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1 that express the type 3 serotonin receptor (5-HT3R).
2 gions of brain that expressed high levels of 5-HT3R.
3 HT(3)R-specific antagonist MDL72222, and the 5-HT(3)R agonist chlorophenylbiguanide readily competed
5 sponses elicited by successive injections of 5-HT(3)R agonists and (2) co-injection of the selective
6 results suggest that the loss of response to 5-HT(3)R agonists is due to desensitization of 5-HT(3)Rs
7 vided evidence that (1) tachyphylaxis to the 5-HT(3)R agonists was not due to impairment of the centr
11 systemic injections of the 5-HT(3) receptor (5-HT(3)R) agonists such as phenylbiguanide (PBG) may inv
12 ellular (i.e., ligand-binding) domain of the 5-HT(3)R and to perform a series of ligand docking exper
18 campal neurons indicates that serotonin, via 5-HT3R, can affect GABA release and suggests the partici
20 -HT(3A) subunit to form a native heteromeric 5-HT(3)R channel in rat CA1 hippocampal interneurons in
21 s to the lining of the pore of the resulting 5-HT3R channel, a mutant nicotinic alpha4 subunit with a
23 ar makeup of the serotonin 5-HT(3) receptor (5-HT(3)R) channel was investigated in rat hippocampal CA
24 en in native and recombinant 5-HT3 receptor (5-HT3R) channels, we reported previously the novel hypot
25 o, improved IBS symptoms and reduced rCBF in 5-HT3R containing regions of the EMS, but not in areas a
27 ns produces two classes of structures of the 5-HT(3)R/dTC complex; only one of these has the 2'N of d
28 ive analysis indicated that more than 90% of 5-HT3R expressing cells are GABAergic in the neocortex a
31 on and immunocytochemistry to determine that 5-HT3R-expressing neurons are mainly GABA-containing cel
33 rected mutagenesis, homology modeling of the 5-HT(3)R extracellular domain, and ligand docking simula
38 cs of desensitization of the 5-HT3 receptor (5-HT3R)-gated ion channel were investigated using whole-
39 ed by exogenous or endogenous 5-HT decreased 5-HT(3)R immunoreactivity at the neuronal cell membrane
42 BA release and suggests the participation of 5-HT3R in the inhibitory regulation of forebrain neurons
44 conclude that the neuronal expression of the 5-HT3R is selective within the GABA neuron population in
49 he hypothesis that the serotonin-3 receptor (5-HT3R) is involved in morphine-induced IEG expression,
54 significantly enhanced the amplitude of the 5-HT(3)R-mediated responses, which is consistent with th
55 d application of 5-HT (50 microM) elicited a 5-HT3R-mediated inward current response that desensitize
56 cantly correlated with rCBF decreases in the 5-HT3R-rich amygdala, ventral striatum, and dorsal pons.
58 cotinic alpha4 subunit co-assembles with the 5-HT3R subunit and forms an integral part of the ion cha
59 usly the novel hypothesis that the serotonin 5-HT3R subunit can co-assemble with the alpha4 subunit o
60 pha4-L285C subunit was co-expressed with the 5-HT3R subunit, both MTSET and silver nitrate (AgNO3), a
61 tudy were to determine the following: (1) if 5-HT(3)R undergoes ligand-induced internalization in mye
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