HT does not activate the 5-HT(3) receptor by itself, nor does it modulate the res

182 time of the recombinant and native neuronal 5-HT(3) receptors by 3- to 6-fold.

183 The inhibition of 5-HT(3) receptors by AEA may contribute to its physiolog

184 work not only unveils the mechanism by which 5-HT3 receptors can reach their axonal localization requ

185 Thus, presynaptic 5-HT3 receptors containing the 5-HT3B subunit might be p

186 Activation of the 5-HT3 receptor decreased the amplitude and lateral exten

187 These observations suggest that 5-HT(3) receptor density at the steady state regulates r

188 Also, 5-HT3 receptor density was greater in H-Agg hamsters wit

189 LTP of sympathetic ganglia is 5-HT(3) receptor-dependent and has been shown to require

190 el lining, but may play an important role in 5-HT3 receptor desensitization.

191 n-selective 5-HT agonist devoid of action at 5-HT3 receptors, did not (n = 18).

192 However, pre-blockade of 5-HT3 receptors eliminated the influence of the antibody

193 eceptor activity and correlated with altered 5-HT(3) receptor expression.

194 have mutated 21 residues in or close to the 5-HT(3) receptor F-loop (Ile(192) to Gly(212)) to Ala or

195 l our results are consistent with a flexible 5-HT(3) receptor F-loop with two regions that have speci

196 he molecular basis for alcohol modulation of 5-HT(3) receptor function has not been determined.

197 udy the mechanism of alcohol potentiation of 5-HT3 receptor function and to analyse effects of alcoho

198 A human recombinant homo-oligomeric 5-HT3 receptor (h5-HT3A) expressed in a human embryonic

199 alter the density of serotonergic fibers or 5-HT3 receptor immunoreactivity or spinal tissue content

200 These data support a role for 5-HT(3) receptors in adolescent cocaine-induced aggressi

201 ioned disgust reactions, while activation of 5-HT(3) receptors in the anterior IC are involved in the

202 These results suggest that activation of 5-HT(3) receptors in the posterior IC is important for t

203 anaesthetized rats investigated the role of 5-HT3 receptors in modulating vagal afferent evoked acti

204 tribution consistent with the involvement of 5-HT3 receptors in modulation of both presynaptic releas

205 current experiment, a potential role for VMN 5-HT3 receptors in the control of lordosis behavior was

206 vations emphasize the potential role for VMN 5-HT3 receptors in the control of lordosis behavior.

207 s, that 5-HT2A receptors are segregated from 5-HT3 receptors in the macaque cerebral cortex.

208 ventromedial medulla and the contribution of 5-HT3 receptors in the trigeminal nucleus caudalis (Vc),

209 Pharmacological blockade of 5-HT3 receptors in vivo or genetic deletion of the 5-HT3

210 amine2A receptors and the ion-channel gating 5-HT3 receptors, in cortical neuron types, which control

211 receptor were limited, the broad effects of 5-HT3 receptor included repetitive and impulsive element

212 This is confirmed for 5-HT3 receptor-induced contractions in the guinea pig il

213 d butanol (ButOH) had similar effects on the 5-HT3 receptor-induced current.

214 ugh serotonin, acting on facilitatory spinal 5-HT3 receptors, influences the final expression of DNIC

215 tive and that the contribution of peripheral 5-HT(3) receptors involves a novel complement of primary

216 The 5-HT(3) receptor is a member of the Cys-loop family of l

217 indicating that the 5-HT(3B) subunit of the 5-HT(3) receptor is expressed in DRG and suggest that se

218 Thus, it is believed that a native neuronal 5-HT(3) receptor is multimeric similar to the related ac

219 at activation of both peripheral and central 5-HT(3) receptors is pronociceptive and that the contrib

220 The 5-hydroxytryptamine(3) (5-HT(3)) receptor is a member of a superfamily of ligand

221 The type 3 serotonin (5-HT(3)) receptor is the only ligand-gated ion channel r

222 tivity because the endogenous ligand for the 5-HT3 receptor is a hydroxylated derivative of tryptopha

223 The 5-HT3 receptor is a member of the Cys-loop ligand-gated

224 The 5-HT3 receptor is a transmitter-gated ion channel of the

225 The type 3 serotonin (5-HT3) receptor is the only ligand-gated ion channel rec

226 Antagonism of 5-HT3 receptors known to promote learning significantly

227 combined with a new model of the nonliganded 5-HT3 receptor, lead to a mechanistic explanation of the

228 trogradely labelled from the colon displayed 5-HT(3) receptor-like immunoreactivity.

229 he lumbar DRG, where they were processed for 5-HT(3) receptor-like immunoreactivity.

230 These data demonstrate that 5-HT3 receptors located in the medial NTS participate in

231 open the possibility that distinct types of 5-HT(3) receptors may be involved in perception and/or p

232 These results suggest that activation of 5-HT(3) receptors may be involved in the production of C

233 partmentalized structural composition of the 5-HT3 receptor may be the basis of functional diversity

234 hetic afferents, at least in part, through a 5-HT(3) receptor mechanism.

235 cardiac afferents during ischaemia through a 5-HT(3) receptor mechanism.

236 ents through a serotonin receptor (subtype 3,5-HT3 receptor) mechanism, before treatment with the ant

237 Therefore, we hypothesized that 5-HT3 receptors mediate CCK-induced Fos-LI in the dorsal

238 The inhibition of the 5-HT3 receptor mediated inward current by low concentrat

239 To determine the relevant sites for 5-HT3 receptor mediated transmission in this region, we

240 nica muscularis mucosae (TMM) assay, and for 5-HT(3) receptor-mediated functional antagonism in the B

241 may play a role in reshaping the efficacy of 5-HT(3) receptor-mediated synaptic transmission.

242 -CNB-5HT released free serotonin that evoked 5-HT(3) receptor-mediated whole-cell currents in NIE-115

243 Ethanol can potentiate serotonin type 3 (5-HT(3)) receptor-mediated responses in various neurons

244 This study suggests that alcohols potentiate 5-HT3 receptor-mediated current by both increasing the r

245 Here, we show that PKC potentiated 5-HT3 receptor-mediated current in Xenopus oocytes expre

246 Ca2+, and Mg2+ concentrations on 5-HT2- and 5-HT3 receptor-mediated depolarizations of the resting m

247 5-HT3 receptor-mediated ion current was recorded from NC

248 ically, in the setting of tissue injury, the 5-HT(3) receptor mediates activation of nociceptors but

249 The exact location of 5-HT3 receptors mediating this action is not clear and m

250 iously, we have shown that serotonin type-3 (5-HT3) receptor mediation of suppression of food intake

251 the mid-to-caudal regions of the NTS and AP, 5-HT3 receptors most significantly mediate neuronal acti

252 ung-specific jugular neurons did not express 5-HT3 receptor mRNA but frequently expressed 5-HT1 or 5-

253 trogradely labelled from the lung, expressed 5-HT3 receptor mRNA.

254 a broad range of compounds that modulate the 5-HT(3) receptor, not through the orthosteric site but b

255 gonists may be due to the desensitization of 5-HT(3) receptors on cardiopulmonary afferents rather th

256 ferents from the colon and the expression of 5-HT(3) receptors on their cell bodies in the dorsal roo

257 T to inappropriate sites in IBS may activate 5-HT3 receptors on extrinsic afferent fibers and motor n

258 lucose regulates the density and function of 5-HT3 receptors on gastric vagal afferent neurones.

259 th the antibody in another group, we blocked 5-HT3 receptors on sensory nerve endings with tropisetro

260 ine have been defined as partial agonists of 5-HT3 receptors on the basis of macroscopic measurements

261 c) tastants and this released 5-HT activates 5-HT3 receptors on the gustatory nerves.

262 intestinal enterochromaffin cells activates 5-HT3 receptors on vagal afferent fibres to mediate lumi

263 al enterochromaffin cells, which acts on the 5-HT3 receptors on vagal afferent fibres to stimulate va

264 rt latency, transient excitation mediated by 5-HT3 receptors, or a delayed onset, more prolonged effe

265 5-HT(3) receptors participate in vagal afferent feedback

266 This raises the possibility that 5-HT3 receptors participating in sympathetic, parasympat

267 oocytes is sufficient to reconstitute native 5-HT(3) receptor properties.

268 sodium channel beta2 subunits or ionotropic 5-HT(3) receptors, proteins with no overt relationship t

269 receptors in vivo or genetic deletion of the 5-HT3 receptors reduces taste nerve responses to acids a

270 Inhibition of 5-HT(3) receptors releases acetylcholine, the endogenous

271 nic acetylcholine receptor and the serotonin 5-HT3 receptor, respectively.

272 In cells exhibiting a 5-HT3 receptor response, 5-HT and 2-methyl-5-HT produced

273 s to recommend the two-drug combination of a 5-HT3 receptor serotonin antagonist and dexamethasone.

274 The three-drug combination of a 5-HT3 receptor serotonin antagonist, dexamethasone, and

275 Blockade of serotonin (5-HT(3)) receptor signalling in the NTS by either the ch

276 s of muscarinic, AMPA, NMDA, GABAA, ATP, and 5-HT3 receptors, spontaneous and evoked postsynaptic cur

277 edial medulla (RVM) in the brainstem and the 5-HT(3) receptor subtype in the spinal dorsal horn are i

278 o increased apparent desensitization of both 5-HT(3) receptor subtypes.

279 T(3)-receptor subunits have been cloned: the 5-HT(3)-receptor subunit A (5-HT(3A)) and the 5-HT(3)-re

280 -HT(3)-receptor subunit A (5-HT(3A)) and the 5-HT(3)-receptor subunit B (5-HT(3B)).

281 Here we describe a new class of 5-HT3-receptor subunit (5-HT3B).

282 There are five 5-HT(3) receptor subunits (A-E), and all functional rece

283 conserved among 5-hydroxytryptamine type 3 (5-HT(3)) receptor subunits and many other subunits of th

284 Two 5-HT(3)-receptor subunits have been cloned: the 5-HT(3)-

285 Uniquely, 5-HT3 receptor subunits (5-HT3A and 5-HT3B) possess a po

286 Two 5-HT3 receptor subunits have been cloned, subunit A (5-H

287 Thus, the prevalent form of 5-HT3 receptor synthesized within the CNS lacks the 5-HT

288 s mesenteric afferents by a direct action on 5-HT3 receptors that are present on vagal mucosal affere

289 Drugs that selectively antagonize 5-HT(3) receptors (the "setrons") are the current gold s

290 final sigma-Conotoxin inactivates the 5-HT3 receptor through competitive antagonism and is a h

291 is a specific competitive antagonist of the 5-HT3 receptor; thus, alphaS-RVIIIA defines a novel fami

292 egulate directly the function and binding of 5-HT3 receptors to ondansetron.

293 s result is explained by the localization of 5-HT(3) receptor transcripts to a previously uncharacter

294 y of the compound for kinetic studies of the 5-HT(3) receptor was demonstrated.

295 d that the interaction of diltiazem with the 5-HT3 receptor was well described by a bimolecular react

296 sponses were reduced, and that the remaining 5-HT3 receptors were hypersensitive.

297 nts is activated directly via stimulation of 5-HT3 receptors, while another population responds to 5-

298 action of L-type Ca2+ channel antagonists on 5-HT3 receptors, whole-cell voltage clamp electrophysiol

299 Consequently, 5-HT(3) receptors with different properties might be pre

300 fibers, serotonin content and the levels of 5-HT3 receptors within the spinal cord at this time poin