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

4 ivity to the dopamine D2 receptor antagonist raclopride.

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

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

7 ated glutamate release in similar fashion as raclopride.

8 g with DA D(2/3) PET assessment using [(11)C]raclopride.

9 lication of the dopamine receptor antagonist raclopride.

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

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

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

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

14 prevented by the D2-like receptor antagonist raclopride.

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

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

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

18 3 receptor (D2/D3) antagonists such as (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 jection of a selective DA D(2/3) antagonist (raclopride, 0.5 mg/kg).

23 al blockage (SCH23390: 0.1 mg/kg/day/5 days; Raclopride: 0.3 mg/kg/day/5 days) of D1R and D2R, and tr

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 r Drd2 antagonists (SCH39166, 1.0 ug/side or raclopride, 1.0 ug/side) during the relapse tests.

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

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

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

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

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

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

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

35 ositron emission tomography (PET) with (11)C-raclopride 24 h post-capture) spent more time feeding in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 [11C]Raclopride and positron emission tomography were used to

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

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

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

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

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

67 8-46 y) received a single injection of (11)C-raclopride, and automatic segmentation of concomitant st

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

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

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

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

72 sing positron emission tomography with (11)C-raclopride as the radiotracer.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 epression and significantly decreased [(11)C]raclopride binding in selected striatal subregions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 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

127 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

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

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

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

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

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

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

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

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

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

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

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

139 We contrasted baseline [(11)C]raclopride D2/3 receptor binding and D2/3 receptor bindi

140 ellular dopamine and leads to reduced [(11)C]raclopride D2/3 receptor binding via competitive displac

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

142 [(11)C]raclopride decrease in binding potential was significant

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

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

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

146 n emission tomography (PET) radioligand [11C]raclopride directly to subsecond dopamine release events

147 tify striatal DA release (measured by [(11)C]raclopride displacement) in response to an intravenous i

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

162 3 radiotracers [(11)C]carfentanil and [(11)C]raclopride have significantly contributed to our underst

163 .54 microM) and dopamine D2 receptors ([(3)H]raclopride, IC(50) = 1.2 microM) are reduced by incorpor

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

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

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

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

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

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

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

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

172 Raclopride in the medial hypothalamus had no effects.

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

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

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

176 ne in D2(-/-) females or coadministered with Raclopride in wild-type females improved SVZ cell prolif

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

178 CH23390, in the NAcS and the D2R antagonist, raclopride, in the NAcC selectively reduced early, perse

179 not D1R antagonism, in the dorsal striatum: raclopride increased errors in the intermediate phase af

180 responses whereas the D2 receptor antagonist raclopride increased the response amplitude.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 globus pallidus, where the change in [(11)C]raclopride nondisplaceable binding potential was approxi

197 and induced a significant decrease in [(11)C]raclopride nondisplaceable binding potential, particular

198 alyses were used to assess changes in [(11)C]raclopride nondisplaceable binding potential.

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

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

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

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

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

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

205 lability was measured as BP(ND) using [(11)C]raclopride PET after antipsychotic discontinuation.

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

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

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

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

210 using fast-scan cyclic voltammetry and [11C]raclopride PET in mice during chemogenetic activation of

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

212 us dopamine release, we collected two [(11)C]raclopride PET scans per participant.

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

214 itored via temporal fluctuations in the [11C]raclopride PET signal.

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

216 minimally conscious state patients using 11C-raclopride PET to estimate dopamine 2-like receptors occ

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

218 ficit was observed, a third and a fourth 11C-raclopride PET were acquired to evaluate changes in dopa

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

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

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

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

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

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

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

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

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

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

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

230 ity in dopamine release at rest using [(11)C]raclopride positron emission tomography (PET), functiona

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

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

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

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

235 sion >59 years old underwent baseline [(11)C]raclopride positron emission tomography followed by open

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

237 C-raclopride positron emission tomography provides an indi

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

239 unterbalanced order, while undergoing [(11)C]raclopride positron emission tomography scans.

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

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

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

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

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

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

246 In contrast, raclopride pretreatment produced inconsistent effects up

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

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

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

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

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

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

253 f presynaptic vesicular DA storage, and [11C]raclopride (RAC), an indicator of D2/D3 receptor availab

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

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

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

257 imol + baclofen, flupenthixol, SCH39166, and raclopride reduced methamphetamine seeking after 15 days

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

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

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

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

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

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

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

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

266 24 matched healthy subjects underwent [(11)C]raclopride scans under a baseline condition and followin

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

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

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

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

271 e detectable temporal variations in the [11C]raclopride signal.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

287 t absent in D2(-/-) females and increased in Raclopride-treated females.

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

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

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

291 0%), the binding potential (BP(ND)) of (11)C-raclopride was found to be around 2.2 for caudate and 2.

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

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

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

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

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

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

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

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