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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 r is the best-characterized heteropentameric 5-HT3 receptor.
7 se and differential expression of 5-HT1A and 5-HT3 receptors.
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 ze a 5-HT-containing pathway which activates 5-HT3 receptors.
12 holecystokinin A receptors and serotonin via 5-HT3 receptors.
13 s high-affinity CCK-A receptors also express 5-HT3 receptors.
14 nly high- or low-affinity CCK-A receptors or 5-HT3 receptors.
15 may also be responsive to serotonin through 5-HT3 receptors.
16 nd 31 units, respectively, by activating the 5-HT3 receptors.
17 and is an antagonist of serotonin 5-HT2 and 5-HT3 receptors.
18 receptor subunit (5-HT3A) yields functional 5-HT3 receptors.
19 ediated by 5-HT in the colonic mucosa and by 5-HT3 receptors.
20 alterations in the neuronal distribution of 5-HT3 receptors.
21 ch activates an inhibitory pathway involving 5-HT3 receptors.
22 e nerve responses apparently by blocking the 5-HT3 receptors.
23 at expression of gLTD involves activation of 5-HT(3) receptor.
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 f 5-HT receptors, including the 5-HT type-3 (5-HT3) receptors.
29 s multimodal subunit-dependent antagonism of 5-HT(3) receptors.
30 gonist, is a potent competitive inhibitor of 5-HT(3) receptors.
31 actions on 5-HT-evoked currents mediated by 5-HT(3) receptors.
32 that was in part mediated by 5-HT acting via 5-HT(3) receptors.
33 smission via a facilitatory action at spinal 5-HT(3) receptors.
34 ic afferent endings via both 5-HT(3) and non-5-HT(3) receptors.
35 me superfamily, including GABA(A), nACh, and 5-HT(3) receptors.
36 atal nicotinic exposure in rat pups: role of 5-HT(3) receptors.
37 y prevented by functional blockade of spinal 5-HT(3) receptors.
38 onses elicited by systemic injections of the 5-HT(3) receptor (5-HT(3)R) agonists such as phenylbigua
42 sal enterochromaffin cells and activation of 5-HT(3) receptors (5-HT(3)Rs) on neurons in the gut wall
45 permeability seen in native and recombinant 5-HT3 receptor (5-HT3R) channels, we reported previously
48 ave the capacity to synthesize two different 5-HT3 receptors, 5-HT3A+/3B- and 5-HT3A+/3B+ receptors.
49 Using a simplified model of the pore of the 5-HT(3) receptor (5HT3R) which restrains the backbone st
50 of the 5-HT3A receptor subunit rendered the 5-HT3 receptor 70-fold more sensitive to serotonin and p
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
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 ione (DNQX) on the excitatory actions of the 5-HT3 receptor agonist 1-phenylbiguanide (PBG) were stud
70 that phenyldiguanide (later recognized as a 5-HT3 receptor agonist) stimulated the firing of C-fibre
71 This initial response was mimicked by the 5-HT3 receptor agonist, 2-methyl-5-HT, whereas 5-methoxy
72 sed with the 5-HT1A receptor agonist and the 5-HT3 receptor agonist, m-chlorophenyl-biguanide (mCPBG;
73 retic application of PBG, a highly selective 5-HT3 receptor agonist, significantly increased activity
74 2-methylserotonin (100 microg kg-1, i.a.), a 5-HT3 receptor agonist, stimulated eleven of twelve affe
79 These findings suggest that tachyphylaxis to 5-HT(3) receptor agonists may be due to the desensitizat
83 pressure and cardiac output elicited by the 5-HT(3)-receptor agonists, phenylbiguanide (100 microg/k
85 ude that colonic sensory neurones expressing 5-HT(3) receptors also functionally express the receptor
88 genetic or pharmacological disruption of the 5-HT(3) receptor, an excitatory serotonin-gated ion chan
89 n the basis of its ability to inactivate the 5-HT3 receptor, an excitatory serotonin-gated ion channe
90 mechanisms underlying the activation of the 5-HT(3) receptor and its contribution to facilitation of
91 ation after mTBI, direct 5-HT effect through 5-HT(3) receptors and indirectly through upregulation of
92 sion of the functional 5-HT3A subunit of the 5-HT3 receptor and the central CB1 cannabinoid receptor
93 erents, mainly through direct stimulation of 5-HT3 receptors and that the action of 5-HT on these aff
94 ether gustatory afferents express functional 5-HT3 receptors and, if so, whether these receptors play
95 notropic glycine receptor, GABA(A) receptor, 5-HT(3) receptor, and nAChR subunits contain a pair of h
96 face at both homomeric and heteromeric human 5-HT(3) receptors, and explain why the competitive pharm
97 e receptors, GABA(A) receptors, serotonin-3 (5-HT(3)) receptors, and glutamate-gated chloride ion cha
98 -application of 5-HT (300 microM), acting at 5-HT3 receptors, and ACh (3 mM) or ATP (1 mM) were addit
99 of disgust and taste avoidance by selective 5-HT(3) receptor antagonism/agonism in the posterior (gr
100 sponses to 2-methyl-5-HT were blocked by the 5-HT(3) receptor antagonist alosetron (2 x 10(-7) M), wh
101 etic risk radiation therapy should receive a 5-HT(3) receptor antagonist before each fraction and for
105 TS-TH-EGFP neurons, an effect blocked by the 5-HT(3) receptor antagonist ondansetron and mimicked by
107 response to acetylcholine was blocked by the 5-HT(3) receptor antagonist renzapride with a similar IC
109 or any highly emetic agents should receive a 5-HT(3) receptor antagonist, dexamethasone, and a neurok
110 etron (300 microg kg(-1), I.V.), a selective 5-HT(3) receptor antagonist, eliminated the afferent's r
115 kg-1, i.v.), or treatment with the selective 5-HT3 receptor antagonist alosetron (30 microg kg-1, i.v
117 1) receptor antagonist in conjunction with a 5-HT3 receptor antagonist and corticosteroid in patients
120 isetron; 500 ng), or were coinfused with the 5-HT3 receptor antagonist and the 5-HT2A/2C receptor ago
122 coefficient = 1.8) that were blocked by the 5-HT3 receptor antagonist ondansetron (IC50 = 103 pM) an
124 led to do so in Tph1(-/-) colon; and (9) the 5-HT3 receptor antagonist ondansetron, which reduced CMM
126 otetralin (DPAT; 0.1 mg/kg and 0.3 mg/kg) or 5-HT3 receptor antagonist tropisetron (0.3 mg/kg) treatm
127 d Fos-LI in the DVC of ondansetron (1 mg/kg; 5-HT3 receptor antagonist) and vehicle-treated rats foll
132 -HT response was completely abolished by the 5-HT3 receptor antagonist, granisetron (0.5 mg kg-1).
133 njection of tropisetron (200 microg kg-1), a 5-HT3 receptor antagonist, significantly attenuated the
135 urthermore, this mutation also converted the 5-HT3 receptor antagonist/very weak partial agonist, apo
136 rolapitant, in combination with a serotonin (5-HT3) receptor antagonist and dexamethasone, for the pr
137 f ondansetron, a selective serotonin type-3 (5-HT3) receptor antagonist, attenuates cholecystokinin (
139 ) and palonosetron (a 5-hydroxytryptamine-3 [5-HT3] receptor antagonist) for the prevention of acute
143 wide dynamic range neurons are inhibited by 5-HT3 receptor antagonists in rats following spinal nerv
144 whisking frequencies, and selective 5-HT2 or 5-HT3 receptor antagonists suppress this rhythmic firing
145 Unilateral infusion of selective 5-HT2 or 5-HT3 receptor antagonists suppresses ipsilateral whiski
146 by DPPIV inhibition or by cholecystokinin or 5-HT3 receptor antagonists, but was inhibited by atropin
150 Probably the most studied modulators of 5-HT(3) receptors are the high affinity competitive 'set
152 oline (nACh) and 5-hydroxytryptamine type 3 (5-HT(3)) receptors are cation-selective ion channels of
154 the modulation of interoceptive circuits, as 5-HT3 receptors are located abundantly on sensory pathwa
160 gle-channel conductance of human recombinant 5-HT3 receptors assembled as homomers of 5-HT3A subunits
162 ain targets but that allosterically modulate 5-HT(3) receptors at clinically relevant concentrations.
163 reas was prepared and tested for 5-HT(4) and 5-HT(3) receptor binding, 5-HT(4) receptor agonism in th
164 us, the data support a modified model of the 5-HT3 receptor binding site and show that loop A plays a
168 hese physiologic data, the effects of spinal 5-HT3 receptor blockade on behavioral hypersensitivity a
169 Second, we examined the effects of hindbrain 5-HT3 receptor blockade on suppression of intake by syst
171 In the present study, activation of spinal 5-HT(3) receptor by intrathecal injection of a selective
175 work not only unveils the mechanism by which 5-HT3 receptors can reach their axonal localization requ
177 R-mApple cells were highly co-expressed with 5-HT3 receptor-containing neurons within the cortex and
185 ptors were not detected in mouse urothelium, 5-HT(3) receptors expressed on bladder sensory neurons p
187 have mutated 21 residues in or close to the 5-HT(3) receptor F-loop (Ile(192) to Gly(212)) to Ala or
188 l our results are consistent with a flexible 5-HT(3) receptor F-loop with two regions that have speci
189 mportant aspects of the mechanistic basis of 5-HT(3) receptor function and modulation by drugs remain
192 udy the mechanism of alcohol potentiation of 5-HT3 receptor function and to analyse effects of alcoho
194 alter the density of serotonergic fibers or 5-HT3 receptor immunoreactivity or spinal tissue content
196 ioned disgust reactions, while activation of 5-HT(3) receptors in the anterior IC are involved in the
197 These results suggest that activation of 5-HT(3) receptors in the posterior IC is important for t
198 anaesthetized rats investigated the role of 5-HT3 receptors in modulating vagal afferent evoked acti
199 tribution consistent with the involvement of 5-HT3 receptors in modulation of both presynaptic releas
201 ventromedial medulla and the contribution of 5-HT3 receptors in the trigeminal nucleus caudalis (Vc),
203 amine2A receptors and the ion-channel gating 5-HT3 receptors, in cortical neuron types, which control
204 receptor were limited, the broad effects of 5-HT3 receptor included repetitive and impulsive element
205 the EC(50) of 5-HT reduced as the density of 5-HT(3) receptors increased, suggesting an effect of rec
208 ugh serotonin, acting on facilitatory spinal 5-HT3 receptors, influences the final expression of DNIC
209 tive and that the contribution of peripheral 5-HT(3) receptors involves a novel complement of primary
212 indicating that the 5-HT(3B) subunit of the 5-HT(3) receptor is expressed in DRG and suggest that se
213 Thus, it is believed that a native neuronal 5-HT(3) receptor is multimeric similar to the related ac
214 at activation of both peripheral and central 5-HT(3) receptors is pronociceptive and that the contrib
217 tivity because the endogenous ligand for the 5-HT3 receptor is a hydroxylated derivative of tryptopha
221 combined with a new model of the nonliganded 5-HT3 receptor, lead to a mechanistic explanation of the
226 ity of high-resolution structures of a mouse 5-HT(3) receptor, many important aspects of the mechanis
227 open the possibility that distinct types of 5-HT(3) receptors may be involved in perception and/or p
228 These results suggest that activation of 5-HT(3) receptors may be involved in the production of C
229 partmentalized structural composition of the 5-HT3 receptor may be the basis of functional diversity
232 ents through a serotonin receptor (subtype 3,5-HT3 receptor) mechanism, before treatment with the ant
235 nica muscularis mucosae (TMM) assay, and for 5-HT(3) receptor-mediated functional antagonism in the B
237 -CNB-5HT released free serotonin that evoked 5-HT(3) receptor-mediated whole-cell currents in NIE-115
238 Ethanol can potentiate serotonin type 3 (5-HT(3)) receptor-mediated responses in various neurons
239 This study suggests that alcohols potentiate 5-HT3 receptor-mediated current by both increasing the r
242 ically, in the setting of tissue injury, the 5-HT(3) receptor mediates activation of nociceptors but
245 iously, we have shown that serotonin type-3 (5-HT3) receptor mediation of suppression of food intake
246 the mid-to-caudal regions of the NTS and AP, 5-HT3 receptors most significantly mediate neuronal acti
248 ung-specific jugular neurons did not express 5-HT3 receptor mRNA but frequently expressed 5-HT1 or 5-
250 a broad range of compounds that modulate the 5-HT(3) receptor, not through the orthosteric site but b
251 gonists may be due to the desensitization of 5-HT(3) receptors on cardiopulmonary afferents rather th
252 ferents from the colon and the expression of 5-HT(3) receptors on their cell bodies in the dorsal roo
253 T to inappropriate sites in IBS may activate 5-HT3 receptors on extrinsic afferent fibers and motor n
254 lucose regulates the density and function of 5-HT3 receptors on gastric vagal afferent neurones.
255 evidence shows mRNA expression of 5-HT2C and 5-HT3 receptors on GLP-1-producing preproglucagon (PPG)
256 th the antibody in another group, we blocked 5-HT3 receptors on sensory nerve endings with tropisetro
257 ine have been defined as partial agonists of 5-HT3 receptors on the basis of macroscopic measurements
259 intestinal enterochromaffin cells activates 5-HT3 receptors on vagal afferent fibres to mediate lumi
260 al enterochromaffin cells, which acts on the 5-HT3 receptors on vagal afferent fibres to stimulate va
261 rt latency, transient excitation mediated by 5-HT3 receptors, or a delayed onset, more prolonged effe
266 sodium channel beta2 subunits or ionotropic 5-HT(3) receptors, proteins with no overt relationship t
267 receptors in vivo or genetic deletion of the 5-HT3 receptors reduces taste nerve responses to acids a
269 s to recommend the two-drug combination of a 5-HT3 receptor serotonin antagonist and dexamethasone.
272 s of muscarinic, AMPA, NMDA, GABAA, ATP, and 5-HT3 receptors, spontaneous and evoked postsynaptic cur
273 edial medulla (RVM) in the brainstem and the 5-HT(3) receptor subtype in the spinal dorsal horn are i
275 T(3)-receptor subunits have been cloned: the 5-HT(3)-receptor subunit A (5-HT(3A)) and the 5-HT(3)-re
279 conserved among 5-hydroxytryptamine type 3 (5-HT(3)) receptor subunits and many other subunits of th
283 e of the vestibule binding site to the human 5-HT(3) receptor, suggesting a common mechanism of modul
285 s mesenteric afferents by a direct action on 5-HT3 receptors that are present on vagal mucosal affere
288 is a specific competitive antagonist of the 5-HT3 receptor; thus, alphaS-RVIIIA defines a novel fami
289 ges in the extracellular domain of the human 5-HT(3) receptor to identify intrareceptor motions durin
291 s result is explained by the localization of 5-HT(3) receptor transcripts to a previously uncharacter
292 eurons was used to investigate expression of 5-HT(3) receptors using single cell RT-PCR, while sensor
294 d that the interaction of diltiazem with the 5-HT3 receptor was well described by a bimolecular react
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
300 fibers, serotonin content and the levels of 5-HT3 receptors within the spinal cord at this time poin