Preventingthereturnoffearinhumansusingreconsolidationupdatemechanisms.pdf

ARTICLES

Preventing the return of fear in humans
using reconsolidation update mechanisms
Daniela Schiller

1,2
, Marie-H. Monfils

1,3
, Candace M. Raio

2
, David C. Johnson

2
, Joseph E. LeDoux

1

& Elizabeth A. Phelps
1,2

Recent research on changing fears has examined targeting reconsolidation. During reconsolidation, stored information is
rendered labile after being retrieved. Pharmacological manipulations at this stage result in an inability to retrieve the
memories at later times, suggesting that they are erased or persistently inhibited. Unfortunately, the use of these
pharmacological manipulations in humans can be problematic. Here we introduce a non-invasive technique to target the
reconsolidation of fear memories in humans. We provide evidence that old fear memories can be updated with non-fearful
information provided during the reconsolidation window. As a consequence, fear responses are no longer expressed, an
effect that lasted at least a year and was selective only to reactivated memories without affecting others. These findings
demonstrate the adaptive role of reconsolidation as a window of opportunity to rewrite emotional memories, and suggest a
non-invasive technique that can be used safely in humans to prevent the return of fear.

Learning about potential dangers in the environment is critical for
adaptive function, but at times fear learning can be maladaptive,
resulting in excessive fear and anxiety. Research on changing fears
has highlighted several techniques, most of which rely on the inhibi-
tion of the learned fear response. An inherent problem with these
inhibition techniques is that the fear may return, for example with
stress1. Recent research on changing fears targeting the reconsolida-
tion process overcomes this challenge to some extent. During recon-
solidation, stored information is rendered labile after being retrieved,
and pharmacological manipulations at this stage result in an inability
to retrieve the memories at later times, suggesting that they are either
erased or persistently inhibited2–6. Although these pharmacological
manipulations are potentially useful for changing learned fears, their
use in humans can be problematic. Here we show that invasive tech-
niques are not necessary to alter fear by targeting reconsolidation.
This is based on the premise that reconsolidation is an adaptive
update mechanism by which new information is incorporated into
old memories3,7,8. By introducing new information during the recon-
solidation period, it may be possible to permanently change the fear
memory. In the present study, we provide evidence in humans that
old fear memories can be updated with non-fearful information
provided during the reconsolidation window. As a consequence, fear
responses are no longer expressed. Furthermore, this effect is specific
to the targeted fear memory, and not others, and persists for at least a
year. These findings demonstrate the adaptive role of reconsolidation
as a window of opportunity to rewrite emotional memories, and
suggest a non-invasive technique that can be used safely and flexibly
in humans to prevent the return of fear.

Pharmacological blockade of reconsolidation

In contrast to the traditional view of memory formation as a one-time
process of consolidation9,10, the reconsolidation hypothesis suggests
that memories are consolidated each time they are retrieved2–6.
Evidence for reconsolidation of emotional memories comes from
studies using pharmacological perturbation after retrieval11–13. The
retrieval-induced plasticity allows the transition from a labile to a
stable state after which memories are no longer prone to interference14.

Why would such a recurrent window of vulnerability exist for old
memories? From an evolutionary perspective, reconsolidation may
serve as an adaptive update mechanism allowing for new information,
available at the time of retrieval, to be integrated into the initial memory
representation3,7,8. This view captures the fluidity of memory and sug-
gests a dynamic process through which memories are formed, updated
and maintained.

Using Pavlovian fear conditioning as a model paradigm, research
in non-human animals has detailed the molecular processes involved
in emotional memory reconsolidation by pharmacologically block-
ing various stages of this process, after which the memory was no
longer expressed. Most of these studies use protein synthesis inhibi-
tors, or other pharmacological agents, that are not safe for use in
humans3,4,6,11–14. Because the ability to impair emotional memories
has important implications for the treatment for anxiety dis s
linked to traumatic memories, such as post-traumatic stress dis
(PTSD), identifying techniques to target reconsolidation that can be
used flexibly and safely in humans is critical. One possibility is to
capitalize on reconsolidation as an update mechanism. If an old fear
memory could be restored while incorporating neutral or more posi-
tive information provided at the time of retrieval, it may be possible
to permanently modify the fearful properties of this memory.

Although this approach captures the very essence of reconsolida-
tion, it has been surprisingly neglected in emotion research in
humans and other animals. Until now, there is only one demonstra-
tion of this approach in non-human animals using fear condition-
ing8, and efforts to alter fear memories by introducing non-fearful
information during initial consolidation have had mixed results15–17.
In humans, studies of motor and declarative memory suggest new
information presented during the reconsolidation window may
interfere with the older memories by either impairing the memory18

or modifying it to incorporate the new information7,19. However,
there is robust evidence that motor, declarative and emotional
memories rely on distinct memory systems in the brain20, and the
reconsolidation process and effect of new information presented
during the reconsolidation window may differ depending on the type
of memory being updated.

1
Center for Neural Science,

2
Psychology Department, New York University, New York, New York 10003, USA.

3
Psychology Department, University of Texas, Austin, Texas 78712, USA.

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Interference of reconsolidation using extinction

In the present study, we sought to capitalize on reconsolidation as an
update mechanism and attempted to alter emotional memories with
new information. We propose that updating a fear memory with
non-fearful information, provided through extinction training,
would rewrite the original fear response and prevent the return of
fear. A recent study in rats8 provides strong evidence in support of
this hypothesis. In brief, 24 h after fear conditioning, rats were
reminded of the conditioned stimulus using a single retrieval trial,
and subsequently underwent extinction training. The extinction
phase was conducted either within or outside the reconsolidation
window, which lasts about 6 h11,18. It was found that fear responses
returned only in rats that underwent extinction after reconsolidation
was completed. In contrast, rats that had extinction training during
the reconsolidation window did not show recovery of fear.

To test this hypothesis in humans, we designed two experiments
examining whether extinction training conducted during the recon-
solidation window would block the return of extinguished fear. In the
first study, three groups of subjects underwent fear conditioning using
a discrimination paradigm with partial reinforcement (Fig. 1a). Two
coloured squares were used. One square (conditioned stimulus1,
hereafter termed CS1) was paired with a mild shock to the wrist
(unconditioned stimulus) on 38% of the trials, whereas the other
square was never paired with shock (CS2). A day later, all three groups
underwent extinction training in which the two conditioned stimuli
were repeatedly presented without the unconditioned stimulus. In two
groups the fear memory was reactivated before extinction using a
single presentation of the CS1. One group (n 5 20) received the
reminder trial 10 min before extinction (within the reconsolidation

window), whereas the second group (n 5 23) was reminded 6 h before
extinction (outside the reconsolidation window11,18). The third group
(n 5 22) was not reminded of the fear memory before extinction train-
ing. Twenty-four hours later, all three groups were presented again
with the conditioned stimuli without the unconditioned stimulus
(re-extinction) to assess spontaneous fear recovery. The measure of
fear was the skin conductance response (SCR). At each stage, the
differential fear response was calculated by subtracting responses to
the CS2 from responses to the CS1.

The results of the spontaneous recovery experiment are presented
in Fig. 1b (see also Supplementary Fig. 1). Subjects that showed suc-
cessful levels of fear acquisition and extinction were included in the
analysis. We verified that these levels were equivalent between the
groups using two-way analysis of variance (ANOVA) with main
effects of group (10 min, 6 h and no reminder) and time (early and
late phase). For both acquisition and extinction there was a significant
main effect of time (F1,62 5 9.92, P , 0.05; F1,62 5 19.59, P , 0.01,
respectively) but no effect of group or interaction. Follow-up t-tests
confirmed that subjects had significantly stronger responses to CS1
than to CS2 during acquisition (late phase; 10-min group: t 5 2.68,
P , 0.05; 6-h group: t 5 3.72, P , 0.05; no-reminder group: t 5 3.72,
P , 0.05), but by the last trial of extinction there was no difference
(10-min group: t 5 20.94; 6-h group: t 5 20.23; no-reminder group:
t 5 20.79; all not significant).

The decrease in fear responses from acquisition (late phase) to
extinction (last trial) for each group was assessed using a two-way
ANOVA with main effects of group (10 min, 6 h and no reminder)
and time (acquisition, extinction). This showed a significant main
effect of time (F1,62 5 29.9, P , 0.01), but no effect of group or inter-
action. Follow-up t-tests confirmed the reduction of fear in all three
groups (10-min group: t 5 2.70, P , 0.05; 6-h group: t 5 4.06,
P , 0.05; no-reminder group: t 5 4.07, P , 0.05), and there was no
difference in the level of fear reduction between the groups (P . 0.5
for all three comparisons).

Spontaneous recovery was assessed using a two-way ANOVA with
main effects of group (10 min, 6 h and no reminder) and time (early
and late phase of re-extinction, defined by the mean first four res-
ponses versus the subsequent four, respectively) showing a significant
main effect of time (F1,62 5 6.26, P , 0.05), and a group 3 time inter-
action (F2,62 5 4.63, P , 0.05). Follow-up t-tests compared the dif-
ferential responses between the last trial of extinction and the first
trial of re-extinction. Spontaneous recovery was found in subjects
who did not receive a reactivation trial before extinction (t 5 2.69,
P , 0.05), or who underwent extinction 6 h after fear reactivation
(t 5 2.66, P , 0.05). In contrast, subjects that had extinction
10 min after reactivation showed no spontaneous recovery
(t 5 0.28, not significant). These results indicate that the spontan-
eous recovery of fear after extinction can be prevented if extinction
training is conducted during the time window in which the fear
memory is proposed to be undergoing reconsolidation.

Persistence of reconsolidation blockade

In this initial study, we used a 24 h interval to test for long-term
memory, which, for practical reasons, is the standard in human fear
recovery experiments16,17,21–23. However, if the fear memory is persis-
tently altered, as would be predicted if we are affecting reconsolidation
of the fear memory, we would expect this effect to last for much longer
time intervals. In an attempt to examine whether the observed block-
ade of fear memory persists, we invited the participants for a follow-up
test after approximately 1 year (10–14 months). Nineteen of the 65
original participants were located and included in the follow-up study
(10-min group, n 5 8; 6-h group, n 5 4; no-reminder group, n 5 7).
We collapsed subjects from the two groups previously showing spon-
taneous recovery (that is, 6 h and no reminder) into one group. As
mentioned earlier, after the spontaneous recovery test, subjects were
re-extinguished using ten non-reinforced presentations of the stimuli
ensuring that all subjects showed no evidence of conditioned fear at

a

b

Day 1 Day 2 Day 3

Group 1: Acquisition Re-extinctionReminder Extinction

Group 2: Acquisition Re-extinctionReminder Extinction

Group 2: Acquisition Re-extinctionNo reminder Extinction

10 min

6 h

Spontaneous recovery: (1st trial of re-extinction) – (last trial of extinction)

10 min 6 h No reminder

* * *
* *

M
e
a
n
d

iff
e
re

n
ti
a
l S

C
R

Acquisition Extinction Re-extinction
–0.05

0.05

0.15

0.25

0.35

Figure 1 | Extinction during reconsolidation prevents spontaneous
recovery of extinguished fear. a, Experimental design and timeline. b, Mean
differential SCRs (CS1 minus CS2) during acquisition (late phase),
extinction (last trial) and re-extinction (first trial) for each experimental
group (10-min reminder, 6-h reminder and no reminder). The three groups
showed equivalent fear acquisition and extinction. Spontaneous recovery
(first trial of re-extinction versus the last trial of extinction) was found in the
group that had not been reminded or that was reminded 6 h before
extinction. In contrast, there was no spontaneous recovery in the group
reminded 10 min before extinction. *P , 0.05 (between acquisition and
extinction, or between extinction and re-extinction within group). Error
bars represent standard errors.

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the conclusion of the initial experiment. This re-extinction allowed us
to conduct a second test of fear recovery a year later. For this second
recovery test, we used a more potent recovery assay, namely reinstate-
ment, in which subjects were exposed to four unsignalled shocks,
followed by non-reinforced presentations of the conditioned stimuli.
The index of fear recovery (Fig. 2 and Supplementary Fig. 2) was the
difference in the conditioned fear response at the end of re-extinction
after the initial spontaneous recovery test and the conditioned fear
response immediately after reinstatement 1 year later. The conditioned
fear response at the end of re-extinction and post-reinstatement was
calculated using a differential SCR score (CS1 minus CS2). A two-
way ANOVA with main factors of group (10 min, 6 h/no-reminder)
and stage (re-extinction, post-reinstatement) showed a significant
main effect of group (F1,17 5 5.89, P , 0.05). The group 3 stage inter-
action was marginally significant (F1,17 5 2.78, P , 0.07, one-tail).
Follow-up one-tail t-test comparisons showed that reinstatement
was significant in the 6-h/no-reminder group (t 5 2.12, P , 0.03),
but not the 10-min group (t 5 0.22, not significant). Moreover, the
reinstatement index was significantly larger in the 6-h/no-reminder
group than the 10-min group (t 5 1.75, P , 0.05). Lastly, a com-
parison of post-reinstatement conditioned fear between the groups
showed a significant difference (t 5 2.18, P , 0.03).

These results indicate that reactivation of a fear memory renders it
labile and extinction training during this lability period leads to a
long lasting blockade of recovery of fear. In contrast, recovery of fear
a year later was observed after regular extinction training. Fear recovery
was also observed when extinction training was conducted with a
sufficient temporal gap after reactivation, presumably allowing for
reconsolidation to be complete.

Specificity of reconsolidation blockade

If interfering with reconsolidation using extinction is to be clinically
useful, it is also important to determine whether it is specific. In real-
life situations, a traumatic event can be associated with several cues,
and each could potentially trigger the recollection of the event and
elicit fear reactions. To assess the specificity of this fear blockade
technique, we examined whether interfering with the reconsolidation
of one fear predictive cue would affect the fate of another, associated
cue.

In a second experiment, more than one stimulus was associated
with the same aversive outcome (Fig. 3a). Specifically, using a within-
subject design, subjects underwent fear conditioning using three
coloured squares. Two squares (CSa1 and CSb1) were paired with
the shock on 38% of the trials. The third square (CS2) was never
paired with the shock. A day later, subjects received a single presenta-
tion of CSa1 and the CS2, but not CSb1. Ten minutes after the
reminder trial, extinction training was conducted (within the recon-
solidation window) using repeated presentations of all conditioned
stimuli without the aversive outcome. Reinstatement of the fear
memory was conducted 24 h later, when subjects returned to the
experiment room and received four unsignalled presentations of
the shock. Ten minutes later, the conditioned stimuli were presented
without the aversive outcome (re-extinction).

The results of the experiment are presented in Fig. 3b (see also
Supplementary Fig. 3). Subjects (n 5 18) that showed successful fear
acquisition and extinction were included. We verified that these
levels were equivalent between the two conditioned stimuli (CSa1
and CSb1) using two-way ANOVAs with main effects of stimulus
(CSa1, CSb1 and CS2) and time (early and late phase, defined by
the mean response during the first and second half of each phase,
respectively). In acquisition, there was a significant main effect of
stimulus (F2,51 5 3.51, P , 0.05) and a stimulus 3 time interaction
(F2,51 5 3.27, P , 0.05). In extinction, there was a significant main
effect of time (F1,51 5 48.74, P , 0.01). Follow-up t-tests were used to
further assess acquisition and extinction of fear. We compared the
mean SCR to CSa1 or CSb1 with the CS2 during the second half
of the acquisition session. Subjects showed significantly stronger res-
ponses to CSa1 than to CS2 (t 5 6.01, P , 0.05), as well as to CSb1
compared to CS2 (t 5 6.68, P , 0.05). Moreover, the level of acquisi-
tion to CSa1 and CSb1 was equivalent (t 5 0.76, not significant). To

R
e
in

st
a
te

m
e
n
t

in
d

e
x

10 min

0.2

0.1

0

–0.1
6 h/

no reminder

*

Figure 2 | Blockade of the return of fear persists one year later. The
reinstatement index is the difference in the conditioned fear response (CS1
minus CS2) at the end of re-extinction after the initial spontaneous
recovery test and the conditioned fear response immediately after
reinstatement a year later. The magnitude of the reinstatement was
significantly higher in the 6-h/no-reminder group than in the 10-min group,
which showed no reinstatement. *P , 0.05; error bars represent standard
errors.

Reinstatement: (1st trial of re-extinction) – (last trial of extinction)

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.1

0

Day 1
Acquisition

CSa+ CSb+ CS–

Day 2
Reminder

10 min 10 min

CSa+ CS–

Extinction
CSa+ CSb+ CS– CSa+ CSb+ CS–

Day 3
Reinstatement

4 × US

Re-extinction

a

b CSa+ (reminded)
CSb+ (not reminded)
CS–

M
e
a
n
S

C
R

* *

*

Acquisition Extinction Re-extinction

Figure 3 | Blockade of the return of fear is specific to reactivated memories.
a, Experimental design and timeline. US, unconditioned stimulus. b, Mean
SCRs (CSa1, CSb1 and CS2) during acquisition (late phase), extinction
(last trial) and re-extinction (first trial). Subjects had equivalent levels of
acquisition and extinction of conditioned fear to the two conditioned
stimuli. The index of fear recovery was the first trial of re-extinction (after
reinstatement) minus the last trial of extinction (before reinstatement). Fear
reinstatement was found only to CSb1 (not reminded before extinction
training), but not to CSa1 (reminded 10 min before extinction training).
*P , 0.05 (between acquisition and extinction, or extinction and re-
extinction for each stimulus). Error bars represent standard errors.

NATURE | Vol 463 | 7 January 2010 ARTICLES

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assess fear extinction, we compared the mean SCR to CSa1 or CSb1
with the CS2 during the last trial of extinction. There were no signifi-
cant differences in responses to CSa1 compared to CS2 (t 5 20.26,
not significant), or to CSb1 compared to CS2 (t 5 20.56, not sig-
nificant), and responses to CSa1 and CSb1 were equally extinguished
(t 5 0.23, not significant). Moreover, subjects had successful reduction
of fear, as assessed by comparing the SCR during the second half of
acquisition with the last trial of extinction, to both CSa1 (t 5 2.62,
P , 0.05) and CSb1 (t 5 4.08, P , 0.05) but not to the CS2
(t 5 20.09, not significant), which was low to begin with.

To assess the recovery of fear, we used a two-way ANOVA with
main effects of stimulus (CSa1, CSb1 and CS2) and time (early and
late phase of re-extinction, defined by the mean first four responses
versus the last four, respectively), which revealed a stimulus 3 time
interaction (F2,51 5 5.14, P , 0.01). Using follow-up t-tests, we com-
pared the SCR during the last trial of extinction (before reinstate-
ment) with the first trial of re-extinction (after reinstatement).
Subjects showed reinstated fear responses only to CSb1, which is
the stimulus that was not reminded before extinction (t 5 2.16,
P , 0.05). In contrast, fear responses to CSa1, which was reminded
10 min before extinction training, did not recover (t 5 0.22, not sig-
nificant). As expected, there were also no fear responses to the CS2
(t 5 0.16, not significant). Thus, extinction during reconsolidation
affected only the reactivated memory and no other trace associated
with the original event.

Discussion

The present findings suggest a new technique to target specific fear
memories and prevent the return of fear after extinction training.
Using two recovery assays, we demonstrated that extinction con-
ducted during the reconsolidation window of an old fear memory
prevented the spontaneous recovery or the reinstatement of fear
responses, an effect that was maintained a year later. Moreover, this
manipulation selectively affected only the reactivated conditioned
stimulus while leaving fear memory to the other non-reactivated
conditioned stimulus intact.

It has been suggested that the adaptive function of reconsolidation
is to allow old memories to be updated each time they are
retrieved3,7,8. In other words, our memory reflects our last retrieval
of it rather than an exact account of the original event. This notion
has received support from interference paradigms targeting motor
and declarative memories7,18,19. These studies demonstrate that new
information provided during reconsolidation could affect old
memories by modifying or interfering with them, but in contrast
to the present study, they do not provide evidence for memory block-
ade. This difference in the effect of new information presented during
reconsolidation on the subsequent qualities of different types of
memory may be due to the diverse nature of the underlying memory
systems. For instance, unlike the distributed cortical representation
of declarative memories20, conditioned fear has a more discrete
neural representation localized in the amygdala24. Indeed, in the
lateral amygdala, pharmacological blockade of the molecular cascade
engaged by retrieval prevents the reconsolidation of fear memories in
rats4. This raises the possibility that our behavioural manipulation,
namely, extinction training during reconsolidation, targeted the
same molecular mechanism.

Although the current behavioural study does not provide direct
evidence that a process of reconsolidation mediates the effects of
extinction training, support for this hypothesis comes from recent
findings in rats8. After fear consolidation, a single isolated retrieval
trial before extinction prevented the recovery of fear in rats.
Interestingly, plasticity in the lateral amygdala induced by the con-
ditioned stimulus retrieval was impaired by the presentation of a
conditioned stimulus 1 h later, indicating possible interference with
the reconsolidation process, similar to the interference caused to
reconsolidation by pharmacological blockade in rats4. Together,
these findings reveal cross-species similarities, which may reflect an

evolutionarily preserved adaptive mechanism whereby the neural
representation of fear memory can be significantly altered through
time-dependent molecular mechanisms triggered by exposure to
fear-eliciting stimuli.

The current results also suggest that timing may have a more
important role in the control of fear than previously appreciated.
Standard extinction training, without previous memory reactivation,
also triggers the fear memory. Given this, one might expect mere
extinction training to have similar effects. That is, the first trial of
extinction might serve as the reminder cue triggering the reconsol-
idation cascade, which is immediately followed by extinction.
However, there is abundant evidence that during standard extinction
training the non-reinforced presentations of the fear-eliciting cue
induce new inhibitory learning, which competes for expression with
the initial fear learning, resulting in the recovery of fear responses in
some circumstances16,17,21–23,25,26. Our findings indicate that the
timing of extinction relative to the reactivation of the memory can
capitalize on reconsolidation mechanisms. Two factors may be
important determinants in this process: the timing of extinction
training relative to retrieval, and/or the chunking of the conditioned
stimulus presentations during extinction relative to reactivation
(that is, the fact that they are massed relative to the single retrieval
trial during the reconsolidation phase). Further studies are required
to disentangle these possibilities.

In conclusion, the present study showed that updating fear memories
with non-fearful information provided through extinction training led
to the blockade of previously learned fear responses and a lasting change
in the original fear memory. These results have significant implications
for the treatment of anxiety dis s. Current forms of therapy rely
heavily on extinction27,28, but the fact that extinguished fear could
recover under certain conditions dampens the resilience of anxiety
patients after treatment. The discovery that certain pharmacological
manipulation can potentially erase memories through effects on recon-
solidation has been encouraging; however, most compounds showing
such effects in various species are toxic to humans. Recently, there has
been promising evidence using compounds that are testable on
humans, namely b-adrenergic receptor blockers29, which also show
effects in trauma patients30, but these effects are not observed in every
case31. The present study proposes that such invasive techniques are not
necessary. Using a more natural intervention that captures the adaptive
purpose of reconsolidation allows a safe and easily implemented way to
prevent the return of fear.

METHODS SUMMARY

Two experiments were designed to examine whether extinction training con-

ducted during the reconsolidation window would block the return of extin-

guished fear. The measure of fear was the SCR. In the first study, three groups

of subjects underwent a discrimination fear conditioning paradigm with partial

reinforcement. Two coloured squares (CS1 and CS2) were used. The CS1 was

paired with a mild shock to the wrist (unconditioned stimulus) on about one-

third of the trials, and the CS2 was never paired with the shock. A day later, all

three groups underwent extinction training (repeated conditioned stimulus pre-

sentations without the unconditioned stimulus). In two groups the fear memory

was reactivated before extinction using a single presentation of the CS1. One

group received the reminder trial 10 min before extinction (within the recon-

solidation window), whereas the second group was reminded 6 h before extinc-

tion (outside the reconsolidation window). The third group was not reminded of

the fear memory before extinction training. To assess spontaneous fear recovery,

a day later all three groups were presented with the conditioned stimuli without

the unconditioned stimulus (re-extinction). About a year later, the return of fear

was assessed again using a different recovery assay (reinstatement).

The second experiment used a within-subject design where subjects under-

went fear conditioning using three coloured squares. Two squares (CSa1 and

CSb1) were paired with the shock on about one-third of the trials. The third

square (CS2) was never paired with the shock. A day later, subjects received a

single presentation of CSa1 and the CS2, but not CSb1. Ten minutes after the

reminder trial, extinction training was conducted (within the reconsolidation

window) using repeated presentations of all conditioned stimuli without the

unconditioned stimulus. Reinstatement of the fear memory was conducted

ARTICLES NATURE | Vol 463 | 7 January 2010

52
Macmillan Publishers Limited. All rights reserved©2010

24 h later, when subjects returned to the experiment room and received four
unsignalled presentations of the shock. Ten minutes later the conditioned stimuli

were presented without the aversive outcome (re-extinction).

Full Methods and any …