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1 mera (Chi22) that only weakly coupled to the 5-HT1B receptor.
2 agamma and Sf9 cell membranes containing the 5-HT1B receptor.
3 one of the serotonin-receptor subtypes, the 5-HT1B receptor.
4 whereas they are relatively unbiased at the 5-HT1B receptor.
5 ludes several ion channels and the serotonin 5-HT1B receptor.
6 region does not show any coupling ability to 5-HT1B receptors.
7 velopment and by signaling and expression of 5-HT1B receptors.
8 serotonin transporter, as well as 5-HT1A and 5-HT1B receptors.
9 because several neuron types in VTA express 5-HT1B receptors.
10 ween Galphai1 and the 5-hydroxytryptamine1B (5-HT1B) receptor.
11 asic, functionally active antagonists of the 5-HT(1B) receptor.
12 excitation probably through 5-HT1A (and not 5-HT1B) receptors.
13 100,635, consistent with the involvement of 5-HT(1B) receptors.
14 ses GABAergic inhibition through presynaptic 5-HT1B receptors; (2) 5-HT decreases the firing of palli
15 resses GABAergic inhibition probably through 5-HT1B receptors; (2) in the external pallidal segment,
16 2+) entry, and we have now demonstrated that 5-HT(1B) receptors (5-HT(1B)Rs) liberate Gbetagamma to i
17 agonist, partial agonist, and antagonist) on 5-HT1B receptor (5-HT1BR) occupancy and the associated h
18 ts suggest that nigral 5-HT, via presynaptic 5-HT1B receptor activation, gates the excitatory STN-->S
19 fects of serotonin1B [5-hydroxytryptamine1B (5-HT1B)] receptor activation on cocaine reinforcement we
20 ryptamine), and L-694,247, and the selective 5-HT(1B) receptor agonist CP 93,129 produced concentrati
21 Results showed that neonatal treatment with 5-HT(1B) receptor agonist robustly impaired sexual behav
23 n of 5-nonyloxytriptamine (NNT), a selective 5-HT(1B) receptor agonist, affects TCA organization in r
24 N-(3-Trifluoromethylphenyl)piperazine, a 5-HT(1B) receptor agonist, potently inhibited 5-HT(1A) r
25 s inhibitory 5-HT effect was mimicked by the 5-HT1B receptor agonist CP93129 and blocked by the 5-HT1
26 the administration to wild-type mice of the 5-HT1B receptor agonist RU24969 results in a striatal in
27 e mice, CP-93,129 (1.4 mumol/kg), a specific 5-HT1B receptor agonist, had no effect in knockout mice.
28 usion of CP 93129 (20, 40, and 80 microM), a 5-HT1B receptor agonist, increased extracellular DA conc
29 uoromethyl)phenyl]-piperazine HCl (TFMPP), a 5-HT1B receptor agonist, reduced in a dose-related manne
30 that intra-tegmental infusion of CP 94253, a 5-HT1B receptor agonist, significantly prolonged the eff
32 phenotype and have reduced responsiveness to 5-HT1B receptor agonists and reduced behavioral reaction
34 conducted to determine whether activation of 5-HT(1B) receptors also alters photic regulation of noct
37 two markers of serotonin neurotransmission, 5-HT(1B) receptors and serotonin reuptake sites, which a
38 H]paroxetine, selective radioligands for the 5-HT(1B) receptors and the serotonin reuptake sites, res
39 of Galphai1 increase agonist binding to the 5-HT1B receptor and receptor stimulation of GTPgammaS bi
41 n pulmonary hypertension and explain how the 5-HT1B receptor and SERT are codependent in regulating S
43 tatin anorectic response may be modulated by 5-HT1B receptors and that a neuronal pathway from the am
44 ffinity (Ki = 17 nM) at its species homolog, 5-HT1B receptors, and at a mutant 5-HT1D beta receptor (
45 by intra-tegmental infusion of SB 216641 (a 5-HT(1B) receptor antagonist), but not BRL 15572 (a 5-HT
46 is effect was blocked by pretreatment with a 5-HT(1B) receptor antagonist, indicating that the behavi
49 in the discovery of novel, de novo designed, 5-HT(1B) receptor antagonists that lack a basic moiety a
50 microscopic immunocytochemical analysis with 5-HT1B receptor antibodies and whole-cell patch-clamp re
54 e of abnormal stimulation of 5-HT(1A) and/or 5-HT(1B) receptors as a result of increased synaptic ava
56 suggest that blockade and activation of VTA 5-HT1B receptors attenuates and potentiates the neuroche
57 , may cause or contribute to the increase in 5-HT(1B) receptor binding in the SCN in middle aged anim
59 pharmacological interventions to interrogate 5-HT1B receptor binding and function and determined bloo
60 s in serotonergic neurotransmission increase 5-HT(1B) receptors but decrease serotonin reuptake sites
61 dicate that the agonist action of NNT at the 5-HT(1B) receptor causes TCA disorganization in rat barr
62 usion and examined for 5-HT afferents to and 5-HT1B receptor-containing neuronal puncta and somata in
63 s in vivo and demonstrate that activation of 5-HT1B receptors contributes to the cellular responses e
64 ng sequence in Galphat either permitted full 5-HT1B receptor coupling to the chimera (Chi24) or only
65 ions within Chi22 (K300Q and L304E) restored 5-HT1B receptor coupling, and again the effects of the t
68 th the structure of the 5-HT2B receptor, the 5-HT1B receptor displays a 3 angstrom outward shift at t
69 nity shift of 5-HT1A receptors compared with 5-HT1B receptors (EC50 values of 6.4 and 12.0 nM, respec
74 In conclusion, these studies indicate that 5-HT(1B) receptor function can be assessed using agonist
75 n (5-HT) turnover and deficient 5-HT(1A) and 5-HT(1B) receptor function in brain regions regulating e
78 rinergic receptor-mediated inhibition of CHO/5-HT1B receptor function was blocked when 5-HT2A recepto
79 ion of 5-HT2A receptors had no effect on CHO/5-HT1B receptor function, although 5-HT2A receptor-media
81 arch has focused on the 5-HT1A receptor, the 5-HT1B receptor has a lesser known role in modulating em
82 ing emotional behaviour and the 5-HT(1A) and 5-HT(1B) receptors have been shown to have distinct role
85 investigate the localisation of 5-HT(1A) and 5-HT(1B) receptors in CeA projection neurones identified
87 y underscores the role played by presynaptic 5-HT(1B) receptors in mediating the effects of cocaine o
88 sent investigation to assess the function of 5-HT(1B) receptors in the modulation of synaptic transmi
91 as designed to assess the involvement of VTA 5-HT1B receptors in mediating the stimulatory effects of
94 GFP injection induced elevated expression of 5-HT1B receptors in neuronal fibers in VTA and increased
95 by examining the subcellular localization of 5-HT1B receptors in the mouse SCN using electron microsc
98 that cocaine acts as an indirect agonist of 5-HT1B receptors in vivo and demonstrate that activation
100 The results suggest that activation of VTA 5-HT1B receptors increases mesolimbic DA neuron activiti
101 gic inputs that are inhibited by presynaptic 5-HT1B receptors; inhibition of excitatory synapses onto
104 results thus demonstrate that stimulation of 5-HT1B receptors is required for fenfluramine-induced an
105 To test the hypothesis that stimulation of 5-HT1B receptors is required for the anorectic effect of
106 ts are in opposition to recent findings with 5-HT1B receptor knock-out mice and may have important on
110 nes retrogradely-labelled with CTb expressed 5-HT(1B) receptor-like immunoreactivity, whereas fewer (
111 alterations in 5-HT afferent innervation and 5-HT1B receptor localization were observed throughout th
112 clock through the activation of presynaptic 5-HT(1B) receptors located on retinal terminals in the s
114 he circadian system by acting at presynaptic 5-HT1B receptors located on retinal axons in the SCN.
115 ctively, and support the suggestion that VTA 5-HT(1B) receptors may be involved in part in mediating
116 he lack of 5-HT2A mediated regulation of CHO/5-HT1B receptors may be due to activation of a third pat
117 reductions found in this study suggest that 5-HT1B receptors may contribute to the etiology or expre
120 n SNr GABA neurons, indicating a presynaptic 5-HT1B receptor-mediated inhibition of glutamate release
121 ay be associated, at least in part, with the 5-HT1B receptor-mediated inhibition of VTA GABA release.
123 ells, 5-hydroxytryptamine (5-HT)1B-like (CHO/5-HT1B) receptor-mediated inhibition of forskolin-stimul
124 ences aggressive behavior, a distinct set of 5-HT1B receptors modulates impulsive behavior during adu
125 as, with bLRs having greater 5-HT1A, but not 5-HT1B, receptor mRNA levels in the septum, hippocampus
126 nterpretation that activation of presynaptic 5-HT(1B) receptors on retinal terminals in the SCN atten
131 ronal circuits and particularly 5-HT(1A) and 5-HT(1B) receptors play a prominent role in the regulati
132 idence suggests that 5-hydroxytriptamine-1B (5-HT1B) receptors play a role in modifying ethanol's rei
134 ion and find that serotonin (5-HT) activates 5-HT(1b) receptors resulting in a long-term depression (
135 its to membranes expressing either 5-HT1A or 5-HT1B receptors shifted the majority of the receptors t
136 h serotonin receptor 1B (5-HTR1B), modulates 5-HT1B receptor signal transduction, and is required for
137 stochemical study, using NPY, alpha-MSH, and 5-HT(1B)-receptor-specific antibodies and slides assesse
138 the behavioral consequences of mCPP-induced 5-HT(1B) receptor stimulation are unmasked in animals de
140 odulating signaling through 5-HT4 as well as 5-HT1B receptors supports the concept that this protein
141 ity requires activation of nucleus accumbens 5-HT1B receptors, the blockade of which prevents social
142 ncrease serotonergic receptor functions (eg, 5-HT(1B) receptors), these data support the need for fur
143 act in concert to mediate the ability of the 5-HT1B receptor to couple specifically to inhibitory G p
144 of the ability of the 5-hydroxytryptamine1B (5-HT1B) receptor to discriminate between G protein heter
145 bilities of the Galphat/Galphai1 chimeras to 5-HT1B receptors using high affinity agonist binding and
147 e contribution of the 5-hydroxytryptamine1B (5-HT1B) receptor, we studied the induction of the immedi
148 retrogradely-labelled neurones positive for 5-HT(1B) receptor were present in both lateral and media
149 tly into DRN using stereotaxic procedure, HA-5-HT(1B) receptors were expressed in serotonergic neuron
150 rcing effects and voluntary intake, and that 5-HT1B receptors within the ventral tegmental area (VTA)
151 dy was designed to assess the involvement of 5-HT1B receptors within the ventral tegmental area (VTA)
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