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1 elective, with subnanomolar affinity for the 5-HT1A receptor.
2 ike effect of D1 and possible involvement of 5-HT1A receptor.
3  intrinsic activity (E max = 26 +/- 2.0%) on 5-HT1A receptor.
4 ceptor in recombinant cells expressing human 5-HT1A receptor.
5 at serotonin is primarily acting through the 5-HT1A receptor.
6  hypothalamus and hippocampus is mediated by 5-HT1A receptors.
7 ed with the known postmortem distribution of 5-HT1A receptors.
8 ylpiperazine ([(18)F]MPPF), an antagonist of 5-HT1A receptors.
9 A, gamma-aminobutyric acid (GABA)B , BZ, and 5-HT1A receptors.
10 HT to a concentration sufficient to activate 5-HT1A receptors.
11 rotonin transporter (SERT) and serotonin 1A (5-HT1A) receptor.
12 h potency and efficacy were increased at the 5-HT(1A) receptor.
13 ilar to the agonist-induced responses of the 5-HT(1A) receptor.
14 hether protection required activation of the 5-HT(1A) receptor.
15 use and human MC respond to 5-HT through the 5-HT(1A) receptor.
16 e on the expression of the gene encoding the 5-HT(1A) receptor.
17 a high affinity (0.1 nM) and selectivity for 5-HT(1A) receptors.
18 at its main pharmacology is mediated via the 5-HT(1A) receptors.
19 sitization rather than downregulation of DRN 5-HT(1A) receptors.
20 ow produce functional desensitization of DRN 5-HT(1A) receptors.
21 eptor domains and substitutes for endogenous 5-HT(1A) receptors.
22 10 specific binding in brain regions rich in 5-HT(1A) receptors.
23 selectivity for 5-HT(2A) versus 5-HT(2C) and 5-HT(1A) receptors.
24 e first promising agonist PET tracer for the 5-HT(1A) receptors.
25 ining NMDA receptor is the primary target of 5-HT(1A) receptors.
26 t inhibited by activation of the 5-HT(5A) or 5-HT(1A) receptors.
27 hereby could provide a measure of functional 5-HT(1A) receptors.
28 ng in CHO cells expressing the serotonin-1A (5-HT(1A)) receptor.
29 , pretreatment with a specific antagonist of 5-HT1A receptors, 4-iodo-N-[2-[4-(methoxyphenyl)-1-piper
30                                      Because 5-HT(1A) receptor (5-HT(1A)R) internalization has been p
31 diating the intracellular traffic of the rat 5-HT(1A) receptor (5-HT(1A)R) toward dendrites.
32 ne ring present in the previously identified 5-HT1A receptor (5-HT1AR) ligand 3.
33 paring Smo with the 5-hydroxytryptamine(1A) (5-HT(1A)) receptor, a quintessential G(i)-coupled recept
34  the lipid dependence of the human serotonin 5-HT1A receptor, a GPCR that is central to neuronal func
35   Taken together, these results suggest that 5-HT(1A) receptor activation is a critical step in the a
36 to reveal the motivational mechanism whereby 5-HT(1A) receptor activation modulates drinking behavior
37 of drug alone via a mechanism dependent upon 5-HT(1A) receptor activation.
38  suppress the antidepressant-like effects of 5-HT1A receptor activation.
39 f so, whether the increase is dependent upon 5-HT1A receptor activation.
40 5-HT(1D) receptors, it exhibited appreciable 5-HT(1A) receptor affinity.
41 his study, we radiolabeled the high-affinity 5-HT(1A) receptor agonist (18)F-F13714 and investigated
42 n of caudal MR serotonergic neurons with the 5-HT(1A) receptor agonist (R)-(+)-8-hydroxy-2(di-n-propy
43 xetine attenuated hypothermia induced by the 5-HT(1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)
44 thesis using bilateral microperfusion of the 5-HT(1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)
45                                The selective 5-HT(1A) receptor agonist 8-hydroxy-2-dipropylaminotetra
46                       Microinjections of the 5-HT(1A) receptor agonist 8-OHDPAT (0.1, 1.0 and 3.0 nmo
47                  (S)-2 proved to be a potent 5-HT(1A) receptor agonist highly selective over alpha(1)
48 he effect of citalopram, whereas exposure to 5-HT(1A) receptor agonist only moderately influenced mal
49 rone treatment attenuated the effects of the 5-HT(1A) receptor agonist, (+/-)-8-hydroxy-2-(di-n-propy
50 s were used to test the possibility that the 5-HT(1A) receptor agonist, 8-hydroxy-2-(di-N-propylamino
51                                          The 5-HT(1A) receptor agonist, 8-OH-DPAT, reduced cAMP accum
52  receptor agonist, apomorphine (APO) and the 5-HT(1A) receptor agonist, 8-OHDPAT (8OH) in a low dose
53                                    Moreover, 5-HT(1A) receptor agonist-induced hypothermia is blunted
54                           Treatment with the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylmino)tet
55 tested for behavior under effective doses of 5-HT1A receptor agonist 8-hydroxy-N, N-dipropyl-2-aminot
56 ted following systemic administration of the 5-HT1A receptor agonist, 8-OH-DPAT, the D2 receptor anta
57                       Treatment with another 5-HT1A receptor agonist, buspirone (1.5 mg/kg, i.p.), re
58 Identical results were obtained with another 5-HT1A receptor agonist, buspirone (1.5 mg/kg, i.p.; n =
59 te brain, in contrast to 8-OH-DPAT, a potent 5-HT1A receptor agonist.
60                                        Three 5-HT1A receptor agonists (8-OH-DPAT, F13714 and F15599)
61                             We conclude that 5-HT1a receptor agonists have two competing effects: rap
62 t years, new chemical entities targeting the 5-HT(1A) receptor (alone or in combination with other mo
63 affinities and functional activities for the 5-HT(1A) receptor and 5-HT transporter.
64                                              5-HT(1A) receptor and alpha(1)-adrenoreceptor (alpha(1)-
65 h K(i) values of approximately 30 nM for the 5-HT(1A) receptor and K(i) values of 5 and 0.5 nM for th
66 series possessed high affinity for the human 5-HT(1A) receptor and many displayed potent antagonist a
67 mal binding) of ((3)H)-WAY 100635 binding to 5-HT(1A) receptors and ((3)H)-ketanserin binding to 5-HT
68 eir in vitro pharmacological profile at both 5-HT(1A) receptors and alpha(1)-adrenoceptor subtypes wa
69 er, curcumin treatment, via up-regulation of 5-HT(1A) receptors and BDNF, may reverse or protect hipp
70        The effects of 5-HT were mediated via 5-HT(1A) receptors and required the function of Galpha(i
71 f dihydrofuroaporphine bind to the serotonin 5-HT1A receptor and exert opposite effects.
72   Further investigation into the role of the 5-HT1A receptor and the potential of [11C]-WAY100635 PET
73 bited these cells directly via activation of 5-HT1A receptors and indirectly via enhanced GABA releas
74 measured in brain is dominated by binding to 5-HT1A receptors and to reveal the extent of defluorinat
75 receptors, direct or indirect stimulation of 5-HT(1A) receptors, and to a lesser extent, reduction in
76  onto Receptor (Type II) cells by activating 5-HT1A receptors, and reducing ATP secretion.
77 -HT release throughout the DR, activation of 5-HT1A receptors, and subsequent inhibition.
78  profile of 5-HT(1A-1D) and 5-HT2 receptors, 5-HT1A receptors, and the serotonin (5-HT) transporter (
79 ing of pallidal neurons through postsynaptic 5-HT1A receptors; and (3) 5-HT postsynaptically excites
80 a and 4ccis emerged as novel and interesting 5-HT(1A) receptor antagonist (pK(i) = 8.70) and a 5-HT(1
81 n of fluoxetine (Prozac), others receiving a 5-HT(1A) receptor antagonist (WAY 100,635; Sigma, St. Lo
82 , its prevention by chronic treatment with a 5-HT(1A) receptor antagonist (WAY-100,635) did not preve
83  at the dosages used in this experiment, the 5-HT(1A) receptor antagonist WAY 100,635 may have positi
84                                The selective 5-HT(1A) receptor antagonist WAY100135 (10 microM) block
85 onin (5-hydroxytryptamine, 5-HT), as did the 5-HT(1A) receptor antagonist WAY100635.
86 by pretreatment with WAY-100635, a serotonin 5-HT(1A) receptor antagonist, in DAT-KO mice, but the dr
87  avoidance learning may be stimulated by the 5-HT(1A) receptor antagonist.
88 nists (8-OH-DPAT, F13714 and F15599) and one 5-HT1A receptor antagonist (MPPF) were compared in terms
89        Instead, CUMI-101 behaved as a potent 5-HT1A receptor antagonist by dose-dependently inhibitin
90 nduced increase in social behaviors, while a 5-HT1A receptor antagonist did not alter affiliative voc
91 infused with WAY100635 (400 to 2000 ng), the 5-HT1A receptor antagonist did not facilitate lordosis r
92                        CUMI-101 behaves as a 5-HT1A receptor antagonist in primate brain, with signif
93 udy showed that CUMI-101 behaved as a potent 5-HT1A receptor antagonist in rat brain.
94 ntagonist SB 216641 (10 microM), but not the 5-HT1A receptor antagonist WAY 100635 (10 microM) or the
95 y 8-OH-DPAT persisted in the presence of the 5-HT1A receptor antagonist WAY-100635, was abolished by
96 antagonist), WAY-100635 (selective serotonin 5-HT1A receptor antagonist) as well as monoamine oxidase
97 1D/1A) receptor antagonist) or WAY 100635 (a 5-HT1A receptor antagonist).
98 contribute to propranolol's action since the 5-HT1A receptor antagonist, (S)-WAY 100135 (P = 0.2), an
99 n emission tomography imaging and a specific 5-HT1A receptor antagonist, [carbonyl-11C]WAY-100635.
100 rying concentrations (200 to 2000 ng) of the 5-HT1A receptor antagonist, N-[2[4-(2-methoxyphenyl)-1-p
101 5-HT2C receptor antagonist, SB242084, or the 5-HT1A receptor antagonist, WAY-100635, and were tested
102 ing serotonin (5-HT) reuptake inhibitors and 5-HT1A receptor antagonists.
103 tative differences in the mechanisms whereby 5-HT(1A) receptors are able to inhibit stimulation of ad
104  studies suggest that spinal and supraspinal 5-HT(1A) receptors are involved in multiple inhibitory m
105                                   Inhibitory 5-HT(1a) receptors are located on serotonin (5-HT) neuro
106 ypercapnia, but not to hypoxia, and that MRR 5-HT1A receptors are also involved in thermoregulation a
107        Presynaptic dorsal raphe neuron (DRN) 5-HT1A receptors are known to have a critical role in af
108                                          The 5-HT1A receptors are located both presynaptically and po
109                                Serotonin 1A (5-HT1A) receptors are involved in several physiological
110 ally interesting to consider and justify the 5-HT(1A) receptor as a new attractive target for drug di
111 formance and 3H-8-OH-DPAT-labeled binding of 5-HT(1a) receptors as well as 125I-LSD-labeled binding o
112 g and is a partial agonist for the serotonin 5-HT(1A) receptors as well as possessing low affinity an
113 hippocampus while increasing the efficacy of 5-HT1A receptors as measured by agonist-stimulated [35S]
114 pharmacology showed that focal activation of 5-HT1A receptors at the axon initial segment (AIS), but
115                                     ANOVA of 5-HT(1A) receptor availability demonstrated a significan
116 is was not associated with MAO-A genotype or 5-HT(1A) receptor availability in these regions.
117  MAO-A activity were associated with greater 5-HT(1A) receptor availability in women, but not in men.
118 we investigated the relationship between DRN 5-HT1A receptor availability and amygdala reactivity to
119  processing and the relationship between DRN 5-HT1A receptor availability and amygdala reactivity.
120                           Alterations in DRN 5-HT1A receptor availability cause phenotypes characteri
121                       Our data show that DRN 5-HT1A receptor availability is linked specifically to t
122               However, it is unknown whether 5-HT1A receptor availability is linked specifically to t
123 we tested drugs that stimulate serotonin 1A (5-HT1A) receptors, based on our previous findings that t
124 ent study, it was found that blockade of the 5-HT(1A) receptor before and after pilocarpine treatment
125  found between 5-HT neuron count or density, 5-HT(1A) receptor binding density, or 5-HTT receptor bin
126 HT neurons, there was a decrease with age in 5-HT(1A) receptor binding in the SIDS cases but no chang
127                                 We estimated 5-HT(1A) receptor binding preoperatively with (18)F-tran
128  as well as a significantly lower density of 5-HT(1A) receptor binding sites (P<or=.01 for all 9 nucl
129                                              5-HT(1A) receptor binding was 29% to 55% lower in 3 medu
130 oleacetic acid (5-HIAA); levels of TPH2; and 5-HT(1A) receptor binding.
131                    A significant increase in 5-HT1A receptor binding density was observed across infa
132                        We observed increased 5-HT1A receptor binding in women who had recovered from
133  exception of the hypoglossal nucleus, where 5-HT1A receptor binding increases while SERT binding rem
134                                              5-HT1A receptor binding is also associated with treatmen
135                        Regional estimates of 5-HT1A receptor binding potential (nondisplaceable) were
136                                     Specific 5-HT1A receptor binding was assessed using the binding p
137                                     However, 5-HT1A receptor binding was associated with a measure of
138 an age, 25.1 +/- 5.8 years).Intervention The 5-HT1A receptor binding was measured using positron emis
139 hey exhibit reduced 5-HT neuron activity and 5-HT1A receptor binding with varying changes in postsyna
140 s receptor decreases it, we examined whether 5-HT(1A) receptor blockade would prevent the seizure-ind
141 d by either 5-HT2A/C receptor stimulation or 5-HT1A receptor blockade of naive control pups.
142                                          The 5-HT(1A) receptor BP was inversely associated with heart
143 so blocked functional desensitization of DRN 5-HT(1A) receptors by uncontrollable stress.
144 nsitivity, suggesting that Rh-CT(5-HT1A) and 5-HT(1A) receptors compete to interact with the same tra
145 A receptor protomer in the hippocampal FGFR1-5-HT1A receptor complex enhancing the FGFR1 signaling.
146 r receptor 1 (FGFR1)-5-hydroxytryptamine 1A (5-HT1A) receptor complexes have been demonstrated and th
147 promoter, so that they are only expressed in 5-HT1A receptor-containing cells.
148                  These data suggest that the 5-HT(1A) receptor contains high and moderate affinity Ca
149                                    The human 5-HT(1A) receptor contains two putative CaM binding moti
150 esults demonstrate that drugs that stimulate 5-HT1A receptors counteract respiratory abnormalities in
151                                The serotonin 5-HT(1A) receptor couples to heterotrimeric G proteins a
152 unexpected, large increase in the inhibitory 5-HT(1A) receptor currents.
153                      A strong correlation of 5-HT(1A) receptor decreases in hippocampus with worsenin
154 ssion tomography (PET) for quantification of 5-HT(1A) receptor densities in the living brains of Alzh
155  compromises the accuracy of measurements of 5-HT1A receptor densities in adjacent areas of brain bec
156 ts applicability to measuring brain regional 5-HT1A receptor densities.
157 esearch with PET for measuring serotonin 1A (5-HT1A) receptor densities in brain regions of human sub
158 ases in social behaviors are 5-HT2A, but not 5-HT1A, receptor dependent.
159 ffects of uncontrollable stress also blocked 5-HT(1A) receptor desensitization.
160        We determined that stimulation of the 5-HT1A receptor did not contribute to this improvement i
161 TM4/TM5 can form an interaction interface in 5-HT(1A) receptor dimers and indicates that specific ami
162 inding in rats was consistent with the known 5-HT(1A) receptors distribution (hippocampus and cortica
163 ) F-Mefway therefore may be used to quantify 5-HT1A receptor distribution in brain regions for the st
164 G protein-coupled receptor that targets into 5-HT(1A) receptor domains and substitutes for endogenous
165 titive control of Gi/o pathway activation in 5-HT1A receptor domains in the dorsal raphe nucleus (DRN
166 ic alpha1 and alpha2 receptors; serotonergic 5-HT1A receptors; dopaminergic D1/5 receptors by using q
167                                              5-HT(1A) receptors exist in high- and low-affinity state
168                 The inhibitory serotonin-1A (5-HT(1A)) receptor exists in two separate populations wi
169 ion of the serotonin 5-hydroxytryptamine-1A (5-HT(1A)) receptor expressed in CHO-K1 cells.
170 be associated with sex-specific variation in 5-HT(1A) receptor expression.
171 l polymorphism in the promoter region of the 5-HT(1A) receptor gene is associated with depression and
172 orphism in the promoter of the serotonin-1A (5-HT(1A)) receptor gene in increased susceptibility to d
173      Altered regulation of the serotonin-1A (5-HT1A) receptor gene is implicated in major depression
174  activities at both the 5-HT transporter and 5-HT1A receptor, good selectivity over the alpha1-adrene
175 of the serotonin 1A (5-hydroxytryptamine 1A [5-HT(1A)]) receptor has been widely used in clinical stu
176 results reveal the broad dependence that the 5-HT1A receptor has on plasma membrane properties, demon
177 tonergic system, including the serotonin 1A (5-HT(1A)) receptor, has been implicated in the pathophys
178  5-HT1A receptors in line with evidence that 5-HT1A receptors have a role in mediating emotional proc
179                                    Serotonin 5-HT1A receptors have been implicated in disorders of th
180           Current PET radioligands targeting 5-HT1A receptors have limitations hindering widespread P
181 -HT1A autoreceptors by being part of a FGFR1-5-HT1A receptor heterocomplex in the midbrain raphe 5-HT
182 e cells, evidence for the existence of FGFR1-5-HT1A receptor heterocomplexes in the dorsal and median
183  that CaM binding and phosphorylation of the 5-HT(1A) receptor i3 loop peptides by protein kinase C a
184     (18) F-Mefway appears to be an effective 5-HT1A receptor imaging agent in all models, including h
185  uptake and, in turn, its spillover on brain 5-HT1A receptor imaging were assessed by PET with venous
186 gh the authors observed a greater density of 5-HT1A receptor immunoreactivity in H-Agg hamsters withi
187 2A), serotonin 2C (5-HT2C) and serotonin 1A (5-HT1A) receptors, implicated in the development of anxi
188 modulin (CaM) co-immunoprecipitates with the 5-HT(1A) receptor in Chinese hamster ovary fibroblasts.
189 tered serotonin transmission by means of the 5-HT(1A) receptor in dysfunction of prefrontal cortex py
190 onfirming the requirement for activating the 5-HT(1A) receptor in initiating this survival pathway.
191 also observed an increased expression of the 5-HT(1A) receptor in ipsapirone-treated control neurons.
192 transfer to show that CaM interacts with the 5-HT(1A) receptor in living cells, representing the firs
193 lso highlight the importance of the cortical 5-HT(1A) receptor in mediating cognition.
194 s of each receptor, Smo is equivalent to the 5-HT(1A) receptor in the assay as it relates to capacity
195 ity, and resulted in better visualization of 5-HT(1A) receptor in the brain.
196 tomography and [(11)C]WAY-100635 to quantify 5-HT(1A) receptors in a group of 31 healthy and unmedica
197 eased [(11)C]CUMI-101 BP(ND) at postsynaptic 5-HT(1A) receptors in several cortical regions, but ther
198  for probing the high-affinity states of the 5-HT(1A) receptors in vitro and in vivo.
199                   Translation of imaging the 5-HT1A receptor in animal models to humans will facilita
200 adiotracer for PET experiments examining the 5-HT1A receptor in neuropsychiatric disorders and drug i
201 rements show simultaneous trafficking of the 5-HT1A receptor in two distinct endosomal recycling path
202                    We therefore knocked down 5-HT1A receptors in either the dorsal raphe (presynaptic
203 ns of decreased immunoreactive perikarya and 5-HT1A receptors in fluoxetine-treated hamsters.
204                                 Knockdown of 5-HT1A receptors in hippocampus, but not dorsal raphe, s
205 rsive stimuli and that this is linked to DRN 5-HT1A receptors in line with evidence that 5-HT1A recep
206  of DA D2 receptors in mPFC or activation of 5-HT1A receptors in OFC increases impulsive choice in th
207 ial of 18F-FCWAY to act as a radioligand for 5-HT1A receptors in rat brain and also revealed extensiv
208 FCWAY, results in effective imaging of brain 5-HT1A receptors in rat.
209 e as an effective platform for investigating 5-HT1A receptors in rodent models of neuropsychiatric co
210 e influence of pharmacological activation of 5-HT1A receptors in specific brain regions, this neuroim
211   Finally, we demonstrate that activation of 5-HT1A receptors in the dBNST is necessary for the anxio
212 r the results suggest that the activation of 5-HT1A receptors in the DRN results from the local relea
213 hat serotonin signaling through postsynaptic 5-HT1A receptors in the hippocampus is critical for the
214 nd Ad-1AP-antisense) were used to manipulate 5-HT1A receptors in the hypothalamus.
215              The density and the function of 5-HT1A receptors in the medial hypothalamus were signifi
216 hypothalamus of SERT knock-out mice restored 5-HT1A receptors in the medial hypothalamus; this effect
217  support earlier findings that activation of 5-HT1A receptors in the mediobasal hypothalamus inhibits
218 itory effects of substance P, implicating DR 5-HT1A receptors in this response.
219 f research have implicated the serotonin 1A (5-HT1A) receptor in major depressive disorder (MDD).
220 ed decreased density of 5-hydroxytryptamine (5-HT1A) receptors in the hypothalamus, amygdala, and dor
221 or the serotonin 1A (5-hydroxytryptamine 1A [5-HT1A]) receptor in recombinant cells expressing human
222 etine persistently upregulated SERT, but not 5-HT1A receptors, in both the neocortex and the hippocam
223            Our goal was to determine whether 5-HT(1A) receptors inhibit opioid release in the spinal
224                      These results show that 5-HT(1A) receptors inhibit opioid release in the spinal
225                              Here, activated 5-HT1A receptors inhibit firing and, thereby, muscle con
226   Here we show that serotonin, by activating 5-HT(1A) receptors, inhibited NMDA receptor-mediated ion
227 e feedback onto receptor cells by activating 5-HT(1A) receptors, inhibiting taste-evoked Ca(2+) mobil
228  previous study has shown that activation of 5-HT(1A) receptors inhibits N-methyl-D-aspartate (NMDA)
229                                          The 5-HT(1A) receptor is a metabotropic G protein-coupled re
230 the serotonergic (5-HT) system, of which the 5-HT1A receptor is an essential component.
231 further demonstrate that tonic activation of 5-HT1A receptors is not responsible for the absence of s
232                        Motor maps derived in 5-HT1A receptor knock-out mice also showed higher moveme
233                               mBMMC from the 5-HT(1A) receptor knockout mouse (5-HT(1A)R(-/-)) did no
234                                 In contrast, 5-HT(1A) receptor levels and G-protein coupling is norma
235 d chronic stimulant effects of cocaine using 5-HT1A receptor ligands in autoreceptor preferring doses
236                                              5-HT1A receptor ligands were ineffective.
237  whereas fewer (approximately 30%) expressed 5-HT(1A) receptor-like immunoreactivity.
238                                   Therefore, 5-HT(1A) receptors likely decrease the analgesia produce
239 ily and displayed a preferential labeling of 5-HT(1A) receptors located in cingulate cortex.
240                                              5-HT(1A) receptor maximal binding in the temporal cortex
241                                The serotonin 5-HT(1A) receptor may modulate some of the negative, cog
242 s favorable in vivo properties for serotonin 5-HT1A receptor measurements in humans.
243                 Moreover, these decreases in 5-HT(1A) receptor measures correlate with decreased gluc
244 sis that the 5-HT(7) but not the 5-HT(5A) or 5-HT(1A) receptors mediate serotonergic phase shifts.
245 m, we provide the first reported profile for 5-HT(1A) receptor-mediated ERK activation using a panel
246 e, but not controllable, tail shock impaired 5-HT(1A) receptor-mediated inhibition of DRN neuronal fi
247  potential significance of these findings to 5-HT(1A) receptor-mediated inhibition of female rat lord
248               This process is underpinned by 5-HT1A receptor-mediated activation of G-protein-coupled
249 nhibitors during development, have amplified 5-HT1A receptor-mediated currents in adulthood.
250 ted depolarization and the appearance of the 5-HT1A receptor-mediated hyperpolarization appears to re
251 hesis in mouse DRN brain slices by recording 5-HT1A receptor-mediated inhibitory postsynaptic current
252 n slices evoked serotonin release produced a 5-HT1A receptor-mediated inhibitory postsynaptic current
253 for the role of progesterone in altering the 5-HT(1A) receptor modulation of lordosis behavior.
254   Here we used computational modeling of the 5-HT(1A) receptor monomer and dimer to predict residues
255                      We also found divergent 5-HT1A receptor mRNA expression within some of these sam
256 ty, we investigated the impact of activating 5-HT1A receptors on post-C5 SCI respiratory dysfunction.
257 1A) receptor antagonist (pK(i) = 8.70) and a 5-HT(1A) receptor partial agonist (pK(i) = 9.25, pD(2) =
258                             As serotonin 1A (5-HT1A) receptors participate in the inhibition of aggre
259  study provides class III evidence that both 5-HT(1A) receptor PET and CMRglc PET can contribute to t
260 a possible role for CaM in the regulation of 5-HT(1A) receptor phosphorylation and desensitization.
261                          Brain serotonin 1A (5-HT1A) receptors play an important role in mood disorde
262 s demonstrate that serotonin, acting through 5-HT1A receptors, plays an excitatory role in forelimb m
263 ntributions of various pre- and postsynaptic 5-HT1A receptor populations to the behavioral effects of
264  lateral and medial parts of the CeA whereas 5-HT(1A) receptor positive neurones were located mainly
265                          Availability of DRN 5-HT1A receptors positively correlated with amygdala con
266 y, in part, be mediated by activation of the 5-HT1A receptor protomer in the hippocampal FGFR1-5-HT1A
267 est to develop an (18)F-labeled full agonist 5-HT(1A) receptor radiotracer.
268 results demonstrate that medial hypothalamic 5-HT1A receptors regulate stress responses and locomotor
269 ey were blocked by antagonists of 5-HT2A and 5-HT1A receptors, respectively.
270                      Targeted suppression of 5-HT(1A) receptor-responsive PPTn neurons also increased
271                     These data indicate that 5-HT(1A) receptor-responsive PPTn neurons normally funct
272                           Serotonin type 1A (5-HT(1A)) receptor-responsive neurons in the pedunculopo
273 ution of Rh-CT(5-HT1A) resembles that of the 5-HT(1A) receptor; Rh-CT(5-HT1A) localizes to somatodend
274  mediated, at least partially, by changes in 5-HT1A receptor sensitivity.
275  additional receptor-interacting proteins in 5-HT(1A) receptor signaling.
276 t 5-HTTLPR effect on receptor binding at the 5-HT(1A) receptor site has been reported in humans, sugg
277  s-carriers) to examine the relation between 5-HT(1A) receptor-specific binding and 5-HTTLPR genotype
278                        Pretreatment with the 5-HT1A receptor-specific antagonist N-[2-[4-(2-methoxyph
279                                              5-HT(1A) receptor stimulation and 5-HT(6) and 5-HT(7) re
280 ists, further evidence for the importance of 5-HT(1A) receptor stimulation in the NOR deficit produce
281 e 5-HT(2A) receptor stimulation, relative to 5-HT(1A) receptor stimulation, both of which can increas
282 ortex, and that the effect is dependent upon 5-HT(1A) receptor stimulation.
283 t have an agonist/antagonist activity at the 5-HT(1A) receptor subtype are known to greatly potentiat
284 l gamma oscillations in both species via the 5-HT1A receptor subtype.
285 pathway--as during motor exercise--activated 5-HT1A receptors that decreased motoneuronal excitabilit
286    Here, we define a mechanism downstream of 5-HT1A receptors that mediates antidepressant-like behav
287 pression-related research has focused on the 5-HT1A receptor, the 5-HT1B receptor has a lesser known
288  on expression and signaling activity of the 5-HT(1A) receptor to a ligand with an intrinsic agonist
289 To evaluate the contribution of hypothalamic 5-HT1A receptors to these phenotypes of SERT knock-out m
290 he dBNST modulates anxiety-like behavior via 5-HT1A receptors under naturalistic conditions.
291                               This effect of 5-HT(1A) receptors was blocked by agents that interfere
292  effect of WAY-100,635, an antagonist to the 5-HT(1A) receptors, was tested.
293        In addition, while the effects of the 5-HT1A receptor were limited, the broad effects of 5-HT3
294 m being protective led to desensitization of 5-HT(1A) receptors, whereas treatments that block the be
295 omography (PET) imaging studies of serotonin 5-HT1A receptors which are implicated in various brain f
296  with an antibody against the serotonin(1A) (5-HT(1A)) receptor, which also mediates inhibitory regul
297 ferent aspects of the depolarization, and of 5-HT1A receptors, which signal the late developing hyper
298 inds selectively to the 5-hydroxytryptamine (5-HT1A) receptor, which is expressed on pyramidal neuron
299 nergic modulation of 5-hydroxytryptamine 1A (5-HT1A) receptors, which hyperpolarizes the activation r
300 e electrophysiological effects of prefrontal 5-HT1A receptors with implications for neuropsychiatric
301                 Interactions between NK1 and 5-HT1A receptors within DR neural networks may contribut

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