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1 e focused upon the effects of activating the dopamine D1 receptor.
2 eases in response to stimulation of striatal dopamine D1 receptors.
3 gic neurons, and (2) excitation initiated by dopamine D1 receptors.
4 c cholinergic, adenosine A2, dopamine D2, or dopamine D1 receptors.
5 g affinity (Ki = 49.3 nM) and selectivity to dopamine D1 receptors.
6 highest binding affinity (Ki = 60.3 nM) for dopamine D1 receptors.
7 uent activation of norepinephrine alpha2 and dopamine D1 receptors.
13 phosphorylation, whereas the effects of the dopamine D1 receptor agonist are blocked by genistein, a
14 lated RGCs, the application of dopamine or a dopamine D1 receptor agonist decreased voltage-activated
16 hr34 DARPP-32 and phospho-Ser845 GluR1 after dopamine D1 receptor agonist or forskolin stimulation.
17 d by treatment of neostriatal neurons with a dopamine D1 receptor agonist or with forskolin, consiste
18 e-treated and normal individuals, whilst the dopamine D1 receptor agonist SKF 38393 (30 mg/kg, i.p.)
19 st dose tested (18 nmol) of a mixture of the dopamine D1 receptor agonist SKF 38393 and the D2 agonis
20 owing by conditioning rats under the partial dopamine D1 receptor agonist SKF 38393 or the opioid ant
21 e administration of a low dose of either the dopamine D1 receptor agonist SKF-38393 or the D2 recepto
23 ain slices of neonatal (P7) rat striatum the dopamine D1 receptor agonist SKF-82958 significantly dec
25 acute behavioral response of DA-/- mice to a dopamine D1 receptor agonist was correlated with c-fos i
26 also attenuated the hyperthermia caused by a dopamine D1 receptor agonist, SKF 38393 (10 mg/kg, s.c.)
27 82958 (SKF), a previously characterized full dopamine D1 receptor agonist, to stimulate the transcrip
29 harmacological roles of Gs- and Golf-coupled dopamine D1 receptor and adenosine A2A receptor in the b
30 an be used to reveal potentially therapeutic dopamine D1 receptor and adenosine A2A receptor ligands
31 ave been developed for 48 antagonists of the dopamine D1 receptor and applied to mining chemical data
37 252a, a Trk tyrosine kinase inhibitor, and a dopamine D1 receptor antagonist could block the effects
38 Systemic administration of the selective dopamine D1 receptor antagonist SCH 23390 [R(+)-7-chloro
40 usion of 10 microg (but not 2 microg) of the dopamine D1 receptor antagonist SCH-23390 greatly impair
42 s sufficient to induce BDNF in the mPFC, and dopamine D1 receptor antagonist treatment blocked the an
43 way were attenuated by pretreatment with the dopamine D1 receptor antagonist, SCH23390, which also ca
44 kDa), in the absence or in the presence of a dopamine D1 receptor antagonist, we provide evidence tha
47 sion of the AMPA-receptor antagonist CNQX or dopamine D1-receptor antagonist SCH-23390 into the DLS b
55 and full intrinsic activity at cloned human dopamine D1 receptors but had much lower affinity at dop
56 One new receptor, DAMB, was identified as a dopamine D1 receptor by sequence analysis and pharmacolo
57 and the previous finding on up-regulation of dopamine D1 receptors by NMDAR activation provide a cell
59 ecause of increased transmission through the dopamine D1 receptor/cAMP-dependent protein kinase pathw
60 These results indicate that stimulation of dopamine D1 receptors can be coupled to the neurotrophin
62 They also demonstrate that activation of dopamine D1 receptors corrects these deficits, through a
63 firing, and that this effect is mediated by dopamine D1 receptor-coupled Ca2+ signalling pathways.
64 rebral cortical areas, substantially reduced dopamine D1 receptor coupling to G(s)-protein, and defic
65 inhibit movement, whereas those that express dopamine D1 receptors (D1+) project to the substantia ni
66 In this study, we show that mice lacking the dopamine D1 receptor (D1R KO mice) manifest greatly redu
67 ss impairs working memory via high levels of dopamine D1 receptor (D1R) activation of cyclic adenosin
68 disease, is associated with an alteration in dopamine D1 receptor (D1R) and glutamate receptor intera
70 inding activity of agonist and antagonist of dopamine D1 receptor (D1R) by using quartz crystal micro
73 omato BAC transgenic mice and found that the dopamine D1 receptor (D1R) is expressed in retinal bipol
74 ntrol of genetic regulatory elements for the dopamine D1 receptor (D1R) or dopamine D2 receptor (D2R)
75 rrent synaptic activity and was reduced by a dopamine D1 receptor (D1R) protein kinase A pathway.
77 , removing NMDARs from MSNs that express the dopamine D1 receptor (D1R) significantly attenuated AMPH
78 Finally, conditional knock-out of Cav1.2 in dopamine D1 receptor (D1R)-expressing cells resulted in
80 gh both angiotensin AT1 receptors (AT1R) and dopamine D1 receptors (D1R) modulates renal sodium excre
83 rt of this, increased activation of striatal dopamine-D1 receptors (D1R) results in desensitization o
84 ippocampal neurons, we demonstrate here that dopamine D1 receptors (D1Rs) and NMDARs form dynamic sur
87 are medium spiny neurons (MSNs) that express dopamine D1 receptors (D1Rs) or D2 receptors (D2Rs), whi
90 mygdala enhanced cue-reward learning through dopamine D1 receptor-dependent mechanisms and suppressed
92 An amphetamine challenge reversed CPD via a dopamine D1-receptor-dependent paradoxical presynaptic p
93 SRT in the rat using direct infusions of the dopamine D1 receptor (DRD1) antagonist SCH 23390 or dopa
94 with a single nucleotide polymorphism in the dopamine D1 receptor (DRD1) gene, which was associated w
96 contrast, decreased dysbindin did not change dopamine D1 receptor (DRD1) levels, or its basal or dopa
97 cortical-limbic induced compulsions in which dopamine D1 receptor-expressing (D1+) neurons in restric
98 cholera toxin (CT) transgene in a subset of dopamine D1 receptor-expressing (D1+) neurons thought to
99 idence that supports a role of Cav1.2 within dopamine D1 receptor-expressing cells of the hippocampus
100 ent of excitatory synaptic transmission onto dopamine D1 receptor-expressing neurons (D1+ neurons) in
101 uced PGE2 targeted EP1 receptors on striatal dopamine D1 receptor-expressing neurons and that this si
102 diacylglycerol lipase alpha (DGLalpha), from dopamine D1 receptor-expressing or adenosine A2a recepto
103 ned mice that lack M4 mAChRs specifically in dopamine D1-receptor-expressing neurons, suggesting that
104 duced hypothyroidismin hamsters (HH) altered dopamine D1 receptor expression, D1 receptor-modulated v
107 f dendritic spines in MSN-D1 (MSN-expressing dopamine D1 receptors) from the core and shell of nucleu
110 PK and JNK signaling pathways is mediated by dopamine D1 receptors in SK-N-MC neuroblastoma cells.
112 d by testing the hypothesis that blockade of dopamine D1 receptors in the VTA attenuates the rewardin
116 t the direct inhibition of NMDA receptors by dopamine D1 receptor ligands is due to the channel pore
117 dies and structure-activity relationships of dopamine D1 receptor ligands suggest that their intrinsi
118 tina that bright-light-induced activation of dopamine D1 receptors located on ON-center cone bipolar
121 deletion of any other NF subunit, amplifies dopamine D1-receptor-mediated motor responses to cocaine
127 ing an amine-accepting binding domain on the dopamine D1 receptor protein that may be further explore
128 e, the PDE10A radioligand (18)F-MNI-659, the dopamine D1 receptor radioligand (11)C-NNC 112, and the
129 e, the PDE10A radioligand (18)F-MNI-659, the dopamine D1 receptor radioligand (11)C-NNC 112, and the
131 twork firing, whereas optimal stimulation of dopamine D1 receptors sculpts network inputs to refine m
135 Although considerable evidence implicates dopamine D1-receptor signaling in the nucleus accumbens
137 FosB and dynorphin-B expression mediated by dopamine D1 receptor stimulation in the development of 3
138 onal state of progestin receptors because of dopamine D1 receptor stimulation, facilitation of lordos
139 (SDS) in mice, here we identified a role of dopamine D1 receptor subtype in mPFC excitatory neurons
140 It is generally assumed that the coupling of dopamine D1 receptors to adenylyl cyclase is mediated by
142 e previously reported that activation of the dopamine D1 receptor triggers a rapid redistribution of
143 neurotensin (NTR1), adrenergic (beta1), and dopamine (D1) receptors were treated with fluorescently
147 NR2A, and NR2B was normal, and activation of dopamine D1 receptors with the agonist SKF-82958 [(+/-)-
148 sensitizing GABAergic input is controlled by dopamine D1 receptors, with horizontal cells serving as
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