ライフサイエンスコーパス: place preference

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

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

3 eptors are necessary for cocaine conditioned place preference.

4 reinstatement of morphine-evoked conditioned place preference.

5 gonists blocked optical self-stimulation and place preference.

6 ug-seeking behaviors, locomotor activity and place preference.

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

8 ively in the NAc reduced cocaine conditioned place preference.

9 rd cues as well as form a social-conditioned place preference.

10 n the NAc of animals conditioned for cocaine place preference.

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

12 ine gain correlated with cocaine conditioned place preference.

13 block the development of alcohol-conditioned place preference.

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

15 rcuit is essential for expression of cocaine place preference.

16 esence of spontaneous pain using conditioned place preference.

17 lasticity in the VTA and cocaine conditioned place preference.

18 behavioral responses by cocaine conditioned place preference.

19 on, behavioral sensitization, or conditioned place preference.

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

21 ide in the VTA disrupted cocaine conditioned place preference.

22 phetamine reward as measured via conditioned place preference.

23 ding locomotor sensitization and conditioned place preference.

24 conditioning, but also enhanced conditioned place preference.

25 induced reinstatement of cocaine conditioned place preference.

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

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

28 -induced synaptic plasticity and conditioned place preference.

29 d propensity for alcohol-induced conditioned place preference.

30 orphine-induced behavioral sensitization and place preference.

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

32 eurons decreased cocaine-induced conditioned place preference.

33 ckdown of Gadd45b blocks cocaine conditioned place preference.

34 uced locomotor sensitization and conditioned place preference.

35 MSNs, in the NAc reduced cocaine conditioned place preference.

36 ocampus is necessary for cocaine conditioned place preference.

37 ampus-dependent behaviors, including cocaine place preference.

38 ronmental cues with reward using conditioned place preference.

39 rove freezing behavior, place avoidance, and place preference.

40 ed optical intracranial self-stimulation and place preference.

41 of dopaminergic VTA-PFC projections elicited place preference.

42 showed unaltered cocaine-induced conditioned place preference.

43 d-limb sensitisation and induced conditioned place preference.

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

45 of extinguished cocaine-induced conditioned place preference.

46 forced instrumental behavior and established place preferences.

47 ersions while leaving intact cocaine-induced place preferences.

48 mental behaviour and establishes conditioned place preferences.

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

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

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

52 ons on the reinstatement of drug-conditioned place preference after extinction of the learned prefere

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

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

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

56 circuit mechanisms of aggression conditioned place preference and aggression self-administration, see

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

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

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

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

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

62 e acquisition of cocaine-induced conditioned place preference and cocaine self-administration.

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

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

65 einforcement, as assessed by the conditioned place preference and drug self-administration procedures

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

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

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

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

70 cocaine-induced reinstatement of conditioned place preference and rapid reductions of cocaine-depende

71 f lateral hypothalamic orexin neurons causes place preference and reduces innate avoidance Endogenous

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

73 be modeled in mice studies using conditioned place preference and self-administration procedures foll

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

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

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

77 potentiates salience attribution in morphine place-preference and fear conditioning assays, CBD coadm

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

79 ine self-administration, cocaine-conditioned place preference, and cocaine-primed reinstatement of dr

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

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

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

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

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

85 periods of hyperactivity and alterations in place preference, are not phenocopied by MK-801, suggest

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

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

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

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

90 syndromes or reward behavior in conditioned-place preference assays in mice, and do not produce depe

91 We performed conditioned place preference assays.

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

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

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

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

96 Finally, SNI mice developed a conditioned place preference based on relief from pain in an IDO1-in

97 Cocaine-conditioned place preference behavior and ex vivo whole-cell electro

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

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

100 in PFC is critical for cocaine locomotor and place preference behaviors.

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

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

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

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

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

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

107 dination, locomotor activity, or conditioned place preference compared with WT littermate controls.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 icantly prevented acute morphine-conditioned place preference (CPP) and stress-induced reinstatement

123 induced reinstatement of cocaine conditioned place preference (CPP) and the effects of low dose guanf

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

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

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

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

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

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

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

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

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

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

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

135 g cells in extinction of cocaine conditioned place preference (CPP) in adult male mice.

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

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

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

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

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

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

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

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

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

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

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

147 ned stimulus can induce a strong conditioned place preference (CPP) or aversion (CPA) in rodents.

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

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

150 vitro was then combined with the conditioned place preference (CPP) paradigm to determine the relatio

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

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

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

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

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

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

157 se potential of pregabalin using conditioned place preference (CPP) paradigm.

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

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

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

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

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

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

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

165 caine (0, 5, 10 mg/kg) using the conditioned place preference (CPP) test.

166 Studies using conditioned place preference (CPP) tests of reward indicate that son

167 5 min before cocaine blocked the conditioned place preference (CPP) to cocaine, but only significantl

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

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

170 nt intensities, and that cocaine conditioned place preference (CPP) training followed by abstinence s

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

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

173 Combining-conditioned place preference (CPP) with molecular analyses, we inves

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 or effects, despite retention of conditioned place preference (CPP).

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

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

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

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

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

195 1, indeed, do not rely only on vision; their place preference depends on the physical distance travel

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

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

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

199 Conditioned place preference, extinction and reinstatement of exting

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

201 6 receptors in iMSNs facilitated conditioned place preference for a low dose of cocaine.

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

203 romoted male-male aggression and conditioned place preference for aggression-paired contexts.

204 alcohol consumption and reduced conditioned place preference for alcohol.

205 We evaluated conditioned place preference for analgesia in 44 calves disbudded or

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

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

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

209 otentiation of ICSS threshold, and decreased place preference for d-Amphetamine during the P Phase.

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

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

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

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

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

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

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

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

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

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

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

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

222 novel object recognition memory and cocaine place preference in male C57BL/6 mice, effects that were

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

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

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

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

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

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

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

230 hat was originally described as 'conditioned place preference' in a two-chamber mouse experiment coul

231 rosocial behaviors (e.g., social-conditioned place preference, increased social interaction, and soci

232 ttention and a lack of D-amphetamine-induced place preference, indicating a disruption of the dopamin

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

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

235 Importantly, place preference is associated with increased activity i

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

237 s activity of orexin neurons correlates with place preference Mediobasal hypothalamic Agrp neurons in

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

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

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

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

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

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

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

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

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

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

248 GAT211 did not induce conditioned place preference or aversion.

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

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

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

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

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

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

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

256 Using various place preference paradigms, we show that activation of K

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

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

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

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

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

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

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

264 ale and female mice in a cocaine conditioned place preference protocol followed by 2 weeks of abstine

265 area of freely moving mice in a conditioned place-preference protocol so as to mediate Pavlovian con

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 ojections also contributed to opioid-induced place preference, suggesting a role in signaling positiv

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

272 dent after conditioning or extinction of the place preference, suggesting that the formation of this

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

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

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

276 0 Hz stimulation was 61.6 s in a "real-time" place preference task; mean preferred duration for 5 Hz

277 mulation (ICSS) procedure, and a conditioned place preference test, respectively.

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

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

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

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

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

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

284 We used conditioned place preference to concomitantly determine the presence

285 Place preference to heroin was not modified, but remarka

286 -primed reinstatement of cocaine conditioned place preference to model drug-associated memories, we f

287 went morphine-induced (10 mg/kg) conditioned-place-preference training, followed by extinction.

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

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

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

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

292 5 knockout mice, whereas cocaine conditioned place preference was retained.

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

294 Conditioned place preference was used to assess the epigenetic lands

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

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

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

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