ライフサイエンスコーパス: 5-HT(3)R

1 5-HT3R-expressing cells with CCK immunoreactivity were o

2 induces apnea via acting on 5-HT receptor 3 (5-HT(3)R) in PCFs, and among the 5-HT(3)R subunits, 5-HT

3 onist) before and after PCF inactivation, 3) 5-HT(3)R currents and the stimulus threshold of the acti

4 t-in-class compound FPPQ, which behaves as a 5-HT(3)R antagonist and a neutral antagonist 5-HT(6)R of

5 Net fluid absorption was decreased by a 5-HT(3)R agonist or by luminal glucose; this was attenua

6 stimulation of beta-cells were blocked by a 5-HT(3)R antagonist and were enhanced by increasing sero

7 gic stimulation of B-cells were blocked by a 5-HT(3)R antagonist and were enhanced by increasing sero

8 atrial bolus injection of phenylbiguanide (a 5-HT(3)R agonist) before and after PCF inactivation, 3)

9 d application of 5-HT (50 microM) elicited a 5-HT3R-mediated inward current response that desensitize

10 ate that epibatidine and mecamylamine act as 5-HT(3)R antagonists.

11 Serotonergic fibres exert background 5-HT3R mediated facilitation of both tactile and nocicep

12 axis to the BJR reflex responses elicited by 5-HT(3)R agonists.

13 The serotonin-gated ion channel (5-HT(3)R) mediates excitatory neuronal communication in

14 ed by exogenous or endogenous 5-HT decreased 5-HT(3)R immunoreactivity at the neuronal cell membrane

15 a sensitive target engagement biomarker for 5-HT(3)R, and support the potential utility of CVN058 in

16 rometry (VCF) to measure simultaneously, for 5-HT(3)R expressed at a cell membrane, conformational ch

17 -HT(3A) subunit to form a native heteromeric 5-HT(3)R channel in rat CA1 hippocampal interneurons in

18 tudy were to determine the following: (1) if 5-HT(3)R undergoes ligand-induced internalization in mye

19 o, improved IBS symptoms and reduced rCBF in 5-HT3R containing regions of the EMS, but not in areas a

20 n the intestinal mucosa results in increased 5-HT(3)R internalization in myenteric neurons.

21 the BJR and that nitrosyl factors influence 5-HT(3)R function.

22 ucosal levels of 5-HT and decreased membrane 5-HT(3)R immunoreactivity by 27%.

23 Thus, combination of 5-HT(3)R antagonism and 5-HT(6)R antagonism, exemplified

24 sponses elicited by successive injections of 5-HT(3)R agonists and (2) co-injection of the selective

25 excitability by shortening the decay time of 5-HT(3)R currents, lowering the stimulus threshold, and

26 responsible for shortening the decay time of 5-HT(3)R-mediated currents.

27 ive analysis indicated that more than 90% of 5-HT3R expressing cells are GABAergic in the neocortex a

28 The co-existence of 5-HT3R and GABA in cortical and hippocampal neurons indi

29 gions of brain that expressed high levels of 5-HT3R.

30 BA release and suggests the participation of 5-HT3R in the inhibitory regulation of forebrain neurons

31 Subjects were not permitted to use other 5-HT(3)R modulators or serotonin reuptake inhibitors.

32 5-HT concentration and strengthened the PCF 5-HT(3)R-mediated apnea.

33 RVM 5-HT neurons that drives pronociceptive 5-HT(3)R signaling in the dorsal horn, and this LS is to

34 h involving the joint modulation of 5-HT(6)R/5-HT(3)R/MAO-B in AD.

35 related peptide, and the serotonin receptor 5-HT(3)R.

36 Serotonin type-3 receptor (5-HT(3)R) antagonists show potential as a treatment for

37 The serotonin type 3 receptor (5-HT(3)R) is a member of the cys-loop ligand-gated ion c

38 systemic injections of the 5-HT(3) receptor (5-HT(3)R) agonists such as phenylbiguanide (PBG) may inv

39 n coupled to the serotonin 5-HT(3) receptor (5-HT(3)R) and to the glycine receptor (GlyR).

40 rating that ondansetron, a 5-HT(3) receptor (5-HT(3)R) antagonist, ameliorates cognitive deficits of

41 ar makeup of the serotonin 5-HT(3) receptor (5-HT(3)R) channel was investigated in rat hippocampal CA

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

43 The serotonin 5-HT(3) receptor (5-HT(3)R) is a member of the cys-loop ligand-gated ion c

44 5-Hydroxytryptamine (5-HT)3 receptor (5-HT3R) antagonists are effective in treating patients w

45 he hypothesis that the serotonin-3 receptor (5-HT3R) is involved in morphine-induced IEG expression,

46 The 5-HT3 receptor (5-HT3R) antagonist Alosetron (Alos) reduces the symptoms

47 en in native and recombinant 5-HT3 receptor (5-HT3R) channels, we reported previously the novel hypot

48 cs of desensitization of the 5-HT3 receptor (5-HT3R)-gated ion channel were investigated using whole-

49 The type 3 serotonin receptor (5-HT3R) is a ligand-gated ion channel whose presence in

50 that express the type 3 serotonin receptor (5-HT3R).

51 s to the lining of the pore of the resulting 5-HT3R channel, a mutant nicotinic alpha4 subunit with a

52 R-a5 signaling) and granisetron (a selective 5-HT(3)R antagonist) alleviates mental dysfunction and y

53 058, a brain-penetrant, potent and selective 5-HT(3)R antagonist, shows efficacy in rodent models of

54 ensitize upon repeated exposure to selective 5-HT(3)R agonists.

55 usly the novel hypothesis that the serotonin 5-HT3R subunit can co-assemble with the alpha4 subunit o

56 Although some 5-HT3R/GABAergic neurons with calretinin (CR) were found

57 on and immunocytochemistry to determine that 5-HT3R-expressing neurons are mainly GABA-containing cel

58 We determined that 5-HT3R/GABA-containing neurons do not exhibit somatostat

59 receptor 3 (5-HT(3)R) in PCFs, and among the 5-HT(3)R subunits, 5-HT(3B) is responsible for shortenin

60 HT(3)R-specific antagonist MDL72222, and the 5-HT(3)R agonist chlorophenylbiguanide readily competed

61 diated hemodynamic responses elicited by the 5-HT(3)R agonists.

62 The PU02 binding site in the 5-HT(3)R corresponds to allosteric sites in anionic Cys-

63 ellular (i.e., ligand-binding) domain of the 5-HT(3)R and to perform a series of ligand docking exper

64 and blocked by intrathecal injection of the 5-HT(3)R antagonist ondansetron; the 5-HT(2A)R antagonis

65 Molecular modeling of the 5-HT(3)R extracellular domain using the antagonist-bound

66 rected mutagenesis, homology modeling of the 5-HT(3)R extracellular domain, and ligand docking simula

67 Cryo-electron microscopy (cryo-EM) of the 5-HT(3)R in complex with serotonin or setrons revealed t

68 ions as a way to map the architecture of the 5-HT(3)R ligand binding domain.

69 dition, the single-channel properties of the 5-HT(3)R were investigated in outside-out patches.

70 ent of the GABA(A)R-a5 or suppression of the 5-HT(3)R within the MC4R(dBNST) neurons not only abolish

71 significantly enhanced the amplitude of the 5-HT(3)R-mediated responses, which is consistent with th

72 ns produces two classes of structures of the 5-HT(3)R/dTC complex; only one of these has the 2'N of d

73 In these cells, serotonin, the 5-HT(3)R-specific antagonist MDL72222, and the 5-HT(3)R

74 VCF recordings show that the 5-HT(3)R has access to four families of conformations en

75 vided evidence that (1) tachyphylaxis to the 5-HT(3)R agonists was not due to impairment of the centr

76 The 5-HT3R/CCK interneurons represent between 35 and 66% of

77 cantly correlated with rCBF decreases in the 5-HT3R-rich amygdala, ventral striatum, and dorsal pons.

78 ng in the kinetics of desensitization of the 5-HT3R channel.

79 To analyze further the role of the 5-HT3R in the CNS, we used in situ hybridization and imm

80 conclude that the neuronal expression of the 5-HT3R is selective within the GABA neuron population in

81 Further characterization of the 5-HT3R/GABAergic neurons was based on their calcium-bind

82 These findings demonstrate that the 5-HT3R antagonist, MDL 72222, can positively modulate mo

83 We suggest that serotonin through the 5-HT3R may regulate GABA and CCK neurotransmission in th

84 ssion, using the selective antagonist to the 5-HT3R, MDL 72222.

85 No reduction was seen when the 5-HT3R was expressed alone or with the wild-type alpha4

86 cotinic alpha4 subunit co-assembles with the 5-HT3R subunit and forms an integral part of the ion cha

87 pha4-L285C subunit was co-expressed with the 5-HT3R subunit, both MTSET and silver nitrate (AgNO3), a

88 These 5-HT3R-expressing interneurons might contain CCK, CB, an

89 results suggest that the loss of response to 5-HT(3)R agonists is due to desensitization of 5-HT(3)Rs

90 campal neurons indicates that serotonin, via 5-HT3R, can affect GABA release and suggests the partici

91 and 5-HT(6)R antagonism and interaction with 5-HT(3)R were determined using molecular dynamic simulat