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 ed by the dopamine D1/D5 receptor antagonist SCH 23390.

10 e decreased immediately after treatment with SCH 23390.

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

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

13 e pretreated with the D1 dopamine antagonist SCH 23390.

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

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

16 -dependent blocking with the D(1) antagonist SCH-23390.

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

18 1 or 2 food pellets, intra-VTA injections of SCH 23390 (0 and 4 microg/0.5 microl) decreased BPs at t

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

20 e effects of the D1-like receptor antagonist SCH 23390 (0.003, 0.01, 0.03 mg/kg) and the D1-like rece

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 (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

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

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

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

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

52 1, an NMDA glutamate receptor antagonist, or SCH 23390, a D1 dopamine receptor antagonist.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 Systemic administration of SCH-23390 (D1 antagonist) slowed probabilistic learning

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

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

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

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

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

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

91 Treatment with SCH 23390 did not have any long-term effects.

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

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

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

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

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

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

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

99 Further comparisons between the effect of SCH-23390/haloperidol on behavioral and resting-state FC

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

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

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

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

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

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

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

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

108 SCH 23390 increased cocaine self-administration on the F

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 re were no sex differences in the effects of SCH 23390 or A77636.

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

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

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

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

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

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

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

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

137 SCH 23390 perfusion decreased the excitability of striat

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

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

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

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

142 by the dopamine D1-like receptor antagonist SCH-23390, providing a potential alternative strategy to

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

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

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

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

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

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

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

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

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

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

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

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

155 conclusion, the D1-like receptor antagonist SCH 23390 reduces nicotine intake and causes sedation in

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

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

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

159 SCH 23390 selectively reversed the apomorphine subsensit

160 Importantly, PL D1 receptor blockade (SCH 23390) shifted the proportion of striatal activity f

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

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

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

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

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

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

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

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

169 The effects of SCH 23390 were investigated 15 min and 24 h after treatm

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