ライフサイエンスコーパス: sulpiride

1 rgic agonist (bromocriptine) and antagonist (sulpiride).

2 ) or maximal D2R blockade (DA + 1 microM (-)-sulpiride).

3 by the D2-like dopamine receptor antagonist sulpiride.

4 amine, SKF-38393, quinpirole, SCH-23390, and sulpiride.

5 administration of the D2 receptor antagonist sulpiride.

6 eaction by a reversible dopamine antagonist, sulpiride.

7 eaction by a reversible dopamine antagonist, sulpiride.

8 eaction by a reversible dopamine antagonist, sulpiride.

9 H23390 but not by the D2 receptor antagonist sulpiride.

10 y blocked by the D2-selective antagonist (-)-sulpiride.

11 npirole: 78.2, 117.3, & 156.4 mM; antagonist sulpiride: 0.3, 0.9, & 2.9 mM) receptors during a simult

12 90 (1 microM), whereas the D2 antagonist (-)-sulpiride (1 microM) was without effect.

13 e blocked by the D2-like dopamine antagonist sulpiride (1 microM).

14 cortex following a single administration of sulpiride (10 mg/kg i.v.).

15 3390 (1.0 mg/kg, i.p.) or the D2 antagonist, sulpiride (10 mg/kg, i.p.) to block the reduction in ext

16 eated or vehicle-pretreated rat neostriatum, sulpiride (10 microM) increased the depolarization-induc

17 de ligands such as raclopride (200-fold) and sulpiride (125-fold).

18 Sulpiride (3 mg/kg i.v.) had no significant effect upon

19 Sulpiride (30 mg/kg i.v.) had a similar effect in the fr

20 Conversely, sulpiride (300 microM), a D2 antagonist, prevented the i

21 ion was prevented partly by superfusion with sulpiride (47% inhibition) and was reduced in D2 mutant

22 idal infusions of the dopamine D2 antagonist sulpiride (50 or 100 ng), the D1-class antagonist SCH-23

23 Coinstillation with S-sulpiride (a specific D(2) receptor antagonist) or propr

24 rochloride, a D1 antagonist, or 0.50 mM S(-)-sulpiride, a D2 antagonist, completely abolished the ICS

25 BA was evaluated by measuring the ability of sulpiride, a D2 dopamine receptor antagonist, to increas

26 Interestingly, 1 mum sulpiride, a D2 receptor antagonist, restored tLTP.

27 TP-channel blocker, was ineffective, as were sulpiride, a D2-receptor antagonist, and tertiapin, a G

28 sed by SCH23390, a D1 antagonist, but not by sulpiride, a D2-selective antagonist.

29 on on neuroplasticity in humans, we combined sulpiride, a selective D2 receptor antagonist, with the

30 emained high at the experiment end (3 h post sulpiride administration).

31 The higher dose of the D2 antagonist sulpiride also increased DA levels and sucrose intake.

32 12909 and D(2) autoreceptors were blocked by sulpiride, although these agents eliminated the differen

33 d received intra-NAc shell microinfusions of sulpiride, amphetamine, and saline.

34 dopaminergic drugs, with opposing effects of sulpiride and methylphenidate.

35 In addition, sulpiride and metoclopramide, drugs with high affinity f

36 We used the D2 receptor antagonist sulpiride and mice lacking the D2 receptor to address th

37 dopaminergic and sigma components defined by sulpiride and PPAP, respectively.

38 uantal size was blocked by the D2 antagonist sulpiride and reversed by L-DOPA.

39 The dopamine antagonists sulpiride and spiperone were both ineffective against th

40 he combined effects of the D(2/3) antagonist sulpiride and the D(4) antagonist L-745,870.

41 e increased DAT activity that was blocked by sulpiride and the protein kinase A selective inhibitor H

42 nt with drugs which served both to decrease (sulpiride) and increase (methylphenidate) dopaminergic t

43 s, D1 and D2 receptor antagonists (SCH23390, sulpiride) and the DA uptake blocker nomifensine were in

44 D1 synaptic signaling by the D2/3 antagonist sulpiride, and 2) the similar localization of aqueous al

45 MS-275, other benzamide derivatives, such as sulpiride, are brain-region selective inhibitors of HDAC

46 the D(2)-like receptor selective antagonist, sulpiride, at 2 Tesla in the brain of the alpha-chloralo

47 Treatment with sulpiride attenuated adaptive coding in both midbrain an

48 tor ([(3)H]SCH23390), and D2 receptor ([(3)H]sulpiride) binding in the dorsal striatum postmortem fro

49 etely reversed by the D2 receptor antagonist sulpiride but not by SCH 23390, a D1 antagonist.

50 Systemic pretreatment with sulpiride, but not SCH23390 (7-chloro-3-methyl-1-phenyl-

51 In contrast, sulpiride by either route of administration failed to bl

52 These data are supportive of the notion that sulpiride causes an increase in frontal dopaminergic fun

53 reatment with SCH-23390 or the D2 antagonist sulpiride confirmed the importance of D1 receptors in me

54 tive antagonists of dopamine (Sch 23390, D1; Sulpiride, D2), glutamate (CPP, competitive NMDA; dizoci

55 The dopamine D2-receptor antagonist sulpiride decreases spontaneous locomotor velocity of pl

56 earning via prediction errors, we found that sulpiride did not disrupt learning, but rather induced p

57 e to D2 receptors (as seen in in situ [(35)S]sulpiride displacement curves) that was robust in contro

58 Specific binding was defined by sulpiride (dopamine receptor ligand), PPAP (sigma recept

59 100 microM SCH 23390) or D2-like (100 microM sulpiride) dopamine receptor antagonists.

60 ested decreased behavioral adaptation in the sulpiride group.

61 idone > (+)-butaclamol > (-)-sulpiride = (+)-sulpiride > (+)-SCH23390 > (-)-butaclamol.

62 tentials, while the selective D2R antagonist sulpiride had the opposite effect.

63 impairing effects of immediate posttraining sulpiride in the spatial task are due to interference wi

64 Conversely, sulpiride increased SSRT but also increased go-trial rea

65 ments induced GP Fos, but that intrapallidal sulpiride induced Fos almost exclusively in PV-lacking p

66 Microdialysis in the NAC showed greater sulpiride-induced DA increases in the NAC of SH vs. DH r

67 In contrast, no sulpiride-induced increase in [3H]GABA overflow was dete

68 The effect of housing conditions on sulpiride-induced increases in extracellular dopamine (D

69 exceed 60%, although with larger lesions the sulpiride-induced response was reduced.

70 Sulpiride infused into the NA either 2 hr posttraining i

71 90 or dopamine D2 receptor (DRD2) antagonist sulpiride into the dorsomedial striatum (DMStr) or nucle

72 fect on response timing, but intra-NAc shell sulpiride microinfusions significantly decreased respons

73 s after lesioning, the stimulatory effect of sulpiride on [3H]GABA overflow was identical to that see

74 esioning, however, the stimulatory effect of sulpiride on electrically evoked [3H]GABA overflow remai

75 2 days later revealed an impairing effect of sulpiride on several retention measures.

76 ate, alone and in combination with 400 mg of sulpiride, on blood oxygenation level-dependent (BOLD) s

77 mmediately followed by intra-NA infusions of sulpiride or saline vehicle.

78 Both SCH-23390 and sulpiride prevented the reduction in extracellular gluta

79 sion into the posterior VTA, and addition of sulpiride reinstated EtOH self-administration.

80 No dose of sulpiride resulted in any significant BOLD signal change

81 r agonist (quinpirole), and a D2 antagonist (sulpiride) suggest that decreases in spiking and RN are

82 [2,3-b]pyridine but not by the D2 antagonist sulpiride, suggesting mediation by D4 receptors.

83 micromol/kg twice a day s.c. for 3 days) and sulpiride (SULP) (12.5 to 50 micromol/kg twice a day for

84 e of D(2)-dopaminergic receptors with either sulpiride (SULP) or 4-(4-chlorophenyl)-1-(1H-indol-3-ylm

85 omazine > domperidone > (+)-butaclamol > (-)-sulpiride = (+)-sulpiride > (+)-SCH23390 > (-)-butaclamo

86 t determined the effects of a D2 antagonist (sulpiride) to reinstate self-administration behavior in

87 nectivity of human caudate nucleus following sulpiride treatment, which is compatible both with the a

88 The effect of sulpiride was defined more specifically in the context o

89 The more salient effect of sulpiride was to increase functional connectivity betwee

90 whereas the D2-receptor-specific antagonist, sulpiride, was over 250 times less effective.

91 , amphetamine and the D2 receptor antagonist sulpiride were without significant effect.

92 of the selective DA D2/3-receptor antagonist sulpiride with genetic analysis of the DA D2 receptor in