ライフサイエンスコーパス: SCH-23390

1 rats that were postoperatively treated with SCH 23390.

2 ntly attenuated by selective D1LR antagonist SCH 23390.

3 eus accumbens which again were attenuated by SCH 23390.

4 ion of the selective D1 receptor antagonist, SCH 23390.

5 the co-administration of the D-1 antagonist, SCH 23390.

6 locked by superfusion with the D1 antagonist SCH 23390.

7 and (2) its modulation by the D1 antagonist SCH 23390.

8 ompletely blocked by the D1/D5 antagonist (+)SCH 23390.

9 iography using the D(1) receptor ligand [3H] SCH 23390.

10 ist (R)-SKF 38393 or the specific antagonist SCH 23390.

11 e pretreated with the D1 dopamine antagonist SCH 23390.

12 ssant response to the dopamine D1 antagonist SCH-23390.

13 tion of the selective D1 receptor antagonist SCH-23390.

14 , and also by the DA D1 receptor antagonist, SCH-23390.

15 1 or 2 food pellets, intra-VTA injections of SCH 23390 (0 and 4 microg/0.5 microl) decreased BPs at t

16 rd consisted of 1 food pellet, injections of SCH 23390 (0, 1, 2, or 4 microg/0.5 microl) in the VTA (

17 lar odorants, whereas both the D, antagonist SCH 23390 (0.025 mg/kg) and the D2 agonist quinpirole (0

18 ion of vehicle or the D1 receptor antagonist SCH 23390 (0.25 or 1.0 microg) prior to systemic (i.p.)

19 elective drugs SKF 81297 (0.1 or 0.4microg), SCH 23390 (0.25 or 1.0microg), quinpirole (1.25 or 5.0mi

20 pendent effects of pre-training infusions of SCH 23390 (0.5, 1.0 and 2.0 microgram) on conditioned fe

21 bens infusion of the D1-receptor antagonist, SCH-23390 (0, .3, 1.0, 3.0 microg), were examined.

22 Systemic injection of either SCH-23390 (0.1 mg/kg) or haloperidol (0.2 mg/kg), relati

23 antagonists raclopride (0.1 and 0.5 mg/kg), SCH-23390 (0.1 mg/kg), or haloperidol (0.1 mg/kg) was wi

24 Infusion of the selective D1 antagonist SCH-23390 (0.15, 0.3, 3.0 nmol) dose-dependently impaire

25 Prior administration of SCH-23390 (0.2 mg/kg), a D(1) antagonist, resulted in a

26 SCH-23390 (0.2 mg/kg), a D1 antagonist, strongly elevate

27 of low doses of the D(1) receptor antagonist SCH-23390 (0.3 nmol) and AP-5 (0.5 nmol) into the accumb

28 sion of the selective D1 receptor antagonist SCH-23390 (0.5-10 microg) blocked this response bilatera

29 SKF 38393; 0.23 microg/side) and antagonist (SCH 23390; 0.25 microg/side).

30 Administration of a D1 antagonist (SCH 23390; 0.5 mg/kg, i.p.) had no effect on the VTA red

31 Their actions were completely reversed by SCH 23390 (1 microM), indicating that endogenous dopamin

32 letely blocked by the D1 receptor antagonist SCH 23390 (1 microM), whereas the D2 antagonist (-)-sulp

33 njections of the D1-like receptor antagonist SCH 23390 (1-4 mug total bilateral dose) into the poster

34 Rats were given intra-mPFC infusions of both SCH 23390 (1.0 microg) and the 5-HT(2C) antagonist RS 10

35 The capacity of the D1 antagonist, SCH-23390 (1.0 mg/kg, i.p.) or the D2 antagonist, sulpir

36 produced by infusion of the D(1) antagonist SCH 23390(1 microg) or the glutamate antagonist NBQX (0.

37 icial CSF (aCSF), the D1 receptor antagonist SCH 23390 (10 microm), or the D2 receptor antagonist eti

38 were completely blocked by the D1 antagonist SCH-23390 (10 microM), which alone had no effect on mRNA

39 usion of the D1 dopamine receptor antagonist SCH-23390 (100 microM) did not alter the carbachol-stimu

40 ride (50 or 100 ng), the D1-class antagonist SCH-23390 (100 ng), the D2-class agonist quinpirole (500

41 KF 82958: 14.6, 43.8, & 143.6 mM; antagonist SCH-23390: 13.4, 40.1, & 60.1 mM) and D2 (agonists quinp

42 ons of the selective D1 receptor antagonist, SCH 23390 (2.0 microgram 0.5 microliter-1 side-1), on th

43 (2.5, 5, and 25 g/side) or the D1 antagonist SCH 23390 (3, 1, 0.3, 0.15, 0.05, and 0.015 nmol/side) i

44 fused rat lungs were coinstilled with DA and SCH 23390 (a specific D(1) receptor antagonist), there w

45 her mimicked by SKF-38393 nor antagonized by SCH-23390 (a selective D1 agonist and antagonist, respec

46 (SKF 38393 and SKF 81297), a D1 antagonist (SCH 23390), a D2 receptor agonist (quinpirole), and a D2

47 D2 receptor antagonist sulpiride but not by SCH 23390, a D1 antagonist.

48 1, an NMDA glutamate receptor antagonist, or SCH 23390, a D1 dopamine receptor antagonist.

49 The antioxidant sodium metabisulfite or SCH 23390, a D1 dopamine receptor-selective antagonist,

50 e rats received bilateral microinjections of SCH 23390, a D1 receptor antagonist.

51 cultures, and this effect was antagonized by SCH 23390, a D1 selective dopamine antagonist.

52 -mediated phosphorylation was antagonized by SCH 23390, a D1-like receptor antagonist.

53 This effect was blocked by SCH-23390, a D1 antagonist, in a dose dependent fashion,

54 ubule cells, an effect that was abolished by SCH-23390, a D1-like receptor antagonist.

55 was evaluated following saline or 0.25mg/kg SCH 23390,a D1 receptor antagonist, while awake hamsters

56 Finally, administration of SCH-23390 alone in the RAIC decreased paw withdrawal lat

57 er, the DA blocking effect was stronger than SCH-23390 alone.

58 Interestingly, bodipy-SCH 23390 also specifically labelled discrete spots of r

59 phenyl-2,3,4,5-tetrahydro-1H-3-benzazepi ne (SCH 23390), although S198A and S199A displayed significa

60 The effect of SKF 81297 was reversed by SCH 23390 (an antagonist at D1/D5 receptors), confirming

61 Injection of SCH 23390, an antagonist of the D(1) class of dopamine r

62 risk of developing HD were scanned with 11C-SCH 23390 and 11C-raclopride to calculate the D1 and D2

63 Benzazepines 1 and 2 (SCH 23390 and SCH 39166, respectively) are two classical

64 Both SCH-23390 and sulpiride prevented the reduction in extra

65 Moreover, asymmetrical infusion of SCH-23390 and the DOR antagonist naltrindole into the NA

66 iate, but not delayed, infusions of both D1 (SCH 23390) and NMDA (AP-5) receptor antagonists signific

67 cocaine, desipramine, SKF-38393, quinpirole, SCH-23390, and sulpiride.

68 Using serial [(11)C]SCH 23390- and [11C]raclopride-PET, we have measured the

69 ), and by the dopamine (DA) (D1) antagonist, SCH-23390, arguing that ACh release, in part, involves a

70 Conversely, intra-PFC infusions of SCH 23390 at the same dose (0.5 microgram/0.5 microliter

71 barrel cortex, and intrastriatal infusion of SCH-23390 attenuated this effect.

72 Pretreatment with the D1 receptor antagonist SCH-23390 before optical VTA stimulation inhibited the a

73 However, the fraction of bodipy-SCH 23390 binding that was specific varied substantially

74 the effect of D1/D5 dopaminergic antagonist SCH 23390, but the infusion of PKC stimulator PMA does n

75 f D1Rs pharmacologically: the D1R antagonist SCH-23390, but not the D2R antagonist raclopride, infuse

76 tion of these drugs resembled the effects of SCH-23390, but whereas the change in basal activity and

77 SCH 23390 by itself had no effect on performance, althou

78 pretreatment with a D1 receptor antagonist, SCH 23390, consistent with drug actions at D1 receptors.

79 Injection of SCH 23390 (D1 DA receptor antagonist) into NA of postpar

80 ists, eticlopride (D2/3, 0.25 mg/kg day) and SCH-23390 (D1, 0.25 mg/kg day), blocked the stereotypic

81 bility of selective antagonists of dopamine (Sch 23390, D1; Sulpiride, D2), glutamate (CPP, competiti

82 ex (mPFC) were taken for analysis of D1 ([3H]SCH-23390), D2 ([3H]Spiperone), and NMDA ([3H]MK-801) re

83 SCH 23390 decreased SSRT with little effect on the go re

84 crophonic potentials, whereas D1R antagonist SCH-23390 decreased microphonic potentials.

85 s did not affect PPT mRNA expression whereas SCH-23390 decreased PPT message levels (-24.5+/-5.4%).

86 Pre-training infusions of SCH 23390 dose-dependently attenuated conditioned freezi

87 ized by the D1-like receptor antagonist R(+)-SCH 23390 (estimated dissociation constant KB = 1.7 micr

88 systems); 2) D1 and D2 receptor antagonists (SCH 23390, eticlopride, raclopride) counteract these eff

89 In contrast to the substantia nigra, SCH 23390 failed to alter the apomorphine sensitivity in

90 crog) of the dopamine D1 receptor antagonist SCH-23390 greatly impaired retrieval and licking of pups

91 zosin, yohimbine, amphetamine, SKF 38393 and SCH 23390 had no effects on cataplexy.

92 stationary reactivity, respectively, whereas SCH-23390 had no effect on these behaviors.

93 Because SCH 23390 has been shown to have agonist-like properties

94 ions of the D-1 dopamine receptor antagonist SCH 23390 HCl (0, 0.8, 1.6, 3.2, and 6.4 microgram total

95 rol injections of the most effective dose of SCH 23390 HCl (6.4 micogram) were made either 1.5 mm dor

96 phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine (SCH 23390) hydrochloride was applied simultaneously via

97 phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine (SCH 23390) hydrochloride, a D1 antagonist, or 0.50 mM S(

98 erin were ineffective, as were injections of SCH 23390 in a site 1 mm dorsal or 1 mm rostral to the e

99 however, the same behavior was unaffected by SCH 23390 in animals tested during the later stages of t

100 SCH-23390 in the medial hypothalamus tended to impair li

101 SCH 23390 increased cocaine self-administration on the F

102 g., escape, jump), whereas the D1 antagonist SCH-23390 increased stationary reactivity (e.g., freezin

103 -tetrahydro-1H-3-benzazep ine hydrochloride (SCH 23390) increased response latencies; however, the sa

104 was displaced by (+)-butaclamol, dopamine or SCH 23390, indicating that it specifically labelled D1 d

105 n of the 5-HT(2C) antagonist failed to alter SCH 23390-induced decreases in METH-induced locomotion a

106 so observed during local eticlopride but not SCH 23390 infusion.

107 stemic and medial or lateral accumbens shell SCH 23390 injections attenuated context-induced reinstat

108 ntrast, core but not lateral or medial shell SCH 23390 injections attenuated discrete-cue-induced rei

109 nt of heroin seeking, whereas accumbens core SCH 23390 injections were ineffective.

110 of muscimol + baclofen into ventral mPFC or SCH 23390 into the accumbens shell had no effect.

111 misphere and D(1)-family receptor antagonist SCH 23390 into the contralateral or ipsilateral accumben

112 npirole into the VTA or of the D1 antagonist SCH 23390 into the LBA caused a decrease in freezing to

113 s assessed immediately after the infusion of SCH 23390 into the NAcc (0.5 microgram/0.5 microliter/si

114 al injections of the dopamine D1 antagonist, SCH 23390 into the prefrontal cortex (PFC), or the nucle

115 nist CNQX or dopamine D1-receptor antagonist SCH-23390 into the DLS before testing restored goal-dire

116 of the dopamine (DA) D1 receptor antagonist SCH-23390 into the lateral septum (LS) blocks ethanol-in

117 nt 1, microinjections of the D(1) antagonist SCH-23390 into the MPOA before each of seven daily 30-mi

118 antagonist eticlopride, or the D5 antagonist SCH-23390, into the AH.

119 to the enhancing effects of haloperidol and SCH 23390 on DA metabolism.

120 ation of dopamine D1 or D2 antagonists (1 mm SCH 23390 or 3 mm raclopride) and were not mimicked by i

121 f the dopamine D1 receptor (DRD1) antagonist SCH 23390 or dopamine D2 receptor (DRD2) antagonist sulp

122 tions of the D1 dopamine receptor antagonist SCH 23390 or the 5-HT2 receptor antagonist ketanserin.

123 large-reward arm and blunted the effects of SCH-23390 or haloperidol.

124 tration of SKF-81297 after pretreatment with SCH-23390 or the D2 antagonist sulpiride confirmed the i

125 ns of high concentrations of D1- (100 microM SCH 23390) or D2-like (100 microM sulpiride) dopamine re

126 that block dopamine receptors (haloperidol, SCH 23390) or reduce stress-induced PFC dopamine turnove

127 of a D1 agonist (SKF 38393), D1 antagonist (SCH 23390), or a vehicle solution.

128 arm after treatment with the D1 antagonist, SCH-23390, or the D2 antagonist, haloperidol.

129 SCH 23390 perfusion decreased the excitability of striat

130 ymptomatic mutation carriers had serial [11C]SCH 23390-PET and showed a mean annual loss of striatal

131 Infusions of SCH 23390 prior to acquisition training, prior to retent

132 We found that SCH 23390 produced a dose-dependent decrease in AMPH- an

133 nsitive to the receptor-selective antagonist SCH 23390, protein kinase A inhibition (KT5720), and MEK

134 T), [DA D3/D2 preferring], Antagonists: R(+)-SCH 23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3

135 leate), but neither DA receptor antagonists [SCH-23390 (R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,

136 Pretreatment with the D1 antagonist SCH-23390 ((R)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-

137 t by using the D1-family receptor antagonist SCH 23390 [R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3

138 he selective dopamine D1 receptor antagonist SCH 23390 [R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3

139 Pretreatment with the D1 dopamine antagonist SCH 23390 [R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,

140 ly, pretreatment with the D1-like antagonist SCH 23390 [R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-

141 of D(1) and D(2) antagonists (raclopride and SCH-23390 [R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3

142 stent with mediation by D(1)-type receptors, SCH-23390 [R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,

143 ulting food intake was decreased by doses of SCH 23390 ranging from 0.05 to 100 nmol/side injected bi

144 The D1/D5 antagonist (+)SCH 23390 reduced early LTP.

145 ata showed that intra-VTA microinjections of SCH 23390 reduced the rewarding effects of food.

146 However, haloperidol and raclopride (but not SCH-23390) reversed the disruptive effect of 30 mg/kg ke

147 vented by the DA D1-like receptor antagonist SCH 23390 (SCH), the DA D2-like receptor antagonist remo

148 sters were treated with saline or 0.25 mg/kg SCH-23390 (SCH), a D(1) receptor antagonist that crosses

149 SCH 23390 selectively reversed the apomorphine subsensit

150 a D1 agonist (SKF 38393) or a D1 antagonist (SCH 23390), suggesting that D1 and D2 receptors are func

151 Conversely, while injection of SCH-23390 suppressed aggressive behavior, these reductio

152 d intertrial interval remained vulnerable to SCH 23390 throughout the experiment.

153 Binding of bodipy-SCH 23390 to live neurons was displaced by (+)-butaclamo

154 The dopamine D1 receptor antagonist SCH 23390 was ineffective both systemically (0.25 mg/kg,

155 scent D1 dopamine receptor antagonist bodipy-SCH 23390 was measured in 2-3-week-old primary striatal

156 r observed when the D(1) receptor antagonist SCH-23390 was infused into the NAcc.

157 of DBS, whereas the D1 receptor antagonist, SCH-23390, was ineffective, suggesting that dopamine sig

158 Co-infusion of the lowest dose of SCH 23390 with a low dose of the NMDA antagonist AP-5 (0