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1 whereas they are relatively unbiased at the 5-HT1B receptor.
2 ludes several ion channels and the serotonin 5-HT1B receptor.
3 mera (Chi22) that only weakly coupled to the 5-HT1B receptor.
4 agamma and Sf9 cell membranes containing the 5-HT1B receptor.
5 one of the serotonin-receptor subtypes, the 5-HT1B receptor.
6 velopment and by signaling and expression of 5-HT1B receptors.
7 serotonin transporter, as well as 5-HT1A and 5-HT1B receptors.
8 because several neuron types in VTA express 5-HT1B receptors.
9 region does not show any coupling ability to 5-HT1B receptors.
10 ween Galphai1 and the 5-hydroxytryptamine1B (5-HT1B) receptor.
11 excitation probably through 5-HT1A (and not 5-HT1B) receptors.
12 ses GABAergic inhibition through presynaptic 5-HT1B receptors; (2) 5-HT decreases the firing of palli
13 resses GABAergic inhibition probably through 5-HT1B receptors; (2) in the external pallidal segment,
14 agonist, partial agonist, and antagonist) on 5-HT1B receptor (5-HT1BR) occupancy and the associated h
15 ts suggest that nigral 5-HT, via presynaptic 5-HT1B receptor activation, gates the excitatory STN-->S
16 fects of serotonin1B [5-hydroxytryptamine1B (5-HT1B)] receptor activation on cocaine reinforcement we
17 s inhibitory 5-HT effect was mimicked by the 5-HT1B receptor agonist CP93129 and blocked by the 5-HT1
18 the administration to wild-type mice of the 5-HT1B receptor agonist RU24969 results in a striatal in
19 e mice, CP-93,129 (1.4 mumol/kg), a specific 5-HT1B receptor agonist, had no effect in knockout mice.
20 usion of CP 93129 (20, 40, and 80 microM), a 5-HT1B receptor agonist, increased extracellular DA conc
21 uoromethyl)phenyl]-piperazine HCl (TFMPP), a 5-HT1B receptor agonist, reduced in a dose-related manne
22 that intra-tegmental infusion of CP 94253, a 5-HT1B receptor agonist, significantly prolonged the eff
24 phenotype and have reduced responsiveness to 5-HT1B receptor agonists and reduced behavioral reaction
28 of Galphai1 increase agonist binding to the 5-HT1B receptor and receptor stimulation of GTPgammaS bi
30 n pulmonary hypertension and explain how the 5-HT1B receptor and SERT are codependent in regulating S
32 tatin anorectic response may be modulated by 5-HT1B receptors and that a neuronal pathway from the am
33 ffinity (Ki = 17 nM) at its species homolog, 5-HT1B receptors, and at a mutant 5-HT1D beta receptor (
36 microscopic immunocytochemical analysis with 5-HT1B receptor antibodies and whole-cell patch-clamp re
40 suggest that blockade and activation of VTA 5-HT1B receptors attenuates and potentiates the neuroche
41 pharmacological interventions to interrogate 5-HT1B receptor binding and function and determined bloo
42 usion and examined for 5-HT afferents to and 5-HT1B receptor-containing neuronal puncta and somata in
43 s in vivo and demonstrate that activation of 5-HT1B receptors contributes to the cellular responses e
44 ng sequence in Galphat either permitted full 5-HT1B receptor coupling to the chimera (Chi24) or only
45 ions within Chi22 (K300Q and L304E) restored 5-HT1B receptor coupling, and again the effects of the t
47 th the structure of the 5-HT2B receptor, the 5-HT1B receptor displays a 3 angstrom outward shift at t
48 nity shift of 5-HT1A receptors compared with 5-HT1B receptors (EC50 values of 6.4 and 12.0 nM, respec
53 rinergic receptor-mediated inhibition of CHO/5-HT1B receptor function was blocked when 5-HT2A recepto
54 ion of 5-HT2A receptors had no effect on CHO/5-HT1B receptor function, although 5-HT2A receptor-media
56 arch has focused on the 5-HT1A receptor, the 5-HT1B receptor has a lesser known role in modulating em
60 as designed to assess the involvement of VTA 5-HT1B receptors in mediating the stimulatory effects of
63 GFP injection induced elevated expression of 5-HT1B receptors in neuronal fibers in VTA and increased
64 by examining the subcellular localization of 5-HT1B receptors in the mouse SCN using electron microsc
67 that cocaine acts as an indirect agonist of 5-HT1B receptors in vivo and demonstrate that activation
69 The results suggest that activation of VTA 5-HT1B receptors increases mesolimbic DA neuron activiti
70 gic inputs that are inhibited by presynaptic 5-HT1B receptors; inhibition of excitatory synapses onto
73 results thus demonstrate that stimulation of 5-HT1B receptors is required for fenfluramine-induced an
74 To test the hypothesis that stimulation of 5-HT1B receptors is required for the anorectic effect of
75 ts are in opposition to recent findings with 5-HT1B receptor knock-out mice and may have important on
78 alterations in 5-HT afferent innervation and 5-HT1B receptor localization were observed throughout th
80 he circadian system by acting at presynaptic 5-HT1B receptors located on retinal axons in the SCN.
81 he lack of 5-HT2A mediated regulation of CHO/5-HT1B receptors may be due to activation of a third pat
82 reductions found in this study suggest that 5-HT1B receptors may contribute to the etiology or expre
85 n SNr GABA neurons, indicating a presynaptic 5-HT1B receptor-mediated inhibition of glutamate release
86 ay be associated, at least in part, with the 5-HT1B receptor-mediated inhibition of VTA GABA release.
88 ells, 5-hydroxytryptamine (5-HT)1B-like (CHO/5-HT1B) receptor-mediated inhibition of forskolin-stimul
89 ences aggressive behavior, a distinct set of 5-HT1B receptors modulates impulsive behavior during adu
90 as, with bLRs having greater 5-HT1A, but not 5-HT1B, receptor mRNA levels in the septum, hippocampus
94 idence suggests that 5-hydroxytriptamine-1B (5-HT1B) receptors play a role in modifying ethanol's rei
95 its to membranes expressing either 5-HT1A or 5-HT1B receptors shifted the majority of the receptors t
96 h serotonin receptor 1B (5-HTR1B), modulates 5-HT1B receptor signal transduction, and is required for
98 odulating signaling through 5-HT4 as well as 5-HT1B receptors supports the concept that this protein
99 ity requires activation of nucleus accumbens 5-HT1B receptors, the blockade of which prevents social
100 act in concert to mediate the ability of the 5-HT1B receptor to couple specifically to inhibitory G p
101 of the ability of the 5-hydroxytryptamine1B (5-HT1B) receptor to discriminate between G protein heter
102 bilities of the Galphat/Galphai1 chimeras to 5-HT1B receptors using high affinity agonist binding and
104 e contribution of the 5-hydroxytryptamine1B (5-HT1B) receptor, we studied the induction of the immedi
105 rcing effects and voluntary intake, and that 5-HT1B receptors within the ventral tegmental area (VTA)
106 dy was designed to assess the involvement of 5-HT1B receptors within the ventral tegmental area (VTA)
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