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1 be dependent on tonic stimulation of the DA D1 receptor.
2 upon the effects of activating the dopamine D1 receptor.
3 changes in protein levels, at least for the D1-receptor.
4 rontal cortex influence temporal control via D1 receptors.
5 P treatment down-regulated the expression of D1 receptors.
6 tive functions, acting predominantly through D1 receptors.
7 ur, in part, via activation of dopamine (DA) D1 receptors.
8 greatly reduced cell-surface localization of D1 receptors.
9 by differentially activating dopamine D2 and D1 receptors.
10 s channel-blocking effect was independent of D1 receptors.
11 whether they are agonists or antagonists for D1 receptors.
12 in-coupled receptors, and lacked activity at D1 receptors.
13 vation of norepinephrine alpha2 and dopamine D1 receptors.
14 cumbens pathway, via, in part, activation of D1 receptors.
15 its cytokine production via dopamine type 1 (D1) receptors.
16 through DA D2 and adenosine A2A, but not DA D1, receptors.
17 dopamine transporter (DAT; [(3)H]mazindol), D1 receptor ([(3)H]SCH23390), and D2 receptor ([(3)H]sul
22 dose-dependent inverted U-shaped effects of D1 receptor activation on neuroplasticity of the motor c
25 ockade following maintained illumination and D1 receptor activation result in minimal GABAA receptor
29 al demonstration that 5-HT1A and D2, but not D1, receptor activity influence a behavioral analog of l
31 slices with NR2A antagonist (NVP-AAM077) and D1 receptor agonist augmented the increase of dendritic
32 active enantiomer of the selective and full D1 receptor agonist dihydrexidine (DAR-0100A) could atte
33 conditioning rats under the partial dopamine D1 receptor agonist SKF 38393 or the opioid antagonist n
35 tration of a low dose of either the dopamine D1 receptor agonist SKF-38393 or the D2 receptor antagon
36 s of neonatal (P7) rat striatum the dopamine D1 receptor agonist SKF-82958 significantly decreases NM
37 hibited opposite regulatory responses to the D1 receptor agonist SKF38393 (1-phenyl-2,3,4-5-tetrahydr
41 nuated the hyperthermia caused by a dopamine D1 receptor agonist, SKF 38393 (10 mg/kg, s.c.), indicat
43 further clinical support to the potential of D1 receptor agonists to treat schizophrenia-spectrum wor
44 n males whereas females rely more heavily on D1 receptors, an effect that could be explained by sexua
46 gical roles of Gs- and Golf-coupled dopamine D1 receptor and adenosine A2A receptor in the brain and
47 d to reveal potentially therapeutic dopamine D1 receptor and adenosine A2A receptor ligands with func
49 factor transmitting the signals derived from D1 receptors and associative pathways to the CaCRE sites
52 hat activate the direct striatal pathway via D1 receptors and inhibit the indirect striato-cortical p
53 P and cGMP, whose synthesis is stimulated by D1 receptors and inhibited by D2 receptors preferentiall
54 ics we found a strong down-regulation of the D1 receptor- and DA transporter (DAT)-binding sites, but
55 emales were less sensitive to the effects of D1-receptor antagonism as compared with their ShA counte
56 rk tyrosine kinase inhibitor, and a dopamine D1 receptor antagonist could block the effects of SKF383
57 ven an intra-mPFC infusion of vehicle or the D1 receptor antagonist SCH 23390 (0.25 or 1.0 microg) pr
60 two injections: first with +/-8-OH-DPAT, the D1 receptor antagonist SCH23390 or their vehicles, and s
61 ent to induce BDNF in the mPFC, and dopamine D1 receptor antagonist treatment blocked the antidepress
62 e, attenuated the action of DBS, whereas the D1 receptor antagonist, SCH-23390, was ineffective, sugg
64 s paper assessed the possibility that the DA D1 receptor antagonist, SCH23390, might inhibit METH-ind
67 ed following saline or 0.25mg/kg SCH 23390,a D1 receptor antagonist, while awake hamsters breathed no
69 he AMPA-receptor antagonist CNQX or dopamine D1-receptor antagonist SCH-23390 into the DLS before tes
70 e effects of intra-accumbens infusion of the D1-receptor antagonist, SCH-23390 (0, .3, 1.0, 3.0 micro
73 ion and patch-clamp recordings, we show that D1 receptors are almost exclusively expressed in the str
76 striatal medium spiny neurons (MSNs) marker, D1-receptor associated signaling protein dopamine-and-cA
78 Importantly, systemic inhibition of dopamine D1 receptors attenuated the stroke-induced increase in o
80 was no correlation between striatal DAT and D1 receptor binding (R(2)=0.07, p=0.33), although DAT an
82 d serotonin levels in basal ganglia; reduced D1 receptor binding in nucleus accumbens; axodendritic p
84 inding (R(2)=0.07, p=0.33), although DAT and D1 receptor binding was positively correlated in subject
86 We also show that maintained darkness and D1 receptor blockade following maintained illumination a
87 ple discrete-trial procedures employed here, D1 receptor blockade preferential reduces Pavlovian and
92 ests; cyclic AMP responses to stimulation of D1 receptors by dopamine was selectively impaired in PrP
93 nd tonic inhibition, the acute activation of D1 receptors (by a selective agonist or indirectly by am
94 esults indicate that stimulation of dopamine D1 receptors can be coupled to the neurotrophin receptor
95 gnificantly, prior activation of presynaptic D1 receptors caused a time-dependent attenuation of mGlu
96 rly growth response 3 (EGR3) is increased in D1 receptor containing MSNs of mice susceptible to socia
98 chronic cocaine treatment is stable only in D1-receptor-containing neurons and that DeltaFosB expres
99 also demonstrate that activation of dopamine D1 receptors corrects these deficits, through a mechanis
100 rtical areas, substantially reduced dopamine D1 receptor coupling to G(s)-protein, and deficits in co
102 ovement, whereas those that express dopamine D1 receptors (D1+) project to the substantia nigra pars
103 tudy, we show that mice lacking the dopamine D1 receptor (D1R KO mice) manifest greatly reduced FAA,
104 s working memory via high levels of dopamine D1 receptor (D1R) activation of cyclic adenosine monopho
106 is associated with an alteration in dopamine D1 receptor (D1R) and glutamate receptor interactions.
109 tivity of agonist and antagonist of dopamine D1 receptor (D1R) by using quartz crystal microbalance (
111 transgenic mice and found that the dopamine D1 receptor (D1R) is expressed in retinal bipolar cells
113 ressing EGFP under the control of either the D1 receptor (D1R) or the D2 receptor (D2R) gene and micr
117 g NMDARs from MSNs that express the dopamine D1 receptor (D1R) significantly attenuated AMPH sensitiz
119 ut approach to selectively delete GRK2 in DA D1 receptor (D1R)-, DA D2 receptor (D2R)-, adenosine 2A
120 conditional knock-out of Cav1.2 in dopamine D1 receptor (D1R)-expressing cells resulted in attenuati
121 from C57BL/6 male mice, that a dopamine (DA) D1 receptor (D1R)-mediated enhancement in glutamate syna
123 ngiotensin AT1 receptors (AT1R) and dopamine D1 receptors (D1R) modulates renal sodium excretion and
124 s, increased activation of striatal dopamine-D1 receptors (D1R) results in desensitization of delta-o
127 lation of DORs in CINs critically influences D1-receptor (D1R)-expressing projection neurons in the N
128 ell but not the core in mice, which required D1 receptors (D1Rs) and mechanistic target of rapamycin
129 l neurons, we demonstrate here that dopamine D1 receptors (D1Rs) and NMDARs form dynamic surface clus
132 ipulation of FEF activity either by blocking D1 receptors (D1Rs) or by stimulating D2 receptors (D2Rs
133 m spiny neurons (MSNs) that express dopamine D1 receptors (D1Rs) or D2 receptors (D2Rs), which drive
139 sic firing, increased SC responses through a D1 receptor-dependent enhancement of excitatory transmis
140 Here we investigate the pathways involved in D1 receptor-dependent ERK1/2 activation using acute stri
143 nhanced cue-reward learning through dopamine D1 receptor-dependent mechanisms and suppressed task-irr
145 r inhibition of engrafted neurons, revealing D1 receptor-dependent regulation of host neuronal circui
147 tamine challenge reversed CPD via a dopamine D1-receptor-dependent paradoxical presynaptic potentiati
148 e rat using direct infusions of the dopamine D1 receptor (DRD1) antagonist SCH 23390 or dopamine D2 r
149 ngle nucleotide polymorphism in the dopamine D1 receptor (DRD1) gene, which was associated with ADHD
151 decreased dysbindin did not change dopamine D1 receptor (DRD1) levels, or its basal or dopamine-indu
152 tina, yet has been reported to do so by only D1 receptor-driven cyclic adenosine monophosphate (cAMP)
153 gest that activation of SN DA neurons and DS D1 receptors during fear extinction render fear extincti
154 e carriers, who are assumed to have a higher D1 receptor efficiency than carriers of the A allele.
156 av1.2 channels within the hippocampus and in D1 receptor-expressing cells in extinction of cocaine-as
157 at supports a role of Cav1.2 within dopamine D1 receptor-expressing cells of the hippocampus for exti
159 veal that in hemiparkinsonian mice, striatal D1 receptor-expressing medium spiny neurons (MSNs) direc
161 citatory synaptic transmission onto dopamine D1 receptor-expressing neurons (D1+ neurons) in the nucl
162 targeted EP1 receptors on striatal dopamine D1 receptor-expressing neurons and that this signaling s
165 Our findings indicate that c-Fos produced in D1 receptor-expressing neurons integrates mechanisms to
167 cerol lipase alpha (DGLalpha), from dopamine D1 receptor-expressing or adenosine A2a receptor-express
168 y neurons (MSSNs) giving rise to the direct (D1 receptor-expressing) and indirect (D2 receptor-expres
169 that lack M4 mAChRs specifically in dopamine D1-receptor-expressing neurons, suggesting that postsyna
170 H23390 (which has been suggested to increase D1 receptor expression in the basal ganglia) did not eli
171 iabetic model, we demonstrate that the renal D1 receptor expression is down-regulated by the extracel
172 othyroidismin hamsters (HH) altered dopamine D1 receptor expression, D1 receptor-modulated ventilatio
175 to cocaine while redistributing postsynaptic D1-receptors from endosomes to plasma membrane, consiste
176 ic spines in MSN-D1 (MSN-expressing dopamine D1 receptors) from the core and shell of nucleus accumbe
180 The effect of oxidative stress on renal D1 receptor function was investigated in healthy animals
183 se in BP, which was accompanied by defective D1 receptor G-protein coupling and loss of natriuretic r
184 xidative stress, normalized BP, and restored D1 receptor G-protein coupling and natriuretic response
185 s that down-regulate the expression of renal D1 receptor gene in diabetes are not well understood.
186 microscopy, we show that neurons expressing D1 receptors have unique morphological and physiological
187 leads to GRK-2 translocation and subsequent D1 receptor hyper-serine phosphorylation and uncoupling.
189 ngs demonstrate that repeated stimulation of D1 receptors in adulthood interacts with the development
192 s of cocaine have shown a leading role of DA D1 receptors in the cascade of cellular events elicited
195 ve shown that the expression and function of D1 receptors in the kidneys are decreased in animal mode
197 investigate a potential modulatory role for D1 receptors in the mPFC in amphetamine (AMPH)- and meth
198 The results indicate an important role for D1 receptors in the postnatal development of ME and SP s
199 ates of dopamine turnover, and activation of D1 receptors in the prefrontal cortex, measures that are
200 respectively, blocked the down-regulation of D1 receptors in the primary renal cells and in the kidne
202 robustly and rapidly induced by cocaine via D1 receptors, in mediating cocaine-induced persistent ne
203 have shown that in the absence of functional D1 receptors, in null mice, the systolic, diastolic, and
204 Single-channel recordings show that direct D1 receptor inhibition of NMDA receptors cannot be obser
205 eliably self-administer cocaine and that the D1 receptor is critical for the reinforcing effects of c
207 l overactivation of ERK1/2 via dopamine (DA) D1 receptors is the hallmark of a supersensitive molecul
210 was a significant decrease in the number of D1 receptor knock-out mice that met criteria for acquisi
212 or and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for
216 triatal slices have shown that activation of D1 receptors leads to cAMP-dependent dephosphorylation o
218 bright-light-induced activation of dopamine D1 receptors located on ON-center cone bipolar cell dend
222 Single social defeat stress (S-SDS) induces D1 receptor-mediated extracellular signal-regulated kina
224 ure results in subsensitivity of the INaT to D1 receptor-mediated inhibition because of a possible in
225 nd co-localized with DeltaFosB, suggesting a D1 receptor-mediated mechanism supporting the LHb involv
226 ulated striatal N/OFQ receptors opposing the D1 receptor-mediated overactivation of the striatonigral
228 of any other NF subunit, amplifies dopamine D1-receptor-mediated motor responses to cocaine while re
229 HH) altered dopamine D1 receptor expression, D1 receptor-modulated ventilation, and ventilatory chemo
231 was a pronounced reduction in dopamine (DA) D1 receptor modulation of both intrinsic firing and evok
235 was decreased specifically in D1 cells, and D1 receptor modulation was normal in D1-YAC128 cells.
237 g is related to changes in expression of the D1 receptor mRNA, suppression in expression of serotoner
238 ive reinforcers in wild-type mice but not in D1 receptor mutant mice, whereas food and intravenous in
240 ltures, suggesting that DA agonists acted on D1 receptors on PFC neurons, altering their excitatory t
241 (an agonist that does not activate homomeric D1 receptors or alter cAMP levels in other systems); 2)
242 sequence of activation of either presynaptic D1 receptors or mGluR2/3 receptors may critically regula
243 recognition performance further suggest that D1 receptors place constraints on the responsiveness of
250 eptors enabling flexible decision making and D1 receptors promoting persistence in choice biases.
253 hyroid hamsters (EH), HH exhibited decreased D1 receptor protein levels in carotid bodies, striatum,
255 the striatum correlated negatively with age (D1 receptor: R(2)=0.12, p<0.05; DAT: R(2)=0.36, p<0.001)
256 E10A radioligand (18)F-MNI-659, the dopamine D1 receptor radioligand (11)C-NNC 112, and the 5-HT2A ra
257 E10A radioligand (18)F-MNI-659, the dopamine D1 receptor radioligand (11)C-NNC 112, and the 5-HT2A ra
259 response in the subcellular distribution of D1 receptors, resulting in alterations in signaling capa
260 A decrease in the expression or function of D1 receptors results in increased sodium retention which
261 ing, whereas optimal stimulation of dopamine D1 receptors sculpts network inputs to refine mental rep
265 sm of the oxidative stress-mediated impaired D1 receptor signaling and hypertension is not known.
266 the protective H3 receptor-mediated brake on D1 receptor signaling and prevents the cell death from e
268 eral lines of evidence suggest that dopamine D1 receptor signaling enhances dendritic excitability an
269 ulation by postsynaptic protein kinase A and D1 receptor signaling were determined in two distinct ag
271 gh considerable evidence implicates dopamine D1-receptor signaling in the nucleus accumbens in motiva
273 authors found that modulation of D2, but not D1, receptors significantly affected rats' odor discrimi
274 energic alpha1-adrenoceptor and dopaminergic D1 receptor stimulation activate feedforward calcium-pro
276 dynorphin-B expression mediated by dopamine D1 receptor stimulation in the development of 3,4-dihydr
278 mechanisms that regulate the consequences of D1 receptor stimulation, favoring activation of GluR1 ra
281 mice, here we identified a role of dopamine D1 receptor subtype in mPFC excitatory neurons in suppre
282 eat stress (R-SDS) reduces the expression of D1 receptor subtype in mPFC of mice susceptible to R-SDS
286 ne-mediated disruption leaves an uninhibited D1 receptor that activates Gs, freely recruits beta-arre
287 ically or genetically, reduced the amount of D1 receptor that was internalized in response to dopamin
289 -methyl-D-aspartate receptor potentiation by D1 receptor to trigger ERK1/2 activation and its subsequ
290 ippocampal pyramidal cells, dopamine acts at D1 receptors to reduce peak Na(+) currents by activation
292 ors, and extends this notion by showing that D1 receptor transmission within the striatum strongly su
295 n the mPFC of the brief access animals while D1 receptors were elevated in the N.Acc shell of the ext
299 ng GABAergic input is controlled by dopamine D1 receptors, with horizontal cells serving as a plausib
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