ライフサイエンスコーパス: raclopride

1 ocked by pretreatment with a D2R antagonist (raclopride).

2 DAT ([11C]cocaine) and DA D2 receptor ([11C]raclopride).

3 isplaces binding of the D(2) ligand, [(11)C]-raclopride.

4 ated glutamate release in similar fashion as raclopride.

5 sitron emission tomography (PET) with [(11)C]raclopride.

6 lication of the dopamine receptor antagonist raclopride.

7 Three rats received a single dose of (11)C-raclopride.

8 atheterized for tail vein injection of (11)C-raclopride.

9 (PET) scans with high specific activity [11C]raclopride.

10 y for the D(2)/D(3)-selective antagonist (-)-raclopride.

11 prevented by the D2-like receptor antagonist raclopride.

12 and the D2/D3R-selective radioligand [(11)C]raclopride.

13 etreatment with the dopamine D2/3 antagonist raclopride.

14 a or in any region when measured with [(11)C]raclopride.

15 3 receptor (D2/D3) antagonists such as (11)C-raclopride.

16 ceable D(2)/D(3) receptor radiotracer [(11)C]raclopride.

17 ivity to the dopamine D2 receptor antagonist raclopride.

18 DG, (11)C-d-threo-methylphenidate, and (11)C-raclopride.

19 0.4, 0.8, and 0.16 mg/kg) or D(2) antagonist raclopride (0, 0.2, 0.4, and 0.8 mg/kg).

20 Administration of raclopride (0.2, 0.6, and 1.2 mg/kg), a D2 antagonist, e

21 on of a selective D2-dopaminergic antagonist raclopride (0.3 nmol/side, bilateral).

22 were evaluated (Haloperidol [0.1 mg/kg] and raclopride [0.2 mg/kg]), for their effects on sham and r

23 jection of a selective DA D(2/3) antagonist (raclopride, 0.5 mg/kg).

24 ydroxy-6-methoxybenzamide (+)-tartrate salt (raclopride; 0, 0.2, or 0.4 mg/kg) on the likelihood and

25 In a fourth animal, raclopride (1 mg/kg) was coinjected with (11)C-racloprid

26 g was examined in pretreatment studies using raclopride (1.0 mg/kg) and d-amphetamine (1.0 mg/kg).

27 e (MPPI) (10 microgram) or the D2 antagonist raclopride (10 microgram).

28 as reversed in the presence of intracortical raclopride (10 microM, 140 min).Taken together, the pres

29 he selective D2 dopamine receptor antagonist raclopride (100 microM) into the SN and was attenuated b

30 beta-(4-fluorophenyl)tropane (CFT, 14 mg) or raclopride (14 mg) to block DAT or D2/D3 binding site, r

31 ent with the dopamine D2 receptor antagonist raclopride (1mg/kg, ip) failed to affect this phenomenon

32 induced by haloperidol (0.5-5 mg/kg i.p.) or raclopride (2 mg/kg s.c.).

33 D2 receptor antagonist haloperidol, but not raclopride (2 mg/kg, i.p.).

34 eased affinity for benzamide ligands such as raclopride (200-fold) and sulpiride (125-fold).

35 sion of the accumbens with the D2 antagonist raclopride (4 microg/side) prevents systemic quinpirole

36 .), or dopamine D2 receptor antagonist, S(-)-raclopride (5 mg/kg, i.p.) but not by capsazepine (40 mg

37 tected with [(11)C]PHNO compared with [(11)C]raclopride (52-64% vs 33-35%, respectively).

38 positron emission tomography (PET) and [C-11]raclopride (a radioligand for the dopamine D2 receptor).

39 emic haloperidol, or intracerebroventricular raclopride (a type 2 dopamine receptor blocker) ameliora

40 D2/3 receptor-binding potential using [(11)C]raclopride (a weak competitive D2/3 receptor antagonist)

41 ist, in a dose dependent fashion, but not by raclopride, a D2 antagonist.

42 into the VTA, but not by equimolar doses of Raclopride, a D2 antagonist.

43 However, raclopride, a D2 selective dopamine antagonist, complete

44 ) and dopamine increases (measured with [11C]raclopride, a D2/D3 receptor ligand with binding that is

45 etized and injected intravenously with (11)C-raclopride, a DRD2-specific ligand, and dynamic PET scan

46 The antipsychotic drug raclopride, a selective D2 receptor antagonist, increase

47 Mass doses of raclopride above tracer levels caused increases in CBV a

48 We scanned 20 controls with [(11)C]raclopride after rested sleep and after 1 night of sleep

49 with positron emission tomography and [(11)C]raclopride, after administration of an injection of plac

50 t on osmotic-induced water drinking, whereas raclopride also reduced water intake.

51 ases in distribution volumes (DVs) of [(11)C]raclopride, although normal reductions in striatal nondi

52 flow was assumed during the bolus PET (11)C-raclopride/AMPH experiment across striatal subregions, w

53 riatum, hippocampus, and cortex, using (11)C-raclopride and (11)C-MPEP, respectively.

54 MRI volumetry, as well as (11)C-raclopride and (18)F-FDG PET, reveal neuronal dysfunctio

55 receptor and mGluR(5) modulation using (11)C-raclopride and 2-(11)C-methyl-6-(2-phenylethynyl)-pyridi

56 ects were followed longitudinally with [11C]-raclopride and [18F]-fluorodeoxyglucose PET imaging, wit

57 After administration of raclopride and d-amphetamine, the (18)F-MCL-524 BPND val

58 preferential dopamine D2 receptor antagonist raclopride and D1 receptor antagonist SCH23390.

59 the combined D(4)-F88V/TMS3 mutants had (-)-raclopride and isomethylbutylamiloride binding propertie

60 ong with MRI and D2DR assessment with [(11)C]raclopride and PET.

61 We used [11C]raclopride and positron emission tomography (PET) to ass

62 Here we use 11C-labelled raclopride and positron emission tomography scans to pro

63 [11C]Raclopride and positron emission tomography were used to

64 ocking mixture of D(1) and D(2) antagonists (raclopride and SCH-23390 [R(+)-7-chloro-8-hydroxy-3-meth

65 The rate of metabolism of [11C]raclopride and the nonspecific binding (cerebellum) were

66 e dopamine receptor antagonists (SCH39166 or raclopride) and the Daun02 chemogenetic inactivation pro

67 D1 or D2 antagonists (1 mm SCH 23390 or 3 mm raclopride) and were not mimicked by injections of the l

68 for the striatal dopamine D2 receptor ([11C]raclopride), and a pharmacologic challenge of the seroto

69 18)F]DOPA), dopamine D2/D3 receptors ([(11)C]raclopride), and serotonin transporter (11)C-N,N-dimethy

70 three radioligands ([(3)H]nemonapride, [(3)H]raclopride, and [(3)H]spiperone) to D(2) dopamine recept

71 8-46 y) received a single injection of (11)C-raclopride, and automatic segmentation of concomitant st

72 es using more than approximately 1-2 nmol/kg raclopride, and scatter correction has a measurable impa

73 n of dopamine D1 (SCH23390) and D2 receptor (raclopride) antagonists reduced gratification of sodium

74 D(1)-selective (SCH23390) or D(2)-selective (raclopride) antagonists.

75 Using [3H]raclopride as the ligand, sub-chronic haloperidol admini

76 In contrast, raclopride as well as saline did not reverse burst firin

77 tients with SZ and 9 HCs with PET and [(11)C]raclopride at baseline and two times (3-5 and 6-10 h) fo

78 he D2/D3 dopamine receptor antagonist [(11)C]raclopride at varying specific activities to anesthetize

79 ith the dopamine receptor radiotracer [(11)C]raclopride, at baseline and again following acute deplet

80 The dopamine D2 receptor antagonist, raclopride, attenuated the action of DBS, whereas the D1

81 hy control subjects were scanned with [(11)C]raclopride before and after stimulant administration (me

82 eated rats with the D(2) receptor antagonist raclopride before systemic AMPH.

83 ubjects underwent two PET scans using [(11)C]raclopride, before and after the administration of a sti

84 ke and methamphetamine-induced change of 11C-raclopride binding (as a measure of DA release) in the p

85 Percent change in [(11)C]raclopride binding after amphetamine (change in nondispl

86 Localization of significant changes in (11)C-raclopride binding after methamphetamine at a voxel leve

87 triatum as assessed by reduced change in 11C-raclopride binding compared with control subjects.

88 The change in [(11)C]raclopride binding correlated significantly with the fal

89 The change in [(11)C]-raclopride binding correlated with preference in the ven

90 which was measured as an increase in [(11)C]raclopride binding following AMPT administration.

91 asured amphetamine-induced changes in [(11)C]raclopride binding in 1) high-risk young adults with a m

92 more, we observed no correlation between 11C-raclopride binding in anterior, posterior or entire puta

93 led that methylphenidate also decreased [11C]raclopride binding in hippocampus and amygdala and that

94 phenidate induced smaller decrements in [11C]raclopride binding in left and right caudate (blunted DA

95 , the results mainly showed decreased [(11)C]raclopride binding in the anterior striatum and limbic A

96 nce exhibited little or no change in [(11)C]-raclopride binding in the cocaine-paired environment.

97 ]DOPA uptake in the anterior putamen, [(11)C]raclopride binding in the posterior striatum, and 2'-met

98 and phenylalanine depletion increased [(11)C]raclopride binding in the striatum by a mean of 6%.

99 The increase in [(11)C]raclopride binding in the striatum was 11.1% (SD=4.4%) i

100 The observed decrease in [11C]raclopride binding is consistent with an increase in dop

101 differential between [3H]nemonapride and [3H]raclopride binding may represent sigma rather than D4 re

102 ET scanning had greater reductions in [(11)C]raclopride binding potential (an indirect measure of dop

103 nd a mean annual 4.8% loss of striatal (11)C-raclopride binding potential (BP) between the first and

104 , as reflected by a 25.2% reduction in (11)C-raclopride binding potential as compared with placebo, b

105 ound when comparing the percentage change of raclopride binding potential between the two Parkinson's

106 greater reduction of ventral striatum (11)C-raclopride binding potential following reward-related cu

107 Modafinil decreased mean (SD) [(11)C]raclopride binding potential in caudate (6.1% [6.5%]; 95

108 ne produced significant reductions in [(11)C]raclopride binding potential in the striatum as a percen

109 that smoked had greater reductions in [(11)C]raclopride binding potential in ventral striatum regions

110 would not likely influence measures of (11)C-raclopride binding potential to a significant extent.

111 rule out the possibility that decreased [11C]raclopride binding reflects decreases in receptor levels

112 Striatal [(11)C]raclopride binding reflects dopamine D(2) receptor avail

113 cocaine-paired environment decreased [(11)C]-raclopride binding relative to the saline-paired environ

114 In DLB, [(3)H]raclopride binding to D2 receptors was significantly red

115 h control subjects, patients had reduced 11C-raclopride binding to D2/D3 receptors at rest in the bil

116 ase during speech production and reduced 11C-raclopride binding to D2/D3 receptors at rest was seen.

117 ping overlapped with a region of reduced 11C-raclopride binding to D2/D3 receptors at rest.

118 were estimated through measurement of [(11)C]raclopride binding with positron emission tomography aft

119 g Scale (UHDRS) scores correlated with (11)C-raclopride binding, but there was no correlation between

120 ound to cause a decrease in the Bmax for [3H]raclopride binding, suggesting that persistently elevate

121 lso show cue-induced displacement of [(11)C]-raclopride binding.

122 HNO binding but no relationship with [(11)C]-raclopride binding.

123 Raclopride blocked 8-OH-DPAT's facilitative effects on e

124 > or =15 cigarettes/day) underwent a [(11)C]raclopride bolus-plus-continuous-infusion PET session.

125 The authors used [(11)C]raclopride bolus-plus-continuous-infusion positron emiss

126 zed significant baseline reductions in (11)C-raclopride BP in both striatal and extrastriatal areas,

127 al, frontal and temporal reductions in (11)C-raclopride BP in Huntington's disease.

128 sease patients also showed attenuated [(11)C]raclopride BP reductions during the same motor paradigm

129 dopamine was blocked by the D(2) antagonist raclopride, but was unaffected by SCH-23990, a D(1) anta

130 er in zQ175 than WT animals by 40% for (11)C-raclopride, by 52% for (18)F-MNI-659, by 28% for (11)C-N

131 er in zQ175 than WT animals by 40% for (11)C-raclopride, by 52% for (18)F-MNI-659, by 28% for (11)C-N

132 It has also been shown that PET with [11C]raclopride can be used to assess changes in brain DA ind

133 Blockade of D2 receptors with raclopride caused a significant increase in the DOPAC/DA

134 binding was tested by blocking D(2/3)R with raclopride (coincubation with 10 muM in vitro, administr

135 ll considerably higher than the doses of 11C-raclopride commonly used in research PET (370-555 MBq).

136 er this reflected dopamine increases ([(11)C]raclopride competes with dopamine for D2/D3 receptor bin

137 Because [11C]raclopride competes with endogenous dopamine for binding

138 es the interaction of a DA function and free raclopride concentration over time and follows directly

139 Micro-PET and autoradiography using [(11)C]raclopride confirmed a strong correlation between high w

140 eceptor antagonists (SCH 23390, eticlopride, raclopride) counteract these effects; 3) these antagonis

141 TS: Positron emission tomography with [(11)C]raclopride (D(2)/D(3) radioligand sensitive to changes i

142 with positron emission tomography and [(11)C]raclopride (D(2)/D(3) receptor radioligand sensitive to

143 used positron emission tomography and [(11)C]raclopride (D2 receptor radioligand that competes with e

144 hical analysis method was used with the [11C]raclopride data to derive the distribution volume of D2

145 e DA D2 receptor antagonist radiotracer [11C]raclopride detected significant activation of DA release

146 nds dopamine, R-(-)propylnorapomorphine, and raclopride did not affect oligomerization of D2L and D2S

147 vian approach and operant lever-press, while raclopride did not.

148 (18)F]FMT and methylphenidate-induced [(11)C]raclopride displacement.

149 ent positron emission tomography with [(11)C]raclopride (dopamine D(2) receptor radioligand that comp

150 using positron emission tomography and [11C]raclopride (dopamine D2 receptor radioligand sensitive t

151 using positron emission tomography and [11C]raclopride (dopamine D2/D3 receptor radioligand) and [11

152 [(1)(1)C]MPH and [(1)(1)C]raclopride dynamic PET scans were performed to image dop

153 response was unaffected by the D2 antagonist raclopride, even at a dose that strongly suppressed loco

154 not 2 microg) of the D2 receptor antagonist raclopride facilitated nursing but did not affect oral m

155 evidenced by reduced displacement of [(11)C]raclopride following amphetamine administration.

156 graphy and radioligands such as F-dopa and C-raclopride for investigating abnormalities of the presyn

157 clopride (1 mg/kg) was coinjected with (11)C-raclopride for the second injection.

158 l labeling of an approved PET tracer, [(11)C]raclopride, for the dopamine D2/D3 receptor by carbonyla

159 Transfer of [11C]raclopride from plasma to brain in the striatum and cere

160 The D2/3 antagonist raclopride had no effect per se, but prevented the quine

161 tween the binding of [3H]nemonapride and [3H]raclopride has been used to quantify dopamine D4 recepto

162 PET and (11)C-raclopride have been used to assess dopamine activity in

163 3 radiotracers [(11)C]carfentanil and [(11)C]raclopride have significantly contributed to our underst

164 .54 microM) and dopamine D2 receptors ([(3)H]raclopride, IC(50) = 1.2 microM) are reduced by incorpor

165 The (11)C-raclopride images of the KO mice showed significantly lo

166 In this study, we use [(11)C]-raclopride imaging in awake rodents to capture cue-induc

167 with positron emission tomography and [(11)C]raclopride in 16 METH abusers, both after placebo and af

168 r availability (measured with PET and [(11)C]raclopride in controls) in striatum, but could not deter

169 The specific binding of [11C]raclopride in dorsal (caudate and putamen) but not in ve

170 pamine D(2)/D(3) receptor imaging with (11)C-raclopride in humans.

171 ositron-emission tomography radioligand [11C]raclopride in nonhuman primates, and (ii) to test the hy

172 affect maternal potentiation and infusion of raclopride in the dorsal striatum did not reverse the bl

173 DA efflux showed an attenuated response to raclopride in the haloperidol alone group; this effect w

174 Raclopride in the medial hypothalamus had no effects.

175 reproducibility of microPET imaging of (11)C-raclopride in the rat brain and the effects of tracer-sp

176 Perfusion with the antagonist raclopride in the same structure produced a moderate red

177 The specific binding of [11C]raclopride in the striatum and thalamus were significant

178 The reduction in binding of raclopride in the striatum positively correlated with th

179 njection of a bolus of [(11)C]PHNO or [(11)C]raclopride in three conditions: baseline; preinjection o

180 y saturation binding of [3H]SCH23390 and [3H]raclopride) in caudate, putamen and nucleus accumbens, o

181 avenous methylphenidate (using PET and [11C] raclopride) in the striatum and in the thalamus.

182 ups showed a similar tolerance effect to the raclopride-induced increase in DA metabolites.

183 gonist SCH-23390, but not the D2R antagonist raclopride, infused into the NAc-S abolished PIT in rats

184 The DVR depended on the mass of tracer (11)C-raclopride injected for doses >1.5 nmol/kg.

185 a was collected for 60 min-starting at (11)C-raclopride injection-and binned into 24 time frames (6 x

186 nt to determine reproducible DVRs from (11)C-raclopride injections of 9.25 MBq (approximately 250 mic

187 ity curves were generated from measured [11C]raclopride input functions.

188 canned with positron emission tomography and raclopride labeled with carbon 11 (D2/D3 receptor radiol

189 ion tomography scanning with the radiotracer raclopride labeled with radioactive carbon (11C) was per

190 on of D(1) and D(2) antagonists SCH23390 and raclopride, like extinction, suppressed responding but,

191 Injection of graded raclopride mass doses revealed a monotonic coupling betw

192 8)F]FMT Ki and the baseline (placebo) [(11)C]raclopride measure, such that participants with greater

193 as the traditionally used radiotracer [(11)C]raclopride measures both high- and low-affinity receptor

194 Test-retest results showed that the (11)C-raclopride microPET DVR was reproducible (change in DVR

195 This study shows that the (11)C-raclopride microPET-derived DVR is reproducible and suit

196 (+)-PHNO (n = 26) and the antagonist [(11)C]-raclopride (n = 35) in healthy humans.

197 the difference in specific binding of [(11)C]raclopride (nondisplaceable binding potential) between b

198 s, we found that the selective D2 antagonist raclopride not only blocked the inhibition induced by D-

199 ular exercise received 2 PET scans with [11C]raclopride on 2 separate days, 1 at baseline and 1 at 5-

200 s were blocked by intranigral application of raclopride, our results suggest that the expression of D

201 sitron Emission Tomography (PET) with [(11)C]raclopride (P<0.0001), while correcting for age, sex, BM

202 tagonist), and dopamine release using [(11)C]raclopride paired with oral methylphenidate administrati

203 Pretreatment with 1 mg of raclopride per kilogram reduced the apparent specific bi

204 t, the subjects were also scanned with [11C]-raclopride PET and structural MRI to measure concurrent

205 availability in vivo as measured with [(11)C]raclopride PET at baseline and during a standardized pai

206 Noiseless simulations of (11)C-raclopride PET curves were performed in a specific bindi

207 In summary, serial (11)C-raclopride PET demonstrates a linear progression of stri

208 All patients had two (11)C-raclopride PET scans 29.2 +/- 12.8 months apart, and six

209 Furthermore, (11)C-raclopride PET showed impairment of the postsynaptic dop

210 Here we report on [11C]raclopride PET studies in which healthy humans performed

211 previously undergone [11C]SCH23390 and [11C]raclopride PET to assess in vivo levels of striatal dopa

212 evaluate serotonin terminal function and 11C-raclopride PET to evaluate dopamine release.

213 volunteers were examined at rest using (11)C-raclopride PET with the radioligand administered as a bo

214 with Huntington's disease using serial (11)C-raclopride PET, a specific marker of D2 dopamine recepto

215 ing clinical assessment and 18F-dopa and 11C-raclopride PET, factors which may influence the function

216 tudy was to investigate in vivo, with [(11)C]raclopride, PET changes in regional brain levels of dopa

217 's disease mutation carriers had serial [11C]raclopride-PET and showed a mean annual loss of striatal

218 Using serial [(11)C]SCH 23390- and [11C]raclopride-PET, we have measured the rate of loss of str

219 nditioned cues and a gambling task on [(11)C]raclopride positron emission tomography (PET) imaging an

220 tes was measured with [(11)C]PHNO and [(11)C]raclopride positron emission tomography (PET) imaging.

221 Notably, the raclopride positron emission tomography (PET) signal in

222 es have demonstrated the ability of the [11C]raclopride positron emission tomography (PET) technique

223 e and participated in a study that used [11C]raclopride positron emission tomography (PET) to quantif

224 ents were studied using 11C-SCH23390 and 11C-raclopride positron emission tomography (PET).

225 Using (11)C-raclopride positron emission tomography after methamphet

226 We used [(11)C]raclopride positron emission tomography and an amphetami

227 onships to cannabis use history using [(11)C]raclopride positron emission tomography and an amphetami

228 Here, by using (11)C-raclopride positron emission tomography imaging, we inve

229 C-raclopride positron emission tomography provides an indi

230 compulsive behaviours) underwent three (11)C-raclopride positron emission tomography scans.

231 or the assessment of tract integrity and 11C-raclopride positron emission tomography to measure cauda

232 patient with Parkinson's disease using [11C]-raclopride positron emission tomography to measure dopam

233 althy volunteers were scanned using [(1)(1)C]raclopride positron emission tomography while they under

234 ain imaging using (18)F-fluorodopa and (11)C-raclopride positron emission tomography.

235 Subjects underwent 60 min of [(1)(1)C]raclopride-positron emission tomography imaging to deter

236 Further, neither SCH23390 nor raclopride pretreatment in the NAcc affected feeding eli

237 In contrast, raclopride pretreatment produced inconsistent effects up

238 dus/putamen also produced an increase, while raclopride produced a decrease, in cataplexy in narcolep

239 PET studies with [11C]raclopride provide an indirect measure of changes in syn

240 iatal neuronal dysfunction measured with 11C-raclopride (RAC) PET, and the role of PK PET as a possib

241 r of dopamine D2-receptor availability (11)C-raclopride (RAC) PET.

242 ons were studied with [(18)F]dopa and [(11)C]raclopride (RAC) PET.

243 ssion tomography with the radioligand [(11)C]raclopride (RAC) to study striatal dopaminergic neurotra

244 s disease gene carriers using PET with (11)C-raclopride (RAC), a specific D(2) receptor ligand and (1

245 reduce the binding potential (BP) of [(11)C]raclopride (RAC; a reflection of striatal DA release) in

246 sing positron emission tomography and [(11)C]raclopride (radioligand sensitive to endogenous dopamine

247 Given that dopamine D1 (SCH23390) and D2 (raclopride) receptor antagonism potently reduce sucrose

248 rast, the dopamine D2/D3 receptor antagonist raclopride reduced the seeking of chocolate-flavored suc

249 e radioligands [(11)C]carfentanil and [(11)C]raclopride, respectively.

250 tance use disorders exhibited smaller [(11)C]raclopride responses, particularly within the right vent

251 ects received single-bolus injections of 11C-raclopride (S-(-)-3,5-dichloro-N-[(1-ethyl-2-pyrrolidiny

252 The difference in [11C]raclopride's specific binding between placebo and methyl

253 potential determined after the initial [11C]raclopride scan did not significantly differ between Tou

254 r completion of a validation study for (11)C-raclopride scans involving 81 subjects, age-associated c

255 When the (11)C-raclopride scans performed 29 months after the baseline

256 24 matched healthy subjects underwent [(11)C]raclopride scans under a baseline condition and followin

257 drug-naive subjects who underwent PET [(11)C]raclopride scans with 0.3 mg/kg d-amphetamine orally and

258 rence and then received two separate [(11)C]-raclopride scans.

259 Drd1 and Drd2 DMS injections of SCH39166 or raclopride selectively decreased methamphetamine seeking

260 with other psychotropic drugs (haloperidol, raclopride, sertraline, and desipramine) that lack reinf

261 animals that had been under the influence of raclopride showed increased head entries in response to

262 Pretreatment with raclopride significantly increased PPI in the DAT (-/-)

263 y the highest equimolar 1600 nmol/kg dose of raclopride significantly reduced sucrose intake in the B

264 eater amphetamine-related reductions in [11C]raclopride specific binding (mean +/- SEM): -22.3% (+/-2

265 amphetamine dose produced a doubling in [11C]raclopride specific binding reductions.

266 ductions (relative to baseline) in the (11)C-raclopride-specific binding parameter (binding potential

267 We applied the nemonapride-raclopride subtraction method to postmortem, non-schizop

268 was observed when D(2)Rs were antagonized by raclopride, suggesting that an acute absence of D(2)Rs c

269 The D2 receptor blocker raclopride suppressed the emission of spontaneous head e

270 When one site was blocked with CFT or raclopride, the binding of the respective ligand to the

271 h the dopamine D2 receptor radioligand (11)C-raclopride, the PDE10A radioligand (18)F-MNI-659, the do

272 h the dopamine D2 receptor radioligand (11)C-raclopride, the PDE10A radioligand (18)F-MNI-659, the do

273 We used PET and [(11)C]raclopride to assess baseline DRD2 availability in 91 pa

274 n tomography scans after injection of [(11)C]raclopride to assess dopamine D(2) receptors and [(18)]f

275 d with positron emission tomography and [11C]raclopride to assess dopamine D2 receptors.

276 positron emission tomography (PET) and [11C]raclopride to assess the availability of dopamine D2 rec

277 g HD were scanned with 11C-SCH 23390 and 11C-raclopride to calculate the D1 and D2 receptor binding p

278 iatum (assessed as reduced binding of [(11)C]raclopride to D2/D3 receptors) in detoxified cocaine abu

279 Binding of the radioligand 11C-labelled raclopride to dopamine D2 receptors is sensitive to leve

280 Binding of raclopride to dopamine receptors in the striatum was sig

281 receptor availability was measured with [11C]raclopride to evaluate its relation to methylphenidate-i

282 D2 receptors were measured with [11C]raclopride to evaluate their relation to methylphenidate

283 at [(11)C]PHNO is more sensitive than [(11)C]raclopride to nicotine- and amphetamine-induced DA relea

284 n DA responses (measured with PET and [(11)C]raclopride) to MP between controls and marijuana abusers

285 lthy subjects were scanned with PET and [11C]raclopride twice in the same day: 7 min after placebo or

286 [(11)C]-raclopride uptake in the saline-paired environment serve

287 In 3 studies, (11)C-raclopride was administered a second time in the same an

288 0%), the binding potential (BP(ND)) of (11)C-raclopride was found to be around 2.2 for caudate and 2.

289 binding (striatum minus cerebellum) of [11C]raclopride was observed.

290 Whole-body radiation dosimetry of 11C-raclopride was performed in healthy human volunteers.

291 eduction in binding potential (BP) of [(11)C]raclopride was seen in both caudate and putamen in healt

292 sitron emission tomography (PET) with [(11)C]raclopride was used to examine IFN-alpha-induced changes

293 Positron emission tomography with [11C]raclopride was used to examine the effects of the intrav

294 graphy imaging with the D2/D3 antagonist 11C-raclopride, we analysed striatal D2/D3 availability at r

295 Here, using PET with [(11)C]raclopride, we identified in the AKT1 gene a new variabl

296 tamine-induced changes in BP(ND) of [(1)(1)C]raclopride were estimated by kinetic modeling.

297 ncreased RC(zmin), BP(ND) estimates of (11)C-raclopride were increased by 12% and 21% for caudate and

298 Two PET studies using [11C]raclopride were performed in 11 normal male subjects bef

299 of D5Rs, flupenthixol, or a D2R antagonist, raclopride, were applied.

300 ne by comparing the specific binding of [11C]raclopride when subjects watched a neutral video (nature