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1 a positive allosteric modulator (PAM) at the dopamine D1 receptor.
2 gets: c-SRC kinase, Smoothened receptor, and dopamine D1 receptor.
3 e focused upon the effects of activating the dopamine D1 receptor.
4 eases in response to stimulation of striatal dopamine D1 receptors.
5 gic neurons, and (2) excitation initiated by dopamine D1 receptors.
6 c cholinergic, adenosine A2, dopamine D2, or dopamine D1 receptors.
7 g affinity (Ki = 49.3 nM) and selectivity to dopamine D1 receptors.
8 highest binding affinity (Ki = 60.3 nM) for dopamine D1 receptors.
9 nd relapse, largely dependent on activity of dopamine D1 receptors.
10 uent activation of norepinephrine alpha2 and dopamine D1 receptors.
11 region-specific pharmacological blockade of dopamine D1-receptors.
18 phosphorylation, whereas the effects of the dopamine D1 receptor agonist are blocked by genistein, a
19 lated RGCs, the application of dopamine or a dopamine D1 receptor agonist decreased voltage-activated
21 hr34 DARPP-32 and phospho-Ser845 GluR1 after dopamine D1 receptor agonist or forskolin stimulation.
22 d by treatment of neostriatal neurons with a dopamine D1 receptor agonist or with forskolin, consiste
23 e-treated and normal individuals, whilst the dopamine D1 receptor agonist SKF 38393 (30 mg/kg, i.p.)
24 st dose tested (18 nmol) of a mixture of the dopamine D1 receptor agonist SKF 38393 and the D2 agonis
25 owing by conditioning rats under the partial dopamine D1 receptor agonist SKF 38393 or the opioid ant
26 e administration of a low dose of either the dopamine D1 receptor agonist SKF-38393 or the D2 recepto
28 ain slices of neonatal (P7) rat striatum the dopamine D1 receptor agonist SKF-82958 significantly dec
30 acute behavioral response of DA-/- mice to a dopamine D1 receptor agonist was correlated with c-fos i
31 also attenuated the hyperthermia caused by a dopamine D1 receptor agonist, SKF 38393 (10 mg/kg, s.c.)
32 82958 (SKF), a previously characterized full dopamine D1 receptor agonist, to stimulate the transcrip
34 This protocol has allowed the synthesis of a dopamine D1 receptor allosteric modulator without recour
35 harmacological roles of Gs- and Golf-coupled dopamine D1 receptor and adenosine A2A receptor in the b
36 an be used to reveal potentially therapeutic dopamine D1 receptor and adenosine A2A receptor ligands
37 ave been developed for 48 antagonists of the dopamine D1 receptor and applied to mining chemical data
41 brain and bound putative GLP-1 receptors on dopamine D1 receptor- and dopamine D2 receptor-expressin
44 252a, a Trk tyrosine kinase inhibitor, and a dopamine D1 receptor antagonist could block the effects
45 Systemic administration of the selective dopamine D1 receptor antagonist SCH 23390 [R(+)-7-chloro
47 usion of 10 microg (but not 2 microg) of the dopamine D1 receptor antagonist SCH-23390 greatly impair
49 s sufficient to induce BDNF in the mPFC, and dopamine D1 receptor antagonist treatment blocked the an
50 way were attenuated by pretreatment with the dopamine D1 receptor antagonist, SCH23390, which also ca
51 kDa), in the absence or in the presence of a dopamine D1 receptor antagonist, we provide evidence tha
54 sion of the AMPA-receptor antagonist CNQX or dopamine D1-receptor antagonist SCH-23390 into the DLS b
62 riments (Daun02 lesioning of vmPFC and acute dopamine D1-receptor blockade with SCH39166 in NAc core
63 and full intrinsic activity at cloned human dopamine D1 receptors but had much lower affinity at dop
64 tive stimulus depended on NAcC AMPA/NMDA and dopamine D1 receptors, but the retrieval of the response
65 One new receptor, DAMB, was identified as a dopamine D1 receptor by sequence analysis and pharmacolo
66 and the previous finding on up-regulation of dopamine D1 receptors by NMDAR activation provide a cell
68 ecause of increased transmission through the dopamine D1 receptor/cAMP-dependent protein kinase pathw
69 These results indicate that stimulation of dopamine D1 receptors can be coupled to the neurotrophin
71 They also demonstrate that activation of dopamine D1 receptors corrects these deficits, through a
72 firing, and that this effect is mediated by dopamine D1 receptor-coupled Ca2+ signalling pathways.
73 rebral cortical areas, substantially reduced dopamine D1 receptor coupling to G(s)-protein, and defic
75 inhibit movement, whereas those that express dopamine D1 receptors (D1+) project to the substantia ni
76 , we demonstrate for the first time that the dopamine D1 receptor (D1DR), the primary mediator of dop
78 ccumbens are differentiated by expression of dopamine D1 receptors (D1DRs) or D2DRs, activation of wh
79 In this study, we show that mice lacking the dopamine D1 receptor (D1R KO mice) manifest greatly redu
80 ss impairs working memory via high levels of dopamine D1 receptor (D1R) activation of cyclic adenosin
81 82) in the CA1 region of the hippocampus via dopamine D1 receptor (D1R) activation, a process largely
82 disease, is associated with an alteration in dopamine D1 receptor (D1R) and glutamate receptor intera
83 y systemic pretreatment of CRF receptor 1 or dopamine D1 receptor (D1R) antagonist and augmented by c
85 onvolute the process of signal bias from the dopamine D1 receptor (D1R) by exploring factors that pro
86 inding activity of agonist and antagonist of dopamine D1 receptor (D1R) by using quartz crystal micro
88 ological studies have clarified the roles of dopamine D1 receptor (D1R) in the medial prefrontal cort
91 omato BAC transgenic mice and found that the dopamine D1 receptor (D1R) is expressed in retinal bipol
92 ntrol of genetic regulatory elements for the dopamine D1 receptor (D1R) or dopamine D2 receptor (D2R)
93 rrent synaptic activity and was reduced by a dopamine D1 receptor (D1R) protein kinase A pathway.
95 , removing NMDARs from MSNs that express the dopamine D1 receptor (D1R) significantly attenuated AMPH
97 Finally, conditional knock-out of Cav1.2 in dopamine D1 receptor (D1R)-expressing cells resulted in
101 cently found that microglial phagocytosis of dopamine D1 receptors (D1R) in the nucleus accumbens (NA
102 gh both angiotensin AT1 receptors (AT1R) and dopamine D1 receptors (D1R) modulates renal sodium excre
105 mory, and Ca(v)1.2 is a downstream target of dopamine D1-receptor (D1R) signaling, we next generated
106 rt of this, increased activation of striatal dopamine-D1 receptors (D1R) results in desensitization o
108 ippocampal neurons, we demonstrate here that dopamine D1 receptors (D1Rs) and NMDARs form dynamic sur
111 are medium spiny neurons (MSNs) that express dopamine D1 receptors (D1Rs) or D2 receptors (D2Rs), whi
115 mygdala enhanced cue-reward learning through dopamine D1 receptor-dependent mechanisms and suppressed
118 An amphetamine challenge reversed CPD via a dopamine D1-receptor-dependent paradoxical presynaptic p
119 Intra-basolateral amygdala antagonism of dopamine D1-receptors did not prevent the reacquisition
120 dient predicted episodic memory and mirrored dopamine D1 receptor distribution, capturing shared func
121 SRT in the rat using direct infusions of the dopamine D1 receptor (DRD1) antagonist SCH 23390 or dopa
122 ctron microscopy (cryo-EM) structures of the dopamine D1 receptor (DRD1) coupled to Gs heterotrimer i
123 with a single nucleotide polymorphism in the dopamine D1 receptor (DRD1) gene, which was associated w
125 contrast, decreased dysbindin did not change dopamine D1 receptor (DRD1) levels, or its basal or dopa
126 Furthermore, this LTP is more prominent in dopamine D1 receptor-expressing (D1) MSNs than D2 MSNs a
127 cortical-limbic induced compulsions in which dopamine D1 receptor-expressing (D1+) neurons in restric
128 cholera toxin (CT) transgene in a subset of dopamine D1 receptor-expressing (D1+) neurons thought to
129 idence that supports a role of Cav1.2 within dopamine D1 receptor-expressing cells of the hippocampus
130 he nucleus accumbens, more specifically, the dopamine D1 receptor-expressing medium spiny neurons (D1
131 own to inhibit glutamatergic transmission in dopamine D1 receptor-expressing medium spiny neurons (D1
132 e the inhibitory function of PSAM(4)-GlyR in dopamine D1 receptor-expressing medium spiny neurons (D1
133 ene expression and muscarinic M4 receptor in dopamine D1 receptor-expressing medium spiny neurons.
134 We also found that HDAC5 functions within dopamine D1 receptor-expressing MSNs to suppress cue-ind
135 ent of excitatory synaptic transmission onto dopamine D1 receptor-expressing neurons (D1+ neurons) in
136 uced PGE2 targeted EP1 receptors on striatal dopamine D1 receptor-expressing neurons and that this si
137 IGNIFICANCE STATEMENT ERK phosphorylation in dopamine D1 receptor-expressing neurons exerts a pivotal
138 ndicate that NCS-Rapgef2 signaling to ERK in dopamine D1 receptor-expressing neurons in the NAc, but
139 ignaling to ERK that underlies plasticity in dopamine D1 receptor-expressing neurons leading to acqui
141 in TS not only potentiated the responses of dopamine D1 receptor-expressing neurons to novel sensory
142 diacylglycerol lipase alpha (DGLalpha), from dopamine D1 receptor-expressing or adenosine A2a recepto
143 insic or synaptic properties on thin-tufted, dopamine D1-receptor-expressing ACC L5 PyNs recorded fro
144 ned mice that lack M4 mAChRs specifically in dopamine D1-receptor-expressing neurons, suggesting that
145 duced hypothyroidismin hamsters (HH) altered dopamine D1 receptor expression, D1 receptor-modulated v
147 in humans, the specific contribution of the dopamine D1 receptor family to these behaviors remained
149 f dendritic spines in MSN-D1 (MSN-expressing dopamine D1 receptors) from the core and shell of nucleu
151 f catechol-based orthosteric agonists of the dopamine D1 receptor has thus far been unsuccessful due
155 areas, among which the IPAC is regulated by dopamine D1 receptor in the mPFC perhaps through direct
156 PK and JNK signaling pathways is mediated by dopamine D1 receptors in SK-N-MC neuroblastoma cells.
160 d by testing the hypothesis that blockade of dopamine D1 receptors in the VTA attenuates the rewardin
164 t the direct inhibition of NMDA receptors by dopamine D1 receptor ligands is due to the channel pore
165 dies and structure-activity relationships of dopamine D1 receptor ligands suggest that their intrinsi
166 tina that bright-light-induced activation of dopamine D1 receptors located on ON-center cone bipolar
169 deletion of any other NF subunit, amplifies dopamine D1-receptor-mediated motor responses to cocaine
170 rats that express Cre recombinase in either dopamine D1 receptor- or adenosine 2a (A2a) receptor-exp
175 ently completed clinical studies suggest the dopamine D1 receptor positive allosteric modulator (PAM)
177 y delays healing, whereas the stimulation of dopamine D1 receptors promotes angiogenesis and expedite
178 ing an amine-accepting binding domain on the dopamine D1 receptor protein that may be further explore
179 e, the PDE10A radioligand (18)F-MNI-659, the dopamine D1 receptor radioligand (11)C-NNC 112, and the
180 e, the PDE10A radioligand (18)F-MNI-659, the dopamine D1 receptor radioligand (11)C-NNC 112, and the
182 twork firing, whereas optimal stimulation of dopamine D1 receptors sculpts network inputs to refine m
186 alk between PKA and ERK1/2 with relevance to dopamine D1 receptor signaling in striatal neurons.
188 Although considerable evidence implicates dopamine D1-receptor signaling in the nucleus accumbens
190 FosB and dynorphin-B expression mediated by dopamine D1 receptor stimulation in the development of 3
191 onal state of progestin receptors because of dopamine D1 receptor stimulation, facilitation of lordos
192 (SDS) in mice, here we identified a role of dopamine D1 receptor subtype in mPFC excitatory neurons
193 It is generally assumed that the coupling of dopamine D1 receptors to adenylyl cyclase is mediated by
195 e previously reported that activation of the dopamine D1 receptor triggers a rapid redistribution of
196 neurotensin (NTR1), adrenergic (beta1), and dopamine (D1) receptors were treated with fluorescently
197 three positive allosteric modulators of the dopamine D1 receptor were found to bind to distinct and
201 (GBC) in association with regional levels of dopamine D1 receptors, which are critical for drug rewar
202 NR2A, and NR2B was normal, and activation of dopamine D1 receptors with the agonist SKF-82958 [(+/-)-
203 sensitizing GABAergic input is controlled by dopamine D1 receptors, with horizontal cells serving as