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1 ) or maximal D2R blockade (DA + 1 microM (-)-sulpiride).
2 rgic agonist (bromocriptine) and antagonist (sulpiride).
3  placebo or selective D2 receptor antagonist sulpiride.
4 nipulating dopamine with methylphenidate and sulpiride.
5 uals and by methylphenidate, but impaired by sulpiride.
6  or the selective D(2/3)-receptor antagonist sulpiride.
7  by the D2-like dopamine receptor antagonist sulpiride.
8 amine, SKF-38393, quinpirole, SCH-23390, and sulpiride.
9 administration of the D2 receptor antagonist sulpiride.
10 eaction by a reversible dopamine antagonist, sulpiride.
11 eaction by a reversible dopamine antagonist, sulpiride.
12 eaction by a reversible dopamine antagonist, sulpiride.
13 H23390 but not by the D2 receptor antagonist sulpiride.
14 y blocked by the D2-selective antagonist (-)-sulpiride.
15 HC-RI was also observed by the antipsychotic sulpiride.
16 npirole: 78.2, 117.3, & 156.4 mM; antagonist sulpiride: 0.3, 0.9, & 2.9 mM) receptors during a simult
17 90 (1 microM), whereas the D2 antagonist (-)-sulpiride (1 microM) was without effect.
18 e blocked by the D2-like dopamine antagonist sulpiride (1 microM).
19  cortex following a single administration of sulpiride (10 mg/kg i.v.).
20 3390 (1.0 mg/kg, i.p.) or the D2 antagonist, sulpiride (10 mg/kg, i.p.) to block the reduction in ext
21 eated or vehicle-pretreated rat neostriatum, sulpiride (10 microM) increased the depolarization-induc
22 de ligands such as raclopride (200-fold) and sulpiride (125-fold).
23                                              Sulpiride (3 mg/kg i.v.) had no significant effect upon
24                                              Sulpiride (30 mg/kg i.v.) had a similar effect in the fr
25                                  Conversely, sulpiride (300 microM), a D2 antagonist, prevented the i
26 ion was prevented partly by superfusion with sulpiride (47% inhibition) and was reduced in D2 mutant
27 idal infusions of the dopamine D2 antagonist sulpiride (50 or 100 ng), the D1-class antagonist SCH-23
28                        Coinstillation with S-sulpiride (a specific D(2) receptor antagonist) or propr
29 rochloride, a D1 antagonist, or 0.50 mM S(-)-sulpiride, a D2 antagonist, completely abolished the ICS
30 BA was evaluated by measuring the ability of sulpiride, a D2 dopamine receptor antagonist, to increas
31                         Interestingly, 1 mum sulpiride, a D2 receptor antagonist, restored tLTP.
32 TP-channel blocker, was ineffective, as were sulpiride, a D2-receptor antagonist, and tertiapin, a G
33 sed by SCH23390, a D1 antagonist, but not by sulpiride, a D2-selective antagonist.
34 thesis capacity, whereas methylphenidate and sulpiride, a selective D2 receptor antagonist, increased
35 on on neuroplasticity in humans, we combined sulpiride, a selective D2 receptor antagonist, with the
36 emained high at the experiment end (3 h post sulpiride administration).
37         The higher dose of the D2 antagonist sulpiride also increased DA levels and sucrose intake.
38 12909 and D(2) autoreceptors were blocked by sulpiride, although these agents eliminated the differen
39 d received intra-NAc shell microinfusions of sulpiride, amphetamine, and saline.
40 dopaminergic drugs, with opposing effects of sulpiride and methylphenidate.
41                                 In addition, sulpiride and metoclopramide, drugs with high affinity f
42           We used the D2 receptor antagonist sulpiride and mice lacking the D2 receptor to address th
43 dopaminergic and sigma components defined by sulpiride and PPAP, respectively.
44 uantal size was blocked by the D2 antagonist sulpiride and reversed by L-DOPA.
45                     The dopamine antagonists sulpiride and spiperone were both ineffective against th
46 he combined effects of the D(2/3) antagonist sulpiride and the D(4) antagonist L-745,870.
47 minergic tone, i.e., the dopamine antagonist sulpiride and the dopamine precursor L-dopa which were b
48 e increased DAT activity that was blocked by sulpiride and the protein kinase A selective inhibitor H
49 nt with drugs which served both to decrease (sulpiride) and increase (methylphenidate) dopaminergic t
50 s, D1 and D2 receptor antagonists (SCH23390, sulpiride) and the DA uptake blocker nomifensine were in
51 D1 synaptic signaling by the D2/3 antagonist sulpiride, and 2) the similar localization of aqueous al
52 MS-275, other benzamide derivatives, such as sulpiride, are brain-region selective inhibitors of HDAC
53 the D(2)-like receptor selective antagonist, sulpiride, at 2 Tesla in the brain of the alpha-chloralo
54                               Treatment with sulpiride attenuated adaptive coding in both midbrain an
55 tor ([(3)H]SCH23390), and D2 receptor ([(3)H]sulpiride) binding in the dorsal striatum postmortem fro
56 etely reversed by the D2 receptor antagonist sulpiride but not by SCH 23390, a D1 antagonist.
57                   Systemic pretreatment with sulpiride, but not SCH23390 (7-chloro-3-methyl-1-phenyl-
58                                 In contrast, sulpiride by either route of administration failed to bl
59 These data are supportive of the notion that sulpiride causes an increase in frontal dopaminergic fun
60 n attenuated shift in the E:I balance in the sulpiride condition, whereas this interaction was not ev
61 reatment with SCH-23390 or the D2 antagonist sulpiride confirmed the importance of D1 receptors in me
62 tive antagonists of dopamine (Sch 23390, D1; Sulpiride, D2), glutamate (CPP, competitive NMDA; dizoci
63                 Methylphenidate improved and sulpiride decreased overall accuracy and response speed.
64          The dopamine D2-receptor antagonist sulpiride decreases spontaneous locomotor velocity of pl
65 earning via prediction errors, we found that sulpiride did not disrupt learning, but rather induced p
66                               The effects of sulpiride did not reach significance.
67 e to D2 receptors (as seen in in situ [(35)S]sulpiride displacement curves) that was robust in contro
68              Specific binding was defined by sulpiride (dopamine receptor ligand), PPAP (sigma recept
69 mocriptine or a dopamine receptor antagonist sulpiride (dopamine study n = 59) and in patients with e
70 100 microM SCH 23390) or D2-like (100 microM sulpiride) dopamine receptor antagonists.
71 d by photolytic release of the D2 antagonist sulpiride from CyHQ-sulpiride was also ~fourfold slower
72 ested decreased behavioral adaptation in the sulpiride group.
73 idone > (+)-butaclamol > (-)-sulpiride = (+)-sulpiride > (+)-SCH23390 > (-)-butaclamol.
74 tentials, while the selective D2R antagonist sulpiride had the opposite effect.
75 se of the D2/D3 dopamine receptor antagonist sulpiride impacts learning about other people's prosocia
76  impairing effects of immediate posttraining sulpiride in the spatial task are due to interference wi
77                                  Conversely, sulpiride increased SSRT but also increased go-trial rea
78 how that in a sample of 76 male participants sulpiride increases the volatility of beliefs, which lea
79 ments induced GP Fos, but that intrapallidal sulpiride induced Fos almost exclusively in PV-lacking p
80      Microdialysis in the NAC showed greater sulpiride-induced DA increases in the NAC of SH vs. DH r
81                              In contrast, no sulpiride-induced increase in [3H]GABA overflow was dete
82          The effect of housing conditions on sulpiride-induced increases in extracellular dopamine (D
83 exceed 60%, although with larger lesions the sulpiride-induced response was reduced.
84                                              Sulpiride infused into the NA either 2 hr posttraining i
85 90 or dopamine D2 receptor (DRD2) antagonist sulpiride into the dorsomedial striatum (DMStr) or nucle
86 fect on response timing, but intra-NAc shell sulpiride microinfusions significantly decreased respons
87 s after lesioning, the stimulatory effect of sulpiride on [3H]GABA overflow was identical to that see
88 esioning, however, the stimulatory effect of sulpiride on electrically evoked [3H]GABA overflow remai
89 2 days later revealed an impairing effect of sulpiride on several retention measures.
90 d the effect of D2 receptor blockade (800 mg sulpiride) on these measures within a randomized, double
91 ate, alone and in combination with 400 mg of sulpiride, on blood oxygenation level-dependent (BOLD) s
92 mmediately followed by intra-NA infusions of sulpiride or saline vehicle.
93                           Both SCH-23390 and sulpiride prevented the reduction in extracellular gluta
94  from metoclopramide through cyproheptadine, sulpiride, propantheline, diphenhydramine, benzhexol, do
95                   The D2 receptor antagonist sulpiride reduces accuracy due to diminished WM involvem
96 sion into the posterior VTA, and addition of sulpiride reinstated EtOH self-administration.
97                                   No dose of sulpiride resulted in any significant BOLD signal change
98 eptadine, (RR = 2.76, 95% C.I. = 2.00-3.82), sulpiride (RR = 2.49, 95% C.I. = 1.65-3.77), propantheli
99 r agonist (quinpirole), and a D2 antagonist (sulpiride) suggest that decreases in spiking and RN are
100 [2,3-b]pyridine but not by the D2 antagonist sulpiride, suggesting mediation by D4 receptors.
101 micromol/kg twice a day s.c. for 3 days) and sulpiride (SULP) (12.5 to 50 micromol/kg twice a day for
102 e of D(2)-dopaminergic receptors with either sulpiride (SULP) or 4-(4-chlorophenyl)-1-(1H-indol-3-ylm
103 omazine > domperidone > (+)-butaclamol > (-)-sulpiride = (+)-sulpiride > (+)-SCH23390 > (-)-butaclamo
104 , as well as the selective D2-receptor agent sulpiride, the latter to strengthen inference about dopa
105 83 participants) from -0.90 (-1.36 to -0.44; sulpiride) to 0.04 (-0.39 to 0.47; flupentixol).
106 t determined the effects of a D2 antagonist (sulpiride) to reinstate self-administration behavior in
107 nectivity of human caudate nucleus following sulpiride treatment, which is compatible both with the a
108 ase of the D2 antagonist sulpiride from CyHQ-sulpiride was also ~fourfold slower in midbrain slices f
109                                The effect of sulpiride was defined more specifically in the context o
110                 No evidence of any effect of sulpiride was found.
111                   The more salient effect of sulpiride was to increase functional connectivity betwee
112 whereas the D2-receptor-specific antagonist, sulpiride, was over 250 times less effective.
113 , amphetamine and the D2 receptor antagonist sulpiride were without significant effect.
114 of the selective DA D2/3-receptor antagonist sulpiride with genetic analysis of the DA D2 receptor in

 
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