ライフサイエンスコーパス: place preference

1 hey received photostimulation (i.e., operant place preference).

2 showed unaltered cocaine-induced conditioned place preference.

3 d-limb sensitisation and induced conditioned place preference.

4 umbens (NAc) and cocaine-induced conditioned place preference.

5 ine gain correlated with cocaine conditioned place preference.

6 block the development of alcohol-conditioned place preference.

7 caine, and it fails to produce a conditioned place preference.

8 rcuit is essential for expression of cocaine place preference.

9 lasticity in the VTA and cocaine conditioned place preference.

10 behavioral responses by cocaine conditioned place preference.

11 on, behavioral sensitization, or conditioned place preference.

12 mice), suppressed opioid-induced conditioned place preference.

13 G9a in the NAc decreases cocaine-conditioned place preference.

14 ide in the VTA disrupted cocaine conditioned place preference.

15 conditioning, but also enhanced conditioned place preference.

16 of extinguished cocaine-induced conditioned place preference.

17 induced reinstatement of cocaine conditioned place preference.

18 t was found to underlie nicotine-conditioned place preference.

19 lates amphetamine (AMPH)-induced conditioned place preference.

20 -induced synaptic plasticity and conditioned place preference.

21 orphine-induced behavioral sensitization and place preference.

22 ound to be necessary for learning a morphine place preference.

23 d to demonstrate significant cocaine-induced place preference.

24 e reward behavior as measured by conditioned place preference.

25 morphine reward, as measured by conditioned place preference.

26 a novel, inescapable open field; and novelty place preference.

27 icantly less hyperlocomotion and conditioned place preference.

28 istent memory of cocaine-induced conditioned place preference.

29 ne-induced reward as measured by conditioned place preference.

30 ventral tegmental area, induced conditioned place preference.

31 s in FS-induced reinstatement of conditioned place preference.

32 e VS and trained to the morphine conditioned place preference.

33 of dopaminergic VTA-PFC projections elicited place preference.

34 eptors are necessary for cocaine conditioned place preference.

35 reinstatement of morphine-evoked conditioned place preference.

36 gonists blocked optical self-stimulation and place preference.

37 GABAergic neurons, which led to a real-time place preference.

38 ively in the NAc reduced cocaine conditioned place preference.

39 ersions while leaving intact cocaine-induced place preferences.

40 mental behaviour and establishes conditioned place preferences.

41 sterior shell of NAS established conditioned place preferences.

42 forced instrumental behavior and established place preferences.

43 ion trials than adults to extinguish cocaine place-preferences.

44 rats were initially conditioned for morphine place preference (8 mg/kg) and then made dependent on mo

45 ent of cocaine sensitization and conditioned place preference, a measure of cocaine reward.

46 ry with local anesthetic elicits conditioned place preference, activates ventral tegmental dopaminerg

47 ral alteration in the locomotor activity and place preference, after IL treatment of 5 days postferti

48 ojections affects behavior using conditioned place preference and a task in which mice learn associat

49 PD325901 persistently blocks cocaine-induced place preference and accelerates extinction following co

50 hanced cocaine sensitization and conditioned place preference and an increase in Alk expression in th

51 ments attenuated cocaine-induced conditioned place preference and blocked the cocaine-induced reducti

52 of oxytocin receptor blockade on both social place preference and cFos expression in the NAc.

53 ayK-8644 (BayK) enhanced cocaine conditioned place preference and cocaine psychomotor activity while

54 e in the NAc, as well as cocaine conditioned place preference and cocaine self-administration.

55 rus and Cre lines during cocaine conditioned place preference and cocaine-induced locomotion.

56 Ac significantly reduced cocaine conditioned place preference and delayed learning of the drug-reinfo

57 positive, reward-like phenotype in real-time place preference and increased locomotor activity in ope

58 Conditioned place preference and locomotor sensitization are rodent

59 elf-administration, METH-induced conditioned place preference and METH- or cue-induced relapse to dru

60 are critical mediators of the expression of place preference and motor adaptations subsequent to rep

61 hat the genotypic differences in conditioned place preference and passive avoidance learning seen in

62 ficient mice exhibit greater ethanol-induced place preference and psychomotor sensitization, and grea

63 We used conditioned place preference and self-administration paradigms to ex

64 which successfully induced both conditioned place preference and sensitization simultaneously in coc

65 in-2 (ChR2) under the VGluT2 promoter causes place preference and supports operant responding for the

66 vely impaired the acquisition of conditioned place preference and the use of spatial information to r

67 shell dynorphin cells induced a KOR-mediated place preference and was positively reinforcing.

68 and the expression of an ethanol conditioned place preference, and abolished stress-induced reinstate

69 ne (3 mg/kg), cocaine (20 mg/kg) conditioned place preference, and active avoidance learning to paire

70 in opioid analgesia, tolerance, conditioned place preference, and self-administration.

71 r activates LH orexin neurons during cocaine place preference, and that this circuit is essential for

72 bility of cocaine to establish a conditioned place preference, and the ability of cocaine-predictive

73 ent in behavioral sensitization, conditioned place-preference, and self-administration of drugs of ab

74 o addiction: locomotor activity, conditioned place preference, anxiety, discrimination, and self-admi

75 xperiment 1) or prior to being placed into a place preference apparatus (Experiment 2).

76 by spatial context-sucrose conditioning in a place preference apparatus characterized by three topogr

77 ce; however, it seems that sensitization and place preference are not necessarily co-expressed to a s

78 xhibit decreased cocaine-induced conditioned place preference, as well as cocaine sensitization.

79 alcohol-induced locomotor sensitization and place preference, as well as excessive alcohol intake an

80 showed no aversive effect in the conditioned place preference assay.

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

82 We performed conditioned place preference assays.

83 (D2-KO), exhibited a significant decrease in place preference associated with cocaine.

84 ks expression of cocaine-induced conditioned place preference at a dose (1)/(300) that of vigabatrin.

85 so enhanced the development of a conditioned place preference at a sub-threshold dose of cocaine (7.5

86 and placebo-pelleted (non-dependent) rats in place preference at any time during abstinence (up to 6

87 ic protein synthesis, in cocaine conditioned place preference, behavioral sensitization, and motor st

88 e, and reinstatement of extinguished cocaine place preference behaviors by stimulation of p38alpha MA

89 e-induced locomotor behavior and conditioned place preference, but had no effect on stress-induced so

90 for nicotine reward as measured by nicotine place preference, but not for another drug of addiction,

91 wever, prazosin-treated mice showed a robust place preference, but vehicle-treated mice did not, sugg

92 te effects on the acquisition of conditioned place preference by significantly enhancing and attenuat

93 airment of extinction of cocaine-conditioned place preference (cocaine-CPP) independent of alpha(2)-A

94 e cocaine hydrochloride established stronger place preferences, cocaine methiodide was also effective

95 plus maze for anxiolytic/anxiogenic effects, place preference conditioning for reward effects, the ta

96 ducing drug-seeking behaviors as measured by place preference conditioning.

97 ly silence NF-kappaB-expressing cells during place preference conditioning.

98 mbens suppresses cocaine-induced conditioned place preference (CPP) acquisition in mice.

99 We show that COC-conditioned place preference (CPP) activates ERK, CREB, Elk-1, and F

100 e acquisition of cocaine-induced conditioned place preference (CPP) and activation of translation elo

101 nown about effects of FR on drug-conditioned place preference (CPP) and brain regional mechanisms tha

102 vity in the VTA affected cocaine conditioned place preference (CPP) and cocaine-evoked synaptic plast

103 for morphine was examined using conditioned place preference (CPP) and drug-induced reinstatement in

104 Conditioned place preference (CPP) and in vivo microdialysis were us

105 llidum (VP) in the expression of conditioned place preference (CPP) and motor adaptations to morphine

106 X4 on two models of food reward: conditioned place preference (CPP) and progressive ratio operant-con

107 pocampus, their role in morphine conditioned place preference (CPP) and reinstatement remains unknown

108 cocaine-primed reinstatement of conditioned place preference (CPP) and relapse of cocaine CPP (drug-

109 Conditioned place preference (CPP) and saccharin (0.2% w/v) self-adm

110 tatement of drug seeking in both conditioned place preference (CPP) and self-administration models.

111 ate would alter morphine-induced conditioned place preference (CPP) and sucrose-reinforced lever-pres

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

113 In a conditioned place preference (CPP) assay, we observed that menthol p

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

115 in differences in heroin-induced conditioned place preference (CPP) between C57BL/6J (C57) and 129P3/

116 utamen (CPu) in morphine-induced conditioned place preference (CPP) by real-time reverse transcriptas

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

118 location cues were studied in 6 conditioned place preference (CPP) experiments with ethanol (2 g/kg)

119 future reinstatement of morphine conditioned place preference (CPP) following a priming dose of morph

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

121 d locomotor sensitization or for conditioned place preference (CPP) for a morphine- or a cocaine-pair

122 no opportunity to consume food (conditioned place preference (CPP) for an environment previously ass

123 neurons varied in proportion to conditioned place preference (CPP) for morphine, cocaine, or food.

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

125 ea (mPOA) on the expression of a conditioned place preference (CPP) for vaginocervical stimulation.

126 hat the magnitude of amphetamine-conditioned place preference (CPP) in behaving rats correlates with

127 but not acquisition, of cocaine conditioned place preference (CPP) in male mice increased Cav1.2 L-t

128 nicotine produced dose-dependent conditioned place preference (CPP) in mice.

129 r acquisition of ethanol-induced conditioned place preference (CPP) in mice.

130 acquisition of oxycodone-induced conditioned place preference (CPP) in rats.

131 ne (AMPH) conditioning induced a conditioned place preference (CPP) in sexually naive (SN), but not p

132 emistry after cocaine (10 mg/kg) conditioned place preference (CPP) in Sprague Dawley rats.

133 d analysis of an animal model of conditioned place preference (CPP) in vivo, we investigated the syna

134 This protocol describes conditioned place preference (CPP) in zebrafish following a single e

135 expression and persistence of a conditioned place preference (CPP) induced by a relatively low dose

136 Conditioned place preference (CPP) is a behavioral assay wherein a r

137 ement of previously extinguished conditioned place preference (CPP) is precipitated by stress or drug

138 Using a cocaine conditioned place preference (CPP) model, we demonstrate that local

139 nt and methods used to establish conditioned place preference (CPP) or aversion (CPA).

140 ed behavior was examined using a conditioned place preference (CPP) paradigm and was shown to be medi

141 We used a conditioned place preference (CPP) paradigm to determine a dose-resp

142 In addition, we employed the conditioned place preference (CPP) paradigm to evaluate positive con

143 We used a standard 4 day conditioned place preference (CPP) paradigm using 20mg/kg cocaine-a

144 caine reward-like effects in the conditioned place preference (CPP) paradigm, using pharmacological a

145 Using conditioned place preference (CPP) paradigm, we observed that GDNF o

146 he unconditioned stimulus in the conditioned place preference (CPP) paradigm.

147 tual cue memory assessed using a conditioned place preference (CPP) paradigm.

148 aine experience assessed using a conditioned place preference (CPP) paradigm.

149 es of cocaine when tested in the conditioned place preference (CPP) procedure and also blocks locomot

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

151 Using a conditioned place preference (CPP) procedure, we found that removal

152 rons in mice following a cocaine-conditioned place preference (CPP) protocol.

153 Using a conditioned place preference (CPP) reinstatement procedure in mice,

154 ediately after a cocaine-induced conditioned place preference (CPP) retrieval trial, beta-AR antagoni

155 eward behavior, assessed using a conditioned place preference (CPP) task, is monitored in mice after

156 nol (EtOH) were examined using a conditioned place preference (CPP) test.

157 5 min before cocaine blocked the conditioned place preference (CPP) to cocaine, but only significantl

158 dminister cocaine and/or display conditioned place preference (CPP) to cocaine, which led to the reev

159 tion, but not the expression, of conditioned place preference (CPP) to cocaine.

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

161 Finally, we show that cocaine conditioned place preference (CPP) training (15 mg/kg; four pairings

162 In the present study, conditioned place preference (CPP) was induced with highly salient n

163 uced locomotor sensitization and conditioned place preference (CPP) were attenuated in tPA-/- mice.

164 reinstatement of the behavior of conditioned place preference (CPP) with sub-threshold priming morphi

165 extinction of a cocaine-induced conditioned place preference (CPP), a task that requires behavioral

166 es examined the effects of E2 on conditioned place preference (CPP), and E2 levels produced in plasma

167 xhibited greater ethanol-induced conditioned place preference (CPP), and showed reduced ethanol stimu

168 bit Fos activation with morphine conditioned place preference (CPP), and whether these cells exhibit

169 nduced behavioral sensitization, conditioned place preference (CPP), cue- and cocaine prime-induced r

170 th fear conditioning and cocaine-conditioned place preference (CPP), during acquisition and extinctio

171 ured by the paradigm of unbiased conditioned place preference (CPP), focusing on GABAergic synaptic a

172 uced locomotor sensitization and conditioned place preference (CPP), mice receiving SB203580 on cocai

173 ed motor sensitization (CMS) and conditioned place preference (CPP), to ascertain whether particular

174 Using reinstatement of conditioned place preference (CPP), we determined whether ceftriaxon

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

176 using evoked sensory stimuli or conditioned place preference (CPP).

177 inistration can be studied using conditioned place preference (CPP).

178 ates stress-induced reinstatement of cocaine place preference (CPP).

179 at mediate extinction of cocaine conditioned place preference (CPP).

180 cific role of the DHC in cocaine conditioned place preference (CPP).

181 he expression of ethanol-induced conditioned place preference (CPP).

182 forcement for the development of conditioned place preference (CPP).

183 ales were tested for amphetamine conditioned place preference (CPP).

184 reinstates extinguished cocaine-conditioned place preference (CPP).

185 nt synapse maturation in cocaine-conditioned place preference (CPP).

186 kg, s.c.) induced locomotion and conditioned place preference (CPP).

187 r in their expression of cocaine-conditioned place preference (CPP).

188 were tested for nicotine-induced conditioned place preference (CPP); voluntary oral nicotine preferen

189 s necessary for morphine-induced conditioned place preference (CPP; a measure of reward) and locomoti

190 ock to elicit pain relief (i.e., conditioned place preference, CPP), revealing the presence of ongoin

191 In contrast, conditioned place preference demonstrated an inverse correlation wit

192 Here, we show that this increased morphine place preference depends upon experiencing drug-stimulus

193 ere subsequently re-conditioned for morphine place preference during protracted abstinence.

194 chedule, but did not affect food conditioned place preference expression.

195 Conditioned place preference, extinction and reinstatement of exting

196 y experienced males did not form conditioned place preference for 0.5 mg/kg morphine.

197 6 receptors in iMSNs facilitated conditioned place preference for a low dose of cocaine.

198 the Ox1r antagonist significantly attenuated place preference for a morphine-, but not a cocaine-pair

199 significantly attenuated the development of place preference for cocaine in rats.

200 on, object location recognition, conditioned place preference for cocaine, or motor learning, when co

201 tor sensitization to cocaine and a decreased place preference for cocaine.

202 uced locomotor sensitization and conditioned place preference for cocaine.

203 -fat diet intake, meal patterns, conditioned place preference for high-fat food, cue-induced reinstat

204 We observed a reduction of conditioned place preference for low doses of the opioid [d-Ala2, N-

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

206 ver repeated mating sessions, or conditioned place preference for mating.

207 -deficient mice display a robust conditioned place preference for morphine when given either caffeine

208 less nicotine and show decreased conditioned place preference for nicotine compared with wild-type mi

209 assessing drug abuse liability; nor was any place preference found after conditioning sessions with

210 ther behavioral sensitization or conditioned place preference; however, it seems that sensitization a

211 ewarding alcohol doses failed to condition a place preference in alpha4 KO mice, paralleling alcohol

212 The ability of alcohol to condition a place preference in each mouse model was also measured.

213 bens by itself sufficed to drive conditioned place preference in freely moving mice.

214 ne was sufficient to condition a significant place preference in Gad2(VTA):Leu9'Ser mice at low nicot

215 hine was ineffective in inducing conditioned place preference in GRK5 knockout mice, whereas cocaine

216 ween locomotor sensitization and conditioned place preference in individual animals.

217 g alcohol dose was sufficient to condition a place preference in Leu9'Ala mice.

218 Here we used conditioned place preference in mice to examine the precise neural c

219 ibitor resulted in a loss of cocaine-induced place preference in opioid-naive animals.

220 ting morphine induced comparable conditioned place preference in ppENK (+/+) and ppENK (-/-) mice.

221 ns reduced expression of cocaine-conditioned place preference in Prkcz(-/-) mice.

222 e extinction of morphine-induced conditioned place preference in rats.

223 th cocaine, nor did they exhibit conditioned place preference in response to cocaine.

224 aine produced reinstatement of an equivalent place preference in Tat-induced GT-tg or C57BL/6J mice;

225 neither significant physical dependence nor place preference in the ED50 dose range.

226 ine produced hyperlocomotion and conditioned place preference in wild-type mice, whereas DKO mice dis

227 imulation, and (3) can establish conditioned place preferences in laboratory animals, suggest that th

228 cocaine methiodide to establish conditioned place preferences in rats with self-administration exper

229 in freely behaving mice promoted conditioned place preference, indicating that such activation is pos

230 ed psychomotor sensitization and conditioned place preference induced by low doses of cocaine.

231 We used an open-field with a removable place preference insert to assess these measures indepen

232 Importantly, place preference is associated with increased activity i

233 enkephalins in morphine-induced conditioned place preference, locomotor sensitization, and analgesic

234 re we show that, in rats, a morphine-induced place preference (mCPP) memory is linked to context-depe

235 und that an established morphine conditioned place preference (mCPP) was persistently disrupted if pr

236 ocampus plays a critical role in linking the place preference memory with the context-conditioned wit

237 hol, and is also observed in the conditioned place preference model in rats and mice.

238 mine release associated with the conditioned place preference model of drug craving.

239 Conditioned place preference (n = 112) and context-induced reinstate

240 tingent pairing of activation caused neither place preference nor aversion.

241 ed to influence cocaine-elicited conditioned place preferences, nor did it produce consistent effects

242 -induced potentiation of cocaine conditioned place preference occurred by a similar mechanism.

243 pite Tat-induced potentiation, extinction of place preference occurred within 21 days, commensurate w

244 ese assays and did not produce a conditioned place preference or aversion, but elicited CB1 receptor-

245 GAT211 did not induce conditioned place preference or aversion.

246 te antinociceptive tolerance, or conditioned-place preference or aversion.

247 analgesic tolerance but not for conditioned place preference or behavioral sensitization induced by

248 erns of stimulation that failed to reinforce place preference or cue-reward associations were able to

249 d not have any effects on water maze escape, place preference or locomotor activity.

250 h concentrations of EtOH and did not develop place preference or locomotor sensitization after repeat

251 ration, KO mice were impaired in conditioned place preference, oral nicotine intake and motor suppres

252 Cocaine produced a significant place preference (p = 0.004) and exposure to the cocaine

253 Furthermore, in the conditioned place preference paradigm with 10 mg/kg morphine conditi

254 Using an unbiased conditioned place preference paradigm with rats, we examined the rol

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

256 d behavioral response (nicotine reward) in a place preference paradigm.

257 of CREB) in the VTA and, using a conditioned place-preference paradigm, found that CREB activation wi

258 f extinction in fear and cocaine conditioned place preference paradigms.

259 mine in the drug discrimination, conditioned place preference, pre-pulse inhibition and open-field te

260 d in mice that were conditioned to a cocaine place preference procedure before stress exposure.

261 ewarding effects of cocaine in a conditioned place preference procedure but did not affect conditione

262 We used a novel conditioned place preference procedure to show that optogenetic inhi

263 In the conditioned place preference procedure, nicotine was sufficient to c

264 dolescent and adult mice using a conditioned place preference procedure.

265 Here, we used a conditioned place-preference procedure to investigate the effects of

266 In the present study, we use a conditioned place preference/reinstatement paradigm in mice to direc

267 Operant place preference scores were highly correlated with self

268 n neutralized an otherwise long-lasting drug-place preference, showing that recoding a spatial memory

269 , or saline, in the setting of a conditioned place preference study.

270 the mouse NAc increased cocaine-conditioned place preference, suggesting an unexpected role for ASIC

271 he extinction of cocaine-induced conditioned place preference, suggesting that the observed effects o

272 simultaneously acquired conditioned cue and place preference task in rats.

273 cc induces avoidance behavior in a real-time place preference task, suggesting that these long-range

274 0 Hz stimulation was 61.6 s in a "real-time" place preference task; mean preferred duration for 5 Hz

275 Using the hot-plate and conditioned place preference test, we investigated opioid-related an

276 duced ongoing pain assessed by a conditioned place preference test.

277 tions, assessed using a socially conditioned place preference test.

278 ted an appetitive response in an optogenetic place preference test.

279 In these studies, we used conditioned place preference to assess the activity of NF-kappaB in

280 ermore, mTOR deletion attenuated conditioned place preference to cocaine and cocaine-induced potentia

281 ve a decreased ability to form a conditioned place preference to cocaine.

282 We used conditioned place preference to concomitantly determine the presence

283 Place preference to heroin was not modified, but remarka

284 2a before daily cocaine showed a significant place preference to the cocaine-paired environment that

285 y-dependent fear conditioning or conditioned place preference using acetophenone.

286 F-kappaB mediates the development of alcohol place preference via its actions in the NAC shell.

287 ine (0, 2.5, 5, 10, or 20 mg/kg) conditioned place preference was assessed.

288 In Experiment 2, a place preference was established with 10 mg/kg cocaine a

289 Conversely, alcohol place preference was increased in Lyn KO mice compared w

290 5 knockout mice, whereas cocaine conditioned place preference was retained.

291 Place preference was tested every 1-2 weeks with no addi

292 Conditioned place preference was used to assess the epigenetic lands

293 erance, physical dependence, and conditioned place preference, we used mice having targeted disruptio

294 earning has a key role in increased morphine place preference when drug is experienced during protrac

295 Daun02 attenuated the development of alcohol place preference when infused into the NAC shell followi

296 Hb glutamatergic fibers produced a real-time place preference, whereas optogenetic stimulation of LHA

297 ist SCH23390 into the PFC blocked adolescent place preferences, whereas microinjections of D(1) agoni

298 ckout mice have enhanced cocaine conditioned place preference, which is reproduced by the focal downr

299 a previously established cocaine-conditioned place preference, while simultaneously enhancing long-te

300 pathway supports positive reinforcement and place preference, while the glutamatergic component medi