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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 extual fear conditioning generated by a weak footshock.
4  response by pressing the lever, terminating footshock.
5 context and novel tone were paired with mild footshock.
6 light or a noise-light compound using a mild footshock.
7 the presence of a good predictor (A) of that footshock.
8 g environment that was initially paired with footshock.
9 d background are normal in their response to footshock.
10 osed CS and a control CS predicted avoidable footshock.
11 but not to odors presented in the absence of footshock.
12 airings of a 10-s odor with a 0.25-s, 0.4-mA footshock.
13 aced into the same context without the CS or footshock.
14 ned to fear a soft tone by pairing it with a footshock.
15  tone no longer predicts the occurrence of a footshock.
16  contexts, I of which was paired with a mild footshock.
17 tly unpaired (random, RND group) manner with footshock.
18 ence or presence of cues associated with the footshock.
19 creased motivation or altered sensitivity to footshock.
20  the level of NE was examined in response to footshock.
21 by reexposure to the tone without additional footshock.
22 g in which a specific context is paired with footshock.
23 ted in SED compared with AW during and after footshock.
24 neutral tone by pairing the tone with a mild footshock.
25 ich did not increase significantly following footshock.
26  when the injections were given 30 min after footshock.
27 aced in a distinct environment and delivered footshock.
28  training context in which they had received footshock.
29 ), or a PACAP agonist (experiment 3) without footshock.
30 d cocaine-seeking behavior in the absence of footshock.
31 e male mice 2 and 4 weeks after a 2 s 1.5 mA footshock.
32 ed neurons were more likely to be excited by footshock.
33 visual CS (CSA) in stage I via pairings with footshock.
34 ons of visual CSA and auditory CS (CSB) with footshock.
35 oked larger amygdala responses than expected footshock.
36 entation of a cue conditioned to inescapable footshock.
37  a lever within a warning period, preventing footshock.
38  robust responses to auditory CSs predicting footshocks.
39 hock arm), and they received four unsignaled footshocks.
40 g compulsively (addicted) in the presence of footshocks.
41 imuli, such as hindpaw pinches or electrical footshocks.
42 cadian rhythm upon removal of light cues and footshocks.
43  were exposed to inescapable, uncontrollable footshocks.
44  an odor aversion associated with early-life footshocks.
45 s trained to drink from a spout were given a footshock (0.35 mA) on Day 5 after approaching the spout
46  the NTS immediately after they were given a footshock (0.35 mA, 0.5 s) in the dark compartment of an
47  mg/kg, i.p.) administered immediately after footshock (0.55 mA for 1 s) potentiated NE release.
48 nfusion of CLN or phosphate buffered saline, footshock (0.8 mA, 1 s), and injected with epinephrine (
49 3 mg/kg), and administration of an escapable footshock (0.8 mA, 1 s).
50                               High-intensity footshock (120, 0.8 mA shocks over 40 min) also elevates
51 n (experiment 1) or exposure to intermittent footshock (15 min, 0.6 mA) and heroin priming injections
52 d on: (1) inhibitory avoidance that involves footshock; (2) a circular maze task that involves escape
53  a water-maze spatial task after being given footshock 30 min before retention testing but are not im
54      Taken together, these data suggest that footshock activates limbic circuitry in the CEA, which i
55            Here we show in rats that stress (footshock) activates the transcription factor cAMP respo
56 odation sessions followed by one exposure to footshock (acute footshock, AFS) or handled similarly wi
57 ailability of the ethanol CS was preceded by footshock, additive effects of these stimuli on respondi
58 tophoresis of the alpha-2 agonist clonidine, footshock administration, and LC stimulation mimicked th
59 followed by one exposure to footshock (acute footshock, AFS) or handled similarly without receiving a
60 adigm was used to compare rats that received footshock after exploring a context to rats that receive
61 ngs of a light conditioned stimulus (CS) and footshock after preexposure either to footshock or to th
62 ning and not after unpaired presentations or footshocks alone.
63 ear memory can arise from paired or unpaired footshock, an effect not predicted by theoretical models
64 g the association between olfactory cues and footshock and add to a growing body of evidence implicat
65 ts possible influence on sleep induced after footshock and after the opportunity to explore a neutral
66 aining, where one tone (CS+) was paired with footshock and another tone (CS-) was presented alone.
67 lter the changes in sleep and EEG induced by footshock and by the opportunity to explore a neutral en
68  in the medial amygdala (MeA) following both footshock and fear recall, but had normal activation in
69 (NE) within the amygdala in response to both footshock and GABAergic compounds.
70 reased freezing behavior in response to mild footshock and produced behavioral activation in the open
71  striatum throughout training on inescapable footshock and signaled active avoidance tasks.
72 rine (NE) release in the amygdala induced by footshock and systemic administration of drugs affecting
73 th the individual and interactive effects of footshock and the CS were significantly greater in previ
74 en the drugs were administered without prior footshock and when the injections were given 30 min afte
75 fear conditioning pairing auditory cues with footshocks and examined extinction behavior, gene expres
76  as repeated stressful events using noxious (footshock) and psychological (restraint) stress.
77 n unconditioned stimulus (US; for example, a footshock), and the resulting CS-US association guides f
78  during a 2-hr baseline, 40 min of scrambled footshock, and a 1-hr recovery.
79 were fear-conditioned by pairing a tone with footshock, and then exposed to chronic unpredictable str
80 em putative dopamine neurons, are excited by footshocks, and acquire a response to auditory stimuli d
81 ere exposed to unpredictable and inescapable footshocks, and fear memory for the shock context was as
82 egular chow or sucrose, and attenuated cue-, footshock-, and yohimbine-induced reinstatement.
83 (i.e., by training rats with a lower, 0.3 mA footshock), AP5 abolished fear-potentiated startle at ea
84 d rats had a stronger memory for the context-footshock association as assessed by all measures of mem
85 ampus on acquisition and retention of T-maze footshock avoidance conditioning.
86 tum to the hippocampus, mice were trained on footshock avoidance in a T-maze.
87 estradiol and estrone on retention of T-maze footshock avoidance in female ovariectomized mice.
88 orms of striatum-dependent memory, including footshock avoidance learning and "response" learning in
89 ent during behavior maintained in a signaled footshock avoidance procedure.
90 ere injected intracerebroventricularly after footshock avoidance training in CD-1 mice.
91 srupted acquisition and retention for T-maze footshock avoidance.
92 mpaired acquisition and retention for T-maze footshock avoidance.
93 osure, all rats received pairings of A and a footshock before assessment of generalized responding (c
94 are reexposed to the unconditioned stimulus (footshock) before drug administration, performance on th
95 nd that repeated forced swim and inescapable footshock both produced aversive behaviors that were blo
96         Dopamine transmission throughout the footshock bout did not predict performance but rather wa
97 of mRNA for TH and c-fos were elevated after footshock but did not differ between SED and AW.
98 e in the brain frontal cortex in response to footshock but does not influence expression of the gene
99 sing neurons before or immediately after the footshock, but not at the time of fear recall, enhanced
100 administered into the rACC immediately after footshock, but not context, training.
101 e responding to odors paired previously with footshock by increasing spontaneous activity and burstin
102 ly trained to associate a tone with a strong footshock by replacing it with a much weaker one during
103 active avoidance, rats avoid a tone-signaled footshock by stepping onto a nearby platform, delaying a
104 in which rats learn to avoid a tone-signaled footshock by stepping onto a nearby platform.
105  We previously demonstrated that a stressor (footshock) can potentiate cocaine seeking in male rats v
106            We show that unsignaled nocturnal footshock caused rats living in an "ethological" apparat
107                   Conditioning with a weaker footshock caused smaller increases in BLA firing rate, b
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 the embedded auditory signal was paired with footshock, control rats were impaired in their ability t
113 ed 50-kHz USVs, whereas a cue that predicted footshock decreased 50-kHz USVs.
114 ns made either before or after training with footshock decreased the level of freezing to conditional
115 we found few effects on somatic responses to footshock, deficits in conditioned fear may reflect alte
116  of a negatively valenced stimulus involving footshock delivery during Pavlovian fear conditioning.
117 nylephrine were infused in the NTS following footshock delivery in one alley of a Y-maze.
118 ards after bar pressing or presentation of a footshock during fear conditioning produced significant
119 re not observed, differences were evident in footshock-elicited ultrasonic vocalizations.
120 formation, by coding for the saliency of the footshock event and by signaling such events to the basa
121                                   Unexpected footshock evoked larger amygdala responses than expected
122 ry conditioned stimulus (CS) was paired with footshock, except when it was preceded by another stimul
123 xposed to a conspecific receiving electrical footshocks exhibited enhanced passive avoidance (PA) lea
124 context freezing was strong in a group given footshock exposure but not in a group given eye shock US
125 ent of cocaine seeking was then tested after footshock exposure in different groups of rats that were
126  additional group was included that received footshock exposure, rather than US reexposure, between e
127  testing, followed 60 min later by stress of footshock exposure.
128 itioned fear responses to a tone paired with footshock extinguish when the tone is presented repeated
129  10 pairings of a 3.7 sec light and a 0.4 mA footshock (fear conditioning).
130 nophobia-like phenotype and when paired with footshocks, fear is robustly enhanced.
131  cocaine seeking by a stressor, intermittent footshock, following intravenous self-administration in
132  adult stress exposure (combination of daily footshock for 10 days and 3 restraint sessions) on (1) m
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 in NGFI-A mRNA was not seen in the immediate-footshock group.
142  mRNA expression than rats of the context-no-footshock group.
143 t received footshock (immediate- and delayed-footshock groups) had greater levels of c-fos mRNA expre
144 lation of translation, long-term memory, and footshock habituation are also revealed.
145 nsights into molecular mechanisms engaged in footshock habituation within distinct MB neurons.
146  the presence of cues previously paired with footshocks, has suggested that the BLC may be a critical
147                  However, rats that received footshock (immediate- and delayed-footshock groups) had
148 er exploring a context to rats that received footshock immediately after placement in the chamber.
149  Pre and Alt-Pre rats received a 2-s, 1.5 mA footshock immediately upon placement in Context A.
150  the light CS than did a group preexposed to footshock in a different context, indicating contextual
151 -eight hours later, rats received the second footshock in a familiar (FAM) or novel (NOV) context.
152  procedure in which rats received unsignaled footshock in a novel observation chamber; freezing behav
153 usion of CRF into VTA has similar effects to footshock in cocaine-experienced animals but fails to ca
154 esion groups showed increased activity after footshock in other studies.
155 chemical cross-sensitization between APO and footshock in such rats is unidirectional and support the
156  knockout mice's increased responsiveness to footshock in the extended test may be an indication of i
157       In Experiment 2, a group preexposed to footshock in the same context showed poorer fear conditi
158                         Male rats were given footshocks in a distinctive context and later tested usi
159 ats acquired a fear memory by receiving mild footshocks in a shock zone on a track, we analyzed place
160 racterized a habituation assay to repetitive footshocks in mixed sex Drosophila groups and demonstrat
161 ional consequences of methamphetamine SA and footshocks in the rat brain.
162 versive training stimulus of a single, brief footshock increased CRH levels in the CEA.
163 nditioning by pairing an auditory cue with a footshock increases the rate of spine elimination.
164 sentation of the same auditory cue without a footshock increases the rate of spine formation.
165                 In contrast to low-intensity footshock, increases in cFos expression within the rostr
166                              A 0.55 mA (2 s) footshock induced a significant increase in NE levels wh
167  nbm corticopetal cholinergic neurons during footshock induced operant suppression.
168 uggest that dopamine input may contribute to footshock- induced activation of cFos expression in the
169 ly, excitotoxic rEPN lesions partly diminish footshock-induced cFos in the LHb and RMTg.
170 ant corticosterone levels displayed enhanced footshock-induced Fos expression in the parvicellular co
171  were measured with the novel open field and footshock-induced freezing tests.
172 ransfer into the OT of intact rats decreased footshock-induced freezing, and this effect was reversed
173 Further, inhibition of the NAshell blocked a footshock-induced increase in dopamine within the PFC an
174 TA antalarmin, but not astressin-2B, blocked footshock-induced reinstatement in LgA rats.
175   Consistent with our previous findings with footshock-induced reinstatement of alcohol seeking in Wi
176 PAC1/VPAC2 antagonist, PACAP 6-38, prevented footshock-induced reinstatement of extinguished cocaine
177                                              Footshock-induced reinstatement was prevented by bilater
178 ine receptor antagonist fluphenazine blocked footshock-induced reinstatement when infused into the PF
179 TA of the contralateral hemisphere prevented footshock-induced reinstatement, whereas ipsilateral man
180                     A differential effect of footshock-induced stress was noted on neuronal subgroups
181                       Here, using increasing footshock intensities in an inhibitory avoidance paradig
182       Furthermore, training with the highest footshock intensity (traumatic experience) led to a sign
183 h levels assessed in rats trained with lower footshock intensity or unshocked controls exposed only t
184    Inhibitory avoidance training with higher footshock intensity produced increased levels of AEA in
185 e demonstrate that habituation to repetitive footshock involves two phases mediated by distinct neuro
186 e association between one stimulus (X) and a footshock is attenuated when X-->footshock training occu
187  retention testing but are not impaired when footshock is given 2 min or 4 h before testing.
188 nstatement of cocaine seeking by a stressor (footshock) is CRF dependent and is augmented in rats tha
189                          The response to the footshock itself is called an activity burst and include
190                     The omission of expected footshock led to a decrease below baseline in the amygda
191 imilarly without receiving any footshock (no footshock, NFS).
192 ) or handled similarly without receiving any footshock (no footshock, NFS).
193  In this model, neither a stressor (electric footshock) nor stress-level corticosterone treatment alo
194                                    The first footshock occurred when rats crossed into the dark chamb
195 on-monotonically related to the intensity of footshock on Day 1.
196    This investigation examined the effect of footshock on responses of 283 spinal dorsal horn neurons
197       Stressed Wistar rats received a single footshock on two occasions.
198                              After the final footshock or NFS session, rats were anesthetized, a lami
199 nt of heroin seeking induced by intermittent footshock or priming injections of heroin.
200 S) and footshock after preexposure either to footshock or to the context alone.
201  to associate a visual stimulus (light) with footshock or were exposed to the light alone.
202          A regimen of inescapable electrical footshocks or no footshocks was then administered.
203 d with either appetitive (food) or aversive (footshock) outcomes.
204                           During the 10 tone-footshock paired training, postshock freezing and USV re
205 nse to postconditioning presentations of the footshock-paired odors but not to odors presented in the
206 t BA projectors become activated by the tone-footshock pairing of fear learning protocols.
207 d fear conditioning, which consisted of tone-footshock pairings, in a third distinct context (context
208 went fear conditioning consisting of 10 tone-footshock pairings.
209                      We then used the T-maze footshock paradigm to test whether a dose of 17 beta-est
210 d in vivo microdialysis to determine whether footshock plus glutamate (50.0 nmol) alters noradrenergi
211 t odor cues that were previously paired with footshock potentiate the acoustic startle response in ra
212 l, the conditioned stimulus, CS) paired with footshock (PRD) and the other half was given the same st
213 he magnitude of the amygdala response to the footshock predicted behavioral responses the following d
214 previous manual restraint (mNE) and after 20 footshocks presented over the course of 30 min alone (FS
215         However, SB and SIB incidence in APO+footshock-primed lesioned rats was nearly tripled.
216 d been associated with a fearful experience (footshock) produces alterations in arousal and sleep tha
217 r conditioning, amygdala responses evoked by footshock progressively decreased, whereas responses evo
218 C and dmPFC to obtain neuronal correlates of footshock-punished EtOH-SA.
219 ward accompanied by varying probabilities of footshock punishment, we recently showed that females ar
220 evels of food reward with the probability of footshock punishment.
221 ward accompanied by varying probabilities of footshock punishment.
222 large reward accompanied by varying risks of footshock punishment.
223 ly trauma exposed rats displayed stereotypic footshock reactivity, yet by adulthood, hippocampus-depe
224 or their axon terminals in the BA during the footshock, reduced the strength of fear memory as tested
225 imbic, cortical, and striatal circuitry in a footshock reinstatement model of relapse to cocaine seek
226 aving mice identified a stable population of footshock-responsive SST-INs during contextual condition
227                     This characterization of footshock-responsive systems identifies cell groups that
228 wley rats were subjected to a combination of footshock/restraint stress in either adolescence (postna
229 MCPG infused into the BLA did not affect the footshock sensitivity.
230                                              Footshock-sensitivity, freezing behavior, and corticoste
231 ions, each coterminating with a 2 s, 0.57 mA footshock separated by a 120 s intertrial interval.
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 els returned to baseline within 30 min after footshock stimulation.
236 f norepinephrine evoked by the unconditioned footshock stimulus.
237 plitude when startle was elicited by a brief footshock stimulus.
238 stered nicotine but cross-sensitizes to mild footshock stress (mFSS).
239 ng where history of caloric restriction with footshock stress (R + S) causes rats to consume twice th
240                      These data suggest that footshock stress activates limbic circuitry of the CEA t
241                                         Mild footshock stress also caused glutamate release in heroin
242                                              Footshock stress and response-contingent presentation of
243 male rats were exposed to acute and repeated footshock stress at prepubertal, peripubteral, and adult
244                                              Footshock stress can reinstate cocaine-seeking behavior
245 the ventral tegmental area (VTA), where mild footshock stress causes CRF release, glutamate release,
246           Exposure of rats to acute electric footshock stress did not by itself reinstate drug-seekin
247 tinguished ethanol-seeking induced by either footshock stress or ethanol-associated discriminative st
248  which is not involved in relapse induced by footshock stress or reexposure to heroin.
249                                              Footshock stress preferentially increased DA utilization
250                           Here, we show that footshock stress produces antinociception in rats by act
251 Studies in rats have shown that intermittent footshock stress reinstates drug seeking after prolonged
252                      Here we report (1) that footshock stress releases CRF in the ventral tegmental a
253 entral pallidum (VP)] blocked the ability of footshock stress to reinstate lever pressing previously
254 ystem, and (4) that, through this circuitry, footshock stress triggers relapse to drug seeking in coc
255 nd showed more freezing in response to acute footshock stress when compared with their saline (SAL) t
256 responsive to acute and chronic intermittent footshock stress, and candidate afferent mediators of hy
257 reased DA utilization in mPFC and associated footshock stress-induced immobility responses, and these
258  in response to conditioned stimuli and mild footshock stress.
259 r altered relapse induced by cocaine cues or footshock stress.
260 ered by either cocaine-priming injections or footshock stress.
261 e) and "emotional" [e.g., restraint (RST) or footshock] stresses.
262 nstatement, first shown with an intermittent footshock stressor in rats trained to self-administer he
263 reduced levels of freezing after inescapable footshocks, suggesting that M(1)R(-/-) mice are hyperact
264                                Unlike males, footshock, tested across a range of intensities, failed
265 ed HPA axis corticosterone response to acute footshock that did not adapt after 10 days of stress exp
266 n innately aversive stimulus, such as a mild footshock (the unconditioned stimulus).
267 conditioned stimulus (US, 2 seconds, 0.57 mA footshock), the context was a continuous background CS.
268 posure enhanced conditioning to an immediate footshock, the context preexposure facilitation effect (
269 a discrete 4-s amyl acetate odor paired with footshock to address several parametric issues that migh
270 r-conditioning paradigm in mice to condition footshock to an odor (conditioned stimulus (CS)).
271  conditioned stimulus previously paired with footshock to reinstate cocaine-induced conditioned place
272 ine self-administration during which we used footshocks to divide rats into animals that continue to
273 50, or 100 ng/0.5 microl) into the NTS after footshock training in a Y-maze discrimination task.
274 ely after either context training (day 1) or footshock training in that context (day 2).
275 s (X) and a footshock is attenuated when X-->footshock training occurs in the presence of a good pred
276 ntial days to separate context training from footshock training.
277 on when administered after either context or 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 ing in response to a tone paired with a weak footshock was immune to the IED, but chemogenetic activa
292 ssociation between an olfactory stimulus and footshock was investigated with a reversible lesion tech
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

 
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