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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

24 5-Hydroxytryptamine (5-HT)3 receptor (5-HT3R) antagonists are effective in treating patients w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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