ライフサイエンスコーパス: footshock

1 the context with an unconditioned stimulus (footshock).

2 ns with 70 dB, 6 kHz tones and 0.5 s, 0.6 mA footshocks).

3 training context in which they had received footshock.

4 the presence of a good predictor (A) of that footshock.

5 g environment that was initially paired with footshock.

6 d background are normal in their response to footshock.

7 osed CS and a control CS predicted avoidable footshock.

8 but not to odors presented in the absence of footshock.

9 airings of a 10-s odor with a 0.25-s, 0.4-mA footshock.

10 aced into the same context without the CS or footshock.

11 ned to fear a soft tone by pairing it with a footshock.

12 tone no longer predicts the occurrence of a footshock.

13 e male mice 2 and 4 weeks after a 2 s 1.5 mA footshock.

14 contexts, I of which was paired with a mild footshock.

15 tly unpaired (random, RND group) manner with footshock.

16 ence or presence of cues associated with the footshock.

17 creased motivation or altered sensitivity to footshock.

18 ed neurons were more likely to be excited by footshock.

19 the level of NE was examined in response to footshock.

20 by reexposure to the tone without additional footshock.

21 g in which a specific context is paired with footshock.

22 ted in SED compared with AW during and after footshock.

23 neutral tone by pairing the tone with a mild footshock.

24 ich did not increase significantly following footshock.

25 visual CS (CSA) in stage I via pairings with footshock.

26 when the injections were given 30 min after footshock.

27 aced in a distinct environment and delivered footshock.

28 ons of visual CSA and auditory CS (CSB) with footshock.

29 crossover every 30 s in order to escape mild footshock.

30 context-no-footshock groups 15 min after the footshock.

31 ed in lesioned rats primed with both APO and footshock.

32 ), or a PACAP agonist (experiment 3) without footshock.

33 oked larger amygdala responses than expected footshock.

34 d cocaine-seeking behavior in the absence of footshock.

35 entation of a cue conditioned to inescapable footshock.

36 a lever within a warning period, preventing footshock.

37 extual fear conditioning generated by a weak footshock.

38 response by pressing the lever, terminating footshock.

39 context and novel tone were paired with mild footshock.

40 light or a noise-light compound using a mild footshock.

41 g compulsively (addicted) in the presence of footshocks.

42 hock arm), and they received four unsignaled footshocks.

43 imuli, such as hindpaw pinches or electrical footshocks.

44 f the sham and half of the BLC rats received footshocks.

45 cadian rhythm upon removal of light cues and footshocks.

46 were exposed to inescapable, uncontrollable footshocks.

47 an odor aversion associated with early-life footshocks.

48 robust responses to auditory CSs predicting footshocks.

49 s trained to drink from a spout were given a footshock (0.35 mA) on Day 5 after approaching the spout

50 the NTS immediately after they were given a footshock (0.35 mA, 0.5 s) in the dark compartment of an

51 mg/kg, i.p.) administered immediately after footshock (0.55 mA for 1 s) potentiated NE release.

52 nfusion of CLN or phosphate buffered saline, footshock (0.8 mA, 1 s), and injected with epinephrine (

53 3 mg/kg), and administration of an escapable footshock (0.8 mA, 1 s).

54 Different groups were given footshocks (0.2, 0.4, 0.8, 1.6 mA) on Day 1.

55 High-intensity footshock (120, 0.8 mA shocks over 40 min) also elevates

56 n (experiment 1) or exposure to intermittent footshock (15 min, 0.6 mA) and heroin priming injections

57 d on: (1) inhibitory avoidance that involves footshock; (2) a circular maze task that involves escape

58 a water-maze spatial task after being given footshock 30 min before retention testing but are not im

59 Taken together, these data suggest that footshock activates limbic circuitry in the CEA, which i

60 Here we show in rats that stress (footshock) activates the transcription factor cAMP respo

61 odation sessions followed by one exposure to footshock (acute footshock, AFS) or handled similarly wi

62 ailability of the ethanol CS was preceded by footshock, additive effects of these stimuli on respondi

63 tophoresis of the alpha-2 agonist clonidine, footshock administration, and LC stimulation mimicked th

64 followed by one exposure to footshock (acute footshock, AFS) or handled similarly without receiving a

65 ber (immediate-footshock group), or received footshock after a 1 min delay (delayed-footshock group).

66 adigm was used to compare rats that received footshock after exploring a context to rats that receive

67 ngs of a light conditioned stimulus (CS) and footshock after preexposure either to footshock or to th

68 0% of lesioned rats primed with APO alone or footshock alone displayed SB and SIB.

69 In lesioned rats primed with APO alone or footshock alone, only neostriatal 3-methoxytyramine (3-M

70 ning and not after unpaired presentations or footshocks alone.

71 ear memory can arise from paired or unpaired footshock, an effect not predicted by theoretical models

72 g the association between olfactory cues and footshock and add to a growing body of evidence implicat

73 ts possible influence on sleep induced after footshock and after the opportunity to explore a neutral

74 lter the changes in sleep and EEG induced by footshock and by the opportunity to explore a neutral en

75 in the medial amygdala (MeA) following both footshock and fear recall, but had normal activation in

76 (NE) within the amygdala in response to both footshock and GABAergic compounds.

77 reased freezing behavior in response to mild footshock and produced behavioral activation in the open

78 rine (NE) release in the amygdala induced by footshock and systemic administration of drugs affecting

79 th the individual and interactive effects of footshock and the CS were significantly greater in previ

80 en the drugs were administered without prior footshock and when the injections were given 30 min afte

81 fear conditioning pairing auditory cues with footshocks and examined extinction behavior, gene expres

82 as repeated stressful events using noxious (footshock) and psychological (restraint) stress.

83 during a 2-hr baseline, 40 min of scrambled footshock, and a 1-hr recovery.

84 were fear-conditioned by pairing a tone with footshock, and then exposed to chronic unpredictable str

85 ere exposed to unpredictable and inescapable footshocks, and fear memory for the shock context was as

86 egular chow or sucrose, and attenuated cue-, footshock-, and yohimbine-induced reinstatement.

87 (i.e., by training rats with a lower, 0.3 mA footshock), AP5 abolished fear-potentiated startle at ea

88 d rats had a stronger memory for the context-footshock association as assessed by all measures of mem

89 ampus on acquisition and retention of T-maze footshock avoidance conditioning.

90 tum to the hippocampus, mice were trained on footshock avoidance in a T-maze.

91 estradiol and estrone on retention of T-maze footshock avoidance in female ovariectomized mice.

92 orms of striatum-dependent memory, including footshock avoidance learning and "response" learning in

93 ent during behavior maintained in a signaled footshock avoidance procedure.

94 ere injected intracerebroventricularly after footshock avoidance training in CD-1 mice.

95 srupted acquisition and retention for T-maze footshock avoidance.

96 mpaired acquisition and retention for T-maze footshock avoidance.

97 osure, all rats received pairings of A and a footshock before assessment of generalized responding (c

98 are reexposed to the unconditioned stimulus (footshock) before drug administration, performance on th

99 0 microgram/kg, i.p.) administered after the footshock blocked the footshock-induced increase in NE l

100 nd that repeated forced swim and inescapable footshock both produced aversive behaviors that were blo

101 of mRNA for TH and c-fos were elevated after footshock but did not differ between SED and AW.

102 e in the brain frontal cortex in response to footshock but does not influence expression of the gene

103 sing neurons before or immediately after the footshock, but not at the time of fear recall, enhanced

104 administered into the rACC immediately after footshock, but not context, training.

105 e responding to odors paired previously with footshock by increasing spontaneous activity and burstin

106 in which rats learn to avoid a tone-signaled footshock by stepping onto a nearby platform.

107 We show that unsignaled nocturnal footshock caused rats living in an "ethological" apparat

108 h seven daily sessions of footshock (chronic footshock, CFS), six accommodation sessions followed by

109 ts were treated with seven daily sessions of footshock (chronic footshock, CFS), six accommodation se

110 Alternatively, once footshocks commenced, animals could initiate an escape r

111 es evoked by the auditory cue that predicted footshock concomitantly increased.

112 , placed in a test chamber without receiving footshock (context-no-footshock group), received footsho

113 the embedded auditory signal was paired with footshock, control rats were impaired in their ability t

114 ed 50-kHz USVs, whereas a cue that predicted footshock decreased 50-kHz USVs.

115 ns made either before or after training with footshock decreased the level of freezing to conditional

116 we found few effects on somatic responses to footshock, deficits in conditioned fear may reflect alte

117 of a negatively valenced stimulus involving footshock delivery during Pavlovian fear conditioning.

118 nylephrine were infused in the NTS following footshock delivery in one alley of a Y-maze.

119 conditional fear cues acquired via immediate footshock delivery.

120 ts in the PVH and killed 2 hours after acute footshock displayed Fos-positive retrogradely labeled ne

121 ards after bar pressing or presentation of a footshock during fear conditioning produced significant

122 nditioned to the distinct environment by the footshock elicits complete immobility termed freezing.

123 Unexpected footshock evoked larger amygdala responses than expected

124 ry conditioned stimulus (CS) was paired with footshock, except when it was preceded by another stimul

125 xposed to a conspecific receiving electrical footshocks exhibited enhanced passive avoidance (PA) lea

126 context freezing was strong in a group given footshock exposure but not in a group given eye shock US

127 ent of cocaine seeking was then tested after footshock exposure in different groups of rats that were

128 additional group was included that received footshock exposure, rather than US reexposure, between e

129 testing, followed 60 min later by stress of footshock exposure.

130 itioned fear responses to a tone paired with footshock extinguish when the tone is presented repeated

131 10 pairings of a 3.7 sec light and a 0.4 mA footshock (fear conditioning).

132 cocaine seeking by a stressor, intermittent footshock, following intravenous self-administration in

133 % of the lever-presses were punished by mild footshock for 9-10 days, whereas for the other group lev

134 stration rats were punished by mild electric footshocks for 10 days with gradual increases in shock i

135 es for methamphetamine were punished by mild footshocks for 5 days.

136 we show that exposing rats to low-intensity footshock (four, 0.5 mA shocks over 20 min) induces cFos

137 ng context 24h prior to receiving a 1.5mA 2s footshock froze significantly more during the context te

138 Footshocks given on Day 1 led to a sensitized excitatory

139 In experiment 3, we tested whether footshocks given on Day 1 would sensitize the excitatory

140 Only the delayed-footshock group displayed a fear response (freezing beha

141 s of the amygdala was greater in the delayed-footshock group than the handled and context-no-footshoc

142 upon being placed in the chamber (immediate-footshock group), or received footshock after a 1 min de

143 mber without receiving footshock (context-no-footshock group), received footshock immediately upon be

144 eived footshock after a 1 min delay (delayed-footshock group).

145 in NGFI-A mRNA was not seen in the immediate-footshock group.

146 mRNA expression than rats of the context-no-footshock group.

147 tshock group than the handled and context-no-footshock groups 15 min after the footshock.

148 RNA expression in the immediate- and delayed-footshock groups did not differ.

149 t received footshock (immediate- and delayed-footshock groups) had greater levels of c-fos mRNA expre

150 the presence of cues previously paired with footshocks, has suggested that the BLC may be a critical

151 However, rats that received footshock (immediate- and delayed-footshock groups) had

152 er exploring a context to rats that received footshock immediately after placement in the chamber.

153 shock (context-no-footshock group), received footshock immediately upon being placed in the chamber (

154 Pre and Alt-Pre rats received a 2-s, 1.5 mA footshock immediately upon placement in Context A.

155 the light CS than did a group preexposed to footshock in a different context, indicating contextual

156 procedure in which rats received unsignaled footshock in a novel observation chamber; freezing behav

157 usion of CRF into VTA has similar effects to footshock in cocaine-experienced animals but fails to ca

158 esion groups showed increased activity after footshock in other studies.

159 chemical cross-sensitization between APO and footshock in such rats is unidirectional and support the

160 knockout mice's increased responsiveness to footshock in the extended test may be an indication of i

161 In Experiment 2, a group preexposed to footshock in the same context showed poorer fear conditi

162 Male rats were given footshocks in a distinctive context and later tested usi

163 ats acquired a fear memory by receiving mild footshocks in a shock zone on a track, we analyzed place

164 ional consequences of methamphetamine SA and footshocks in the rat brain.

165 c cell groups activated in response to acute footshock included ones associated with the processing o

166 versive training stimulus of a single, brief footshock increased CRH levels in the CEA.

167 nditioning by pairing an auditory cue with a footshock increases the rate of spine elimination.

168 sentation of the same auditory cue without a footshock increases the rate of spine formation.

169 In contrast to low-intensity footshock, increases in cFos expression within the rostr

170 A 0.55 mA (2 s) footshock induced a significant increase in NE levels wh

171 nbm corticopetal cholinergic neurons during footshock induced operant suppression.

172 uggest that dopamine input may contribute to footshock- induced activation of cFos expression in the

173 ant corticosterone levels displayed enhanced footshock-induced Fos expression in the parvicellular co

174 were measured with the novel open field and footshock-induced freezing tests.

175 ransfer into the OT of intact rats decreased footshock-induced freezing, and this effect was reversed

176 Further, inhibition of the NAshell blocked a footshock-induced increase in dopamine within the PFC an

177 administered after the footshock blocked the footshock-induced increase in NE levels.

178 TA antalarmin, but not astressin-2B, blocked footshock-induced reinstatement in LgA rats.

179 Consistent with our previous findings with footshock-induced reinstatement of alcohol seeking in Wi

180 PAC1/VPAC2 antagonist, PACAP 6-38, prevented footshock-induced reinstatement of extinguished cocaine

181 Footshock-induced reinstatement was prevented by bilater

182 ine receptor antagonist fluphenazine blocked footshock-induced reinstatement when infused into the PF

183 TA of the contralateral hemisphere prevented footshock-induced reinstatement, whereas ipsilateral man

184 A differential effect of footshock-induced stress was noted on neuronal subgroups

185 Here, using increasing footshock intensities in an inhibitory avoidance paradig

186 Furthermore, training with the highest footshock intensity (traumatic experience) led to a sign

187 h levels assessed in rats trained with lower footshock intensity or unshocked controls exposed only t

188 Inhibitory avoidance training with higher footshock intensity produced increased levels of AEA in

189 nd the magnitude of the increase varied with footshock intensity.

190 e association between one stimulus (X) and a footshock is attenuated when X-->footshock training occu

191 retention testing but are not impaired when footshock is given 2 min or 4 h before testing.

192 nstatement of cocaine seeking by a stressor (footshock) is CRF dependent and is augmented in rats tha

193 The response to the footshock itself is called an activity burst and include

194 The omission of expected footshock led to a decrease below baseline in the amygda

195 imilarly without receiving any footshock (no footshock, NFS).

196 ) or handled similarly without receiving any footshock (no footshock, NFS).

197 In this model, neither a stressor (electric footshock) nor stress-level corticosterone treatment alo

198 on-monotonically related to the intensity of footshock on Day 1.

199 This investigation examined the effect of footshock on responses of 283 spinal dorsal horn neurons

200 After the final footshock or NFS session, rats were anesthetized, a lami

201 nt of heroin seeking induced by intermittent footshock or priming injections of heroin.

202 S) and footshock after preexposure either to footshock or to the context alone.

203 to associate a visual stimulus (light) with footshock or were exposed to the light alone.

204 A regimen of inescapable electrical footshocks or no footshocks was then administered.

205 d with either appetitive (food) or aversive (footshock) outcomes.

206 During the 10 tone-footshock paired training, postshock freezing and USV re

207 nse to postconditioning presentations of the footshock-paired odors but not to odors presented in the

208 d fear conditioning, which consisted of tone-footshock pairings, in a third distinct context (context

209 went fear conditioning consisting of 10 tone-footshock pairings.

210 We then used the T-maze footshock paradigm to test whether a dose of 17 beta-est

211 d in vivo microdialysis to determine whether footshock plus glutamate (50.0 nmol) alters noradrenergi

212 t odor cues that were previously paired with footshock potentiate the acoustic startle response in ra

213 l, the conditioned stimulus, CS) paired with footshock (PRD) and the other half was given the same st

214 he magnitude of the amygdala response to the footshock predicted behavioral responses the following d

215 previous manual restraint (mNE) and after 20 footshocks presented over the course of 30 min alone (FS

216 However, SB and SIB incidence in APO+footshock-primed lesioned rats was nearly tripled.

217 /20 rats) during APO priming, but not during footshock priming.

218 d been associated with a fearful experience (footshock) produces alterations in arousal and sleep tha

219 r conditioning, amygdala responses evoked by footshock progressively decreased, whereas responses evo

220 large reward accompanied by varying risks of footshock punishment.

221 evels of food reward with the probability of footshock punishment.

222 ward accompanied by varying probabilities of footshock punishment.

223 ly trauma exposed rats displayed stereotypic footshock reactivity, yet by adulthood, hippocampus-depe

224 imbic, cortical, and striatal circuitry in a footshock reinstatement model of relapse to cocaine seek

225 This characterization of footshock-responsive systems identifies cell groups that

226 ther dlPAG lesions nor vPAG lesions affected footshock sensitivity (experiment 4) or consumption on a

227 MCPG infused into the BLA did not affect the footshock sensitivity.

228 Footshock-sensitivity, freezing behavior, and corticoste

229 The effects of footshock sensitization (priming), apomorphine (APO) pri

230 ions, each coterminating with a 2 s, 0.57 mA footshock separated by a 120 s intertrial interval.

231 Exposure to a single 30 minute footshock session induced maximal Fos expression in the

232 and/or Fos induction after aversive stimuli (footshocks, shock-predictive cues, food deprivation, or

233 Rats exposed to a footshock show conditional fear when reexposed to the sh

234 The group preexposed to footshock showed poorer fear conditioning to the light C

235 Footshock stimulation increased NE levels and the magnit

236 els returned to baseline within 30 min after footshock stimulation.

237 f norepinephrine evoked by the unconditioned footshock stimulus.

238 plitude when startle was elicited by a brief footshock stimulus.

239 stered nicotine but cross-sensitizes to mild footshock stress (mFSS).

240 ng where history of caloric restriction with footshock stress (R + S) causes rats to consume twice th

241 These data suggest that footshock stress activates limbic circuitry of the CEA t

242 Mild footshock stress also caused glutamate release in heroin

243 Footshock stress and response-contingent presentation of

244 male rats were exposed to acute and repeated footshock stress at prepubertal, peripubteral, and adult

245 Footshock stress can reinstate cocaine-seeking behavior

246 the ventral tegmental area (VTA), where mild footshock stress causes CRF release, glutamate release,

247 Exposure of rats to acute electric footshock stress did not by itself reinstate drug-seekin

248 tinguished ethanol-seeking induced by either footshock stress or ethanol-associated discriminative st

249 which is not involved in relapse induced by footshock stress or reexposure to heroin.

250 Footshock stress preferentially increased DA utilization

251 Here, we show that footshock stress produces antinociception in rats by act

252 Studies in rats have shown that intermittent footshock stress reinstates drug seeking after prolonged

253 Here we report (1) that footshock stress releases CRF in the ventral tegmental a

254 entral pallidum (VP)] blocked the ability of footshock stress to reinstate lever pressing previously

255 ystem, and (4) that, through this circuitry, footshock stress triggers relapse to drug seeking in coc

256 nd showed more freezing in response to acute footshock stress when compared with their saline (SAL) t

257 responsive to acute and chronic intermittent footshock stress, and candidate afferent mediators of hy

258 reased DA utilization in mPFC and associated footshock stress-induced immobility responses, and these

259 in response to conditioned stimuli and mild footshock stress.

260 r altered relapse induced by cocaine cues or footshock stress.

261 refrontal DA and behavioral effects of acute footshock stress; and (3) these effects of repeated nico

262 e) and "emotional" [e.g., restraint (RST) or footshock] stresses.

263 nstatement, first shown with an intermittent footshock stressor in rats trained to self-administer he

264 reduced levels of freezing after inescapable footshocks, suggesting that M(1)R(-/-) mice are hyperact

265 ed HPA axis corticosterone response to acute footshock that did not adapt after 10 days of stress exp

266 conditioned stimulus (US, 2 seconds, 0.57 mA footshock), the context was a continuous background CS.

267 posure enhanced conditioning to an immediate footshock, the context preexposure facilitation effect (

268 a discrete 4-s amyl acetate odor paired with footshock to address several parametric issues that migh

269 r-conditioning paradigm in mice to condition footshock to an odor (conditioned stimulus (CS)).

270 conditioned stimulus previously paired with footshock to reinstate cocaine-induced conditioned place

271 ine self-administration during which we used footshocks to divide rats into animals that continue to

272 50, or 100 ng/0.5 microl) into the NTS after footshock training in a Y-maze discrimination task.

273 ely after either context training (day 1) or footshock training in that context (day 2).

274 s (X) and a footshock is attenuated when X-->footshock training occurs in the presence of a good pred

275 ntial days to separate context training from footshock training.

276 on when administered after either context or footshock training.

277 ons prevented the disruptive effects of high footshock training.

278 into the hippocampus after context, but not footshock, training.

279 nditioning consisted of the delivery of tone-footshock trials in a novel observation chamber, and fre

280 l-reinforced responses were punished by mild footshock; two other groups either received noncontingen

281 nditional stimulus (CS) and a co-terminating footshock unconditional stimulus (US).

282 y conditional stimulus (CS) with an aversive footshock [unconditional stimulus (US)], rats received a

283 to discrete conditioned stimuli (CSs) and a footshock unconditioned stimulus (US) and proposed that

284 Training consisted of 2 CS-footshock unconditioned stimulus pairings.

285 imulus (CS)] that was previously paired with footshocks [unconditioned stimulus (US)].

286 retrieval of an association between a CS and footshock US.

287 flation procedure (i.e., exposure to intense footshock USs) to assess the contribution of S-S associa

288 An unsignaled footshock was consistently paired with the CXT+, and no

289 on in the DG did not further increase when a footshock was delivered in the novel context.

290 less-steel grid floor through which a single footshock was delivered.

291 ssociation between an olfactory stimulus and footshock was investigated with a reversible lesion tech

292 tartle to cues paired with 0.6-mA and 1.6-mA footshocks was evaluated.

293 n of inescapable electrical footshocks or no footshocks was then administered.

294 activity on brain noradrenergic response to footshock were examined.

295 ctive avoidance learning to paired light and footshock were indistinguishable in these four mouse lin

296 ntagonist naltrexone, whereas the effects of footshock were selectively reversed by the corticotropin

297 on a fear-conditioning task (CS paired with footshock) were then trained on an escape-from-fear task

298 tioned auditory stimulus (CS+) was paired to footshocks whereas a second (CS-) was not.

299 ctory cues paired with normally subthreshold footshock, whereas the antagonist completely blocked emo

300 s to olfactory cues paired previously with a footshock, whereas this associative responding was preve