ライフサイエンスコーパス: conditioned place preference

1 ssion exclusively in the NAc reduced cocaine conditioned place preference.

2 social reward cues as well as form a social-conditioned place preference.

3 nucleus accumbens (NAc) and cocaine-induced conditioned place preference.

4 ersistent spine gain correlated with cocaine conditioned place preference.

5 intake and block the development of alcohol-conditioned place preference.

6 dminister cocaine, and it fails to produce a conditioned place preference.

7 essed the presence of spontaneous pain using conditioned place preference.

8 f synaptic plasticity in the VTA and cocaine conditioned place preference.

9 Mzeta on the behavioral responses by cocaine conditioned place preference.

10 tor activation, behavioral sensitization, or conditioned place preference.

11 signaling (mice), suppressed opioid-induced conditioned place preference.

12 ibitory peptide in the VTA disrupted cocaine conditioned place preference.

13 es in methamphetamine reward as measured via conditioned place preference.

14 tenuated cue conditioning, but also enhanced conditioned place preference.

15 viors, including locomotor sensitization and conditioned place preference.

16 ut not drug-induced reinstatement of cocaine conditioned place preference.

17 ant path that was found to underlie nicotine-conditioned place preference.

18 ionally modulates amphetamine (AMPH)-induced conditioned place preference.

19 the nicotine-induced synaptic plasticity and conditioned place preference.

20 wed increased propensity for alcohol-induced conditioned place preference.

21 as5 in NAc neurons decreased cocaine-induced conditioned place preference.

22 rmal morphine reward behavior as measured by conditioned place preference.

23 n diminishes morphine reward, as measured by conditioned place preference.

24 as9 gene knockdown of Gadd45b blocks cocaine conditioned place preference.

25 layed significantly less hyperlocomotion and conditioned place preference.

26 nd more persistent memory of cocaine-induced conditioned place preference.

27 d for morphine-induced reward as measured by conditioned place preference.

28 but not the ventral tegmental area, induced conditioned place preference.

29 show deficits in FS-induced reinstatement of conditioned place preference.

30 ts of morphine as measured by acquisition of conditioned place preference.

31 ut not the shell or ventral pallidum induced conditioned place preference.

32 o influence feeding, locomotor activity, and conditioned place preference.

33 eport that zebrafish exhibit cocaine-induced conditioned place preference.

34 with footshock to reinstate cocaine-induced conditioned place preference.

35 but not D2R-MSNs, in the NAc reduced cocaine conditioned place preference.

36 ventral hippocampus is necessary for cocaine conditioned place preference.

37 sociate environmental cues with reward using conditioned place preference.

38 cocaine-induced locomotor sensitization and conditioned place preference.

39 e, however, showed unaltered cocaine-induced conditioned place preference.

40 reduced hind-limb sensitisation and induced conditioned place preference.

41 rexpressing G9a in the NAc decreases cocaine-conditioned place preference.

42 einstatement of extinguished cocaine-induced conditioned place preference.

43 egions of the VS and trained to the morphine conditioned place preference.

44 HT1A autoreceptors are necessary for cocaine conditioned place preference.

45 ne, blocked reinstatement of morphine-evoked conditioned place preference.

46 orces instrumental behaviour and establishes conditioned place preferences.

47 into the posterior shell of NAS established conditioned place preferences.

48 the development of cocaine sensitization and conditioned place preference, a measure of cocaine rewar

49 rom the injury with local anesthetic elicits conditioned place preference, activates ventral tegmenta

50 c manipulations on the reinstatement of drug-conditioned place preference after extinction of the lea

51 of these projections affects behavior using conditioned place preference and a task in which mice le

52 logical and circuit mechanisms of aggression conditioned place preference and aggression self-adminis

53 e exhibit enhanced cocaine sensitization and conditioned place preference and an increase in Alk expr

54 rol pretreatments attenuated cocaine-induced conditioned place preference and blocked the cocaine-ind

55 with (+/-)-BayK-8644 (BayK) enhanced cocaine conditioned place preference and cocaine psychomotor act

56 ibutes to the acquisition of cocaine-induced conditioned place preference and cocaine self-administra

57 ular dopamine in the NAc, as well as cocaine conditioned place preference and cocaine self-administra

58 ssociated virus and Cre lines during cocaine conditioned place preference and cocaine-induced locomot

59 as4 in the NAc significantly reduced cocaine conditioned place preference and delayed learning of the

60 n and drug reinforcement, as assessed by the conditioned place preference and drug self-administratio

61 Conditioned place preference and locomotor sensitization

62 bited METH self-administration, METH-induced conditioned place preference and METH- or cue-induced re

63 emonstrate that the genotypic differences in conditioned place preference and passive avoidance learn

64 ink between cocaine-induced reinstatement of conditioned place preference and rapid reductions of coc

65 bachol induce reward; such injections induce conditioned place preference and rats learn quickly to s

66 We used conditioned place preference and self-administration par

67 seeking can be modeled in mice studies using conditioned place preference and self-administration pro

68 mpared with their wild-type controls in both conditioned place preference and sensitization behaviors

69 ned protocol which successfully induced both conditioned place preference and sensitization simultane

70 ions selectively impaired the acquisition of conditioned place preference and the use of spatial info

71 sed eating behavior and also caused positive conditioned place preferences and increased positive hed

72 rain-stimulation reward, (2) cocaine-induced conditioned place preference, and (3) cocaine-triggered

73 ) dose-dependently attenuate cocaine-induced conditioned place preference, and (3) dose-dependently a

74 inistration and the expression of an ethanol conditioned place preference, and abolished stress-induc

75 or amphetamine (3 mg/kg), cocaine (20 mg/kg) conditioned place preference, and active avoidance learn

76 enuated cocaine self-administration, cocaine-conditioned place preference, and cocaine-primed reinsta

77 tor 4 (TLR4) in opioid analgesia, tolerance, conditioned place preference, and self-administration.

78 ocomotor activity, behavioral sensitization, conditioned place preference, and striatal dopamine rele

79 mbens, the ability of cocaine to establish a conditioned place preference, and the ability of cocaine

80 its involvement in behavioral sensitization, conditioned place-preference, and self-administration of

81 s relevant to addiction: locomotor activity, conditioned place preference, anxiety, discrimination, a

82 king MCH1R exhibit decreased cocaine-induced conditioned place preference, as well as cocaine sensiti

83 ndence, and showed no aversive effect in the conditioned place preference assay.

84 instatement of cocaine-seeking behavior in a conditioned place preference assay.

85 We performed conditioned place preference assays.

86 t withdrawal syndromes or reward behavior in conditioned-place preference assays in mice, and do not

87 It also blocks expression of cocaine-induced conditioned place preference at a dose (1)/(300) that of

88 caffeine also enhanced the development of a conditioned place preference at a sub-threshold dose of

89 Finally, SNI mice developed a conditioned place preference based on relief from pain i

90 Cocaine-conditioned place preference behavior and ex vivo whole-

91 r of dendritic protein synthesis, in cocaine conditioned place preference, behavioral sensitization,

92 both cocaine-induced locomotor behavior and conditioned place preference, but had no effect on stres

93 e had opposite effects on the acquisition of conditioned place preference by significantly enhancing

94 duces an impairment of extinction of cocaine-conditioned place preference (cocaine-CPP) independent o

95 l motor coordination, locomotor activity, or conditioned place preference compared with WT littermate

96 nucleus accumbens suppresses cocaine-induced conditioned place preference (CPP) acquisition in mice.

97 We show that COC-conditioned place preference (CPP) activates ERK, CREB,

98 r blocked the acquisition of cocaine-induced conditioned place preference (CPP) and activation of tra

99 Little is known about effects of FR on drug-conditioned place preference (CPP) and brain regional me

100 CaMKII activity in the VTA affected cocaine conditioned place preference (CPP) and cocaine-evoked sy

101 r preference for morphine was examined using conditioned place preference (CPP) and drug-induced rein

102 Conditioned place preference (CPP) and in vivo microdial

103 e ventral pallidum (VP) in the expression of conditioned place preference (CPP) and motor adaptations

104 mesolimbic EX4 on two models of food reward: conditioned place preference (CPP) and progressive ratio

105 y in the hippocampus, their role in morphine conditioned place preference (CPP) and reinstatement rem

106 y attenuated cocaine-primed reinstatement of conditioned place preference (CPP) and relapse of cocain

107 Conditioned place preference (CPP) and saccharin (0.2% w

108 nduced reinstatement of drug seeking in both conditioned place preference (CPP) and self-administrati

109 (V2a) significantly prevented acute morphine-conditioned place preference (CPP) and stress-induced re

110 methylphenidate would alter morphine-induced conditioned place preference (CPP) and sucrose-reinforce

111 g in stress-induced reinstatement of cocaine conditioned place preference (CPP) and the effects of lo

112 ine pairing with environmental cues (ie, the conditioned place preference (CPP) apparatus) triggers a

113 In a conditioned place preference (CPP) assay, we observed th

114 attenuates the intensity of cocaine-induced conditioned place preference (CPP) behaviors in female r

115 y shown strain differences in heroin-induced conditioned place preference (CPP) between C57BL/6J (C57

116 nd caudate putamen (CPu) in morphine-induced conditioned place preference (CPP) by real-time reverse

117 Utilizing a rat paradigm of conditioned place preference (CPP) combined with ankle m

118 and spatial location cues were studied in 6 conditioned place preference (CPP) experiments with etha

119 ch predicts future reinstatement of morphine conditioned place preference (CPP) following a priming d

120 Female rats exhibit a conditioned place preference (CPP) for a context paired

121 phine-induced locomotor sensitization or for conditioned place preference (CPP) for a morphine- or a

122 ch there was no opportunity to consume food (conditioned place preference (CPP) for an environment pr

123 in LH orexin neurons varied in proportion to conditioned place preference (CPP) for morphine, cocaine

124 ncountered and, subsequently, will display a conditioned place preference (CPP) for that environment.

125 paired with environmental cues establishes a conditioned place preference (CPP) for that environment.

126 preoptic area (mPOA) on the expression of a conditioned place preference (CPP) for vaginocervical st

127 R)-expressing cells in extinction of cocaine conditioned place preference (CPP) in adult male mice.

128 also found that the magnitude of amphetamine-conditioned place preference (CPP) in behaving rats corr

129 ch adrenal hormones regulate cocaine-induced conditioned place preference (CPP) in either sex.

130 extinction, but not acquisition, of cocaine conditioned place preference (CPP) in male mice increase

131 e find that nicotine produced dose-dependent conditioned place preference (CPP) in mice.

132 did not alter acquisition of ethanol-induced conditioned place preference (CPP) in mice.

133 hibited the acquisition of oxycodone-induced conditioned place preference (CPP) in rats.

134 at amphetamine (AMPH) conditioning induced a conditioned place preference (CPP) in sexually naive (SN

135 mmunohistochemistry after cocaine (10 mg/kg) conditioned place preference (CPP) in Sprague Dawley rat

136 in vitro and analysis of an animal model of conditioned place preference (CPP) in vivo, we investiga

137 This protocol describes conditioned place preference (CPP) in zebrafish followin

138 compare the expression and persistence of a conditioned place preference (CPP) induced by a relative

139 Conditioned place preference (CPP) is a behavioral assay

140 Reinstatement of previously extinguished conditioned place preference (CPP) is precipitated by st

141 eral amygdala memory in the consolidation of conditioned place preference (CPP) memory.

142 In this study, we used the conditioned place preference (CPP) model to investigate

143 Using a cocaine conditioned place preference (CPP) model, we demonstrate

144 n unconditioned stimulus can induce a strong conditioned place preference (CPP) or aversion (CPA) in

145 the equipment and methods used to establish conditioned place preference (CPP) or aversion (CPA).

146 MPH) motivated behavior was examined using a conditioned place preference (CPP) paradigm and was show

147 ysiology in vitro was then combined with the conditioned place preference (CPP) paradigm to determine

148 We used a conditioned place preference (CPP) paradigm to determine

149 In addition, we employed the conditioned place preference (CPP) paradigm to evaluate

150 We used a standard 4 day conditioned place preference (CPP) paradigm using 20mg/k

151 otine and cocaine reward-like effects in the conditioned place preference (CPP) paradigm, using pharm

152 Using conditioned place preference (CPP) paradigm, we observed

153 (AMPH) as the unconditioned stimulus in the conditioned place preference (CPP) paradigm.

154 ated the abuse potential of pregabalin using conditioned place preference (CPP) paradigm.

155 aired contextual cue memory assessed using a conditioned place preference (CPP) paradigm.

156 red with cocaine experience assessed using a conditioned place preference (CPP) paradigm.

157 moderate doses of cocaine when tested in the conditioned place preference (CPP) procedure and also bl

158 Previous work using the conditioned place preference (CPP) procedure implicates

159 Using a conditioned place preference (CPP) procedure, we found t

160 pocretin neurons in mice following a cocaine-conditioned place preference (CPP) protocol.

161 Using a conditioned place preference (CPP) reinstatement procedu

162 58 has been shown to block expression of the conditioned place preference (CPP) response to cocaine i

163 efore or immediately after a cocaine-induced conditioned place preference (CPP) retrieval trial, beta

164 which food-reward behavior, assessed using a conditioned place preference (CPP) task, is monitored in

165 of the amygdala impair acquisition of a food conditioned place preference (CPP) task.

166 rats were subsequently trained in a cocaine conditioned place preference (CPP) task.

167 ysis, behavioral activity assessments, and a conditioned place preference (CPP) test were used to inv

168 esign, or cocaine (0, 5, 10 mg/kg) using the conditioned place preference (CPP) test.

169 istered ethanol (EtOH) were examined using a conditioned place preference (CPP) test.

170 Studies using conditioned place preference (CPP) tests of reward indic

171 of U50488 15 min before cocaine blocked the conditioned place preference (CPP) to cocaine, but only

172 still self-administer cocaine and/or display conditioned place preference (CPP) to cocaine, which led

173 the acquisition, but not the expression, of conditioned place preference (CPP) to cocaine.

174 This treatment enhanced conditioned place preference (CPP) to morphine (2 x 10 m

175 eated rats, MDMA-treated rats did not form a conditioned place preference (CPP) to sex.

176 Finally, we show that cocaine conditioned place preference (CPP) training (15 mg/kg; f

177 with different intensities, and that cocaine conditioned place preference (CPP) training followed by

178 In the present study, conditioned place preference (CPP) was induced with high

179 Cocaine-induced locomotor sensitization and conditioned place preference (CPP) were attenuated in tP

180 Combining-conditioned place preference (CPP) with molecular analys

181 nstrated by reinstatement of the behavior of conditioned place preference (CPP) with sub-threshold pr

182 ly regulates extinction of a cocaine-induced conditioned place preference (CPP), a task that requires

183 resent studies examined the effects of E2 on conditioned place preference (CPP), and E2 levels produc

184 s quinine, exhibited greater ethanol-induced conditioned place preference (CPP), and showed reduced e

185 to VTA exhibit Fos activation with morphine conditioned place preference (CPP), and whether these ce

186 on cocaine-induced behavioral sensitization, conditioned place preference (CPP), cue- and cocaine pri

187 ce, using both fear conditioning and cocaine-conditioned place preference (CPP), during acquisition a

188 reward measured by the paradigm of unbiased conditioned place preference (CPP), focusing on GABAergi

189 cocaine-induced locomotor sensitization and conditioned place preference (CPP), mice receiving SB203

190 s, conditioned motor sensitization (CMS) and conditioned place preference (CPP), to ascertain whether

191 Using reinstatement of conditioned place preference (CPP), we determined whethe

192 aine (10 mg/kg, s.c.) induced locomotion and conditioned place preference (CPP).

193 id not differ in their expression of cocaine-conditioned place preference (CPP).

194 was assessed using evoked sensory stimuli or conditioned place preference (CPP).

195 ith drug administration can be studied using conditioned place preference (CPP).

196 ined the specific role of the DHC in cocaine conditioned place preference (CPP).

197 s (NAc) in the expression of ethanol-induced conditioned place preference (CPP).

198 the rewarding effects of AMPH as measured by conditioned place preference (CPP).

199 ase the reward value of food, as assessed by conditioned place preference (CPP).

200 the effects of forced swim stress on cocaine-conditioned place preference (CPP).

201 s no locomotor effects, despite retention of conditioned place preference (CPP).

202 PFC) is necessary for acquisition of cocaine-conditioned place preference (CPP).

203 of NAc silent synapse maturation in cocaine-conditioned place preference (CPP).

204 injections of AMPH and blocked AMPH-induced conditioned place preference (CPP).

205 ppocampus that mediate extinction of cocaine conditioned place preference (CPP).

206 uder as reinforcement for the development of conditioned place preference (CPP).

207 od of 7 d, males were tested for amphetamine conditioned place preference (CPP).

208 a (VTA), and reinstates extinguished cocaine-conditioned place preference (CPP).

209 littermates were tested for nicotine-induced conditioned place preference (CPP); voluntary oral nicot

210 d that NE was necessary for morphine-induced conditioned place preference (CPP; a measure of reward)

211 ous nerve block to elicit pain relief (i.e., conditioned place preference, CPP), revealing the presen

212 In contrast, conditioned place preference demonstrated an inverse cor

213 nforcement schedule, but did not affect food conditioned place preference expression.

214 Conditioned place preference, extinction and reinstateme

215 , as sexually experienced males did not form conditioned place preference for 0.5 mg/kg morphine.

216 creased 5-HT6 receptors in iMSNs facilitated conditioned place preference for a low dose of cocaine.

217 D2 neurons promoted male-male aggression and conditioned place preference for aggression-paired conte

218 A) decreased alcohol consumption and reduced conditioned place preference for alcohol.

219 We evaluated conditioned place preference for analgesia in 44 calves

220 ct recognition, object location recognition, conditioned place preference for cocaine, or motor learn

221 cocaine-induced locomotor sensitization and conditioned place preference for cocaine.

222 how and high-fat diet intake, meal patterns, conditioned place preference for high-fat food, cue-indu

223 We observed a reduction of conditioned place preference for low doses of the opioid

224 amphetamine reward, indicated by sensitized conditioned place preference for low-dose (0.5 mg/kg) am

225 l behavior over repeated mating sessions, or conditioned place preference for mating.

226 st, dopamine-deficient mice display a robust conditioned place preference for morphine when given eit

227 -administer less nicotine and show decreased conditioned place preference for nicotine compared with

228 o exhibit either behavioral sensitization or conditioned place preference; however, it seems that sen

229 ucleus accumbens by itself sufficed to drive conditioned place preference in freely moving mice.

230 Also, morphine was ineffective in inducing conditioned place preference in GRK5 knockout mice, wher

231 tionship between locomotor sensitization and conditioned place preference in individual animals.

232 Here we used conditioned place preference in mice to examine the prec

233 mber, indicating morphine induced comparable conditioned place preference in ppENK (+/+) and ppENK (-

234 leus accumbens reduced expression of cocaine-conditioned place preference in Prkcz(-/-) mice.

235 acilitate the extinction of morphine-induced conditioned place preference in rats.

236 ly paired with cocaine, nor did they exhibit conditioned place preference in response to cocaine.

237 Morphine produced hyperlocomotion and conditioned place preference in wild-type mice, whereas

238 cal brain stimulation, and (3) can establish conditioned place preferences in laboratory animals, sug

239 chloride and cocaine methiodide to establish conditioned place preferences in rats with self-administ

240 published, what was originally described as 'conditioned place preference' in a two-chamber mouse exp

241 exhibited prosocial behaviors (e.g., social-conditioned place preference, increased social interacti

242 ing neurons in freely behaving mice promoted conditioned place preference, indicating that such activ

243 an exacerbated psychomotor sensitization and conditioned place preference induced by low doses of coc

244 the role of enkephalins in morphine-induced conditioned place preference, locomotor sensitization, a

245 We found that an established morphine conditioned place preference (mCPP) was persistently dis

246 ne, and alcohol, and is also observed in the conditioned place preference model in rats and mice.

247 nges in dopamine release associated with the conditioned place preference model of drug craving.

248 Conditioned place preference (n = 112) and context-induc

249 ockdown failed to influence cocaine-elicited conditioned place preferences, nor did it produce consis

250 that stress-induced potentiation of cocaine conditioned place preference occurred by a similar mecha

251 ciated with an increase in NAcc dopamine and conditioned place preference only under certain testing

252 tivity in these assays and did not produce a conditioned place preference or aversion, but elicited C

253 GAT211 did not induce conditioned place preference or aversion.

254 velopment of analgesic tolerance but not for conditioned place preference or behavioral sensitization

255 effects, acute antinociceptive tolerance, or conditioned-place preference or aversion.

256 ute administration, KO mice were impaired in conditioned place preference, oral nicotine intake and m

257 Furthermore, in the conditioned place preference paradigm with 10 mg/kg morp

258 Using an unbiased conditioned place preference paradigm with rats, we exam

259 ding effects of morphine, as measured in the conditioned place preference paradigm, were substantiall

260 attenuation of alcohol reward, measured in a conditioned place preference paradigm.

261 the reinforcing properties of morphine in a conditioned place preference paradigm.

262 preference (i.e. relieved ongoing pain) in a conditioned place preference paradigm.

263 gative form of CREB) in the VTA and, using a conditioned place-preference paradigm, found that CREB a

264 solidation of extinction in fear and cocaine conditioned place preference paradigms.

265 ects of ketamine in the drug discrimination, conditioned place preference, pre-pulse inhibition and o

266 nuated the rewarding effects of cocaine in a conditioned place preference procedure but did not affec

267 We used a novel conditioned place preference procedure to show that opto

268 In the conditioned place preference procedure, nicotine was suf

269 n both periadolescent and adult mice using a conditioned place preference procedure.

270 Here, we used a conditioned place-preference procedure to investigate th

271 T2-Cre:Ai9 male and female mice in a cocaine conditioned place preference protocol followed by 2 week

272 al tegmental area of freely moving mice in a conditioned place-preference protocol so as to mediate P

273 In the present study, we use a conditioned place preference/reinstatement paradigm in m

274 ns of heroin, or saline, in the setting of a conditioned place preference study.

275 ng ASIC1A in the mouse NAc increased cocaine-conditioned place preference, suggesting an unexpected r

276 creases their development of cocaine-induced conditioned place preference, suggesting reduced sensiti

277 ccurred in the extinction of cocaine-induced conditioned place preference, suggesting that the observ

278 the rewarding properties of morphine in the conditioned place preference test were greater in the be

279 ial self-stimulation (ICSS) procedure, and a conditioned place preference test, respectively.

280 Using the hot-plate and conditioned place preference test, we investigated opioi

281 exes, and reduced ongoing pain assessed by a conditioned place preference test.

282 cial interactions, assessed using a socially conditioned place preference test.

283 cocaine reward/reinforcement, as measured by conditioned place-preference testing.

284 In these studies, we used conditioned place preference to assess the activity of N

285 Furthermore, mTOR deletion attenuated conditioned place preference to cocaine and cocaine-indu

286 mice also have a decreased ability to form a conditioned place preference to cocaine.

287 We used conditioned place preference to concomitantly determine

288 - and stress-primed reinstatement of cocaine conditioned place preference to model drug-associated me

289 shifted the dose-response curve for cocaine-conditioned place preference to the left, indicating alt

290 s then underwent morphine-induced (10 mg/kg) conditioned-place-preference training, followed by extin

291 ith olfactory-dependent fear conditioning or conditioned place preference using acetophenone.

292 vity to cocaine (0, 2.5, 5, 10, or 20 mg/kg) conditioned place preference was assessed.

293 Conditioned place preference was established by EM-1 inj

294 A conditioned place preference was evident in controls and

295 rence in GRK5 knockout mice, whereas cocaine conditioned place preference was retained.

296 Conditioned place preference was used to assess the epig

297 algesia, tolerance, physical dependence, and conditioned place preference, we used mice having target

298 Carbachol produced conditioned place preferences when injected into the pos

299 that p11 knockout mice have enhanced cocaine conditioned place preference, which is reproduced by the

300 tinction of a previously established cocaine-conditioned place preference, while simultaneously enhan