Emerging Trends in The Social and Behavioral Sciences

Mechanisms of Fear Reduction

Item

Title

Mechanisms of Fear Reduction

Author

Lancaster, Cynthia L.

Monfils, Marie‐H.

Research Area

Psychopathology

Topic

Mental Illness Diagnosis and Treatment

Abstract

Over the past century, numerous theories have been advanced toward a unified account of fear reduction and have achieved various degrees of empirical support. Here, we first provide a brief overview of the basic models that account for fear acquisition, then we provide a review of several of the most prominent theories of fear reduction, and finally, we describe important cutting‐edge directions for future research.

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Identifier

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extracted text

Mechanisms of Fear Reduction
CYNTHIA L. LANCASTER and MARIE-H. MONFILS

Abstract
Over the past century, numerous theories have been advanced toward a unified
account of fear reduction and have achieved various degrees of empirical support.
Here, we first provide a brief overview of the basic models that account for fear
acquisition, then we provide a review of several of the most prominent theories of
fear reduction, and finally, we describe important cutting-edge directions for future
research.

Although it is clear that fear reduction occurs across a broad range of
biological organisms (Harris, 1943), there is no single, widely accepted
theory for the mechanism of fear reduction. Over the past century, numerous theories have been advanced and have achieved various degrees of
empirical support. Here, we first provide a brief overview of the basic
models that account for fear acquisition, then we provide a review of several
of the most prominent theories of fear reduction, and finally, we describe
important cutting-edge directions for future research.
We have divided the theories into three broad categories: procedural
models, cognitive models, and neurobiological models. Procedural models,
as defined here, focus primarily on which particular procedures are seen
as most critical for achieving fear reduction. This perspective aligns well
with early work in behaviorism, a movement that focused on observable
procedures and responses. Cognitive models, as defined here, propose that
changes in conscious cognition play a key role in fear reduction. Note that
cognitive models imply the importance of cognitive change as a mechanism,
though cognitive change might be facilitated by behavioral methods (cf.,
Bandura, 1977). The perspective of cognitive models aligns closely with the
cognitive movement and more recent research in psychotherapy. Neurobiological models provide theories on the specific mechanisms of neural
plasticity and the changes of biological systems that are associated with
fear reduction. Behavioral neuroscience and nonhuman animal models of
Emerging Trends in the Social and Behavioral Sciences. Edited by Robert Scott and Stephen Kosslyn.
© 2015 John Wiley & Sons, Inc. ISBN 978-1-118-90077-2.

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

fear reduction have provided the foundation for the development of the
neurobiological models.
“Behavior therapists have had more success in developing clinical treatments
for phobia than in explaining how fear is learned and unlearned.”
—Reiss (1980, p. 380)

FEAR ACQUISITION
Pavlov’s (1927) model of classical conditioning is one of the most important
accounts of fear acquisition. According to this model, fear can be acquired
through pairing an initially neutral stimulus (conditioned stimulus (CS))
with another inherently aversive stimulus (unconditioned stimulus (US)).
For example, in the famous little Albert experiments, young Albert learned
to fear a white rat though classical conditioning (Watson & Rayner, 1920).
At first, Albert showed signs of interest in the rat, but after being repeatedly
presented with a loud noise, the presence of the rat alone elicited distress.
Albert had thus learned to fear the rat, and this fear response generalized
to similar stimuli. Since the little Albert experiments, extensive data have
been gathered through additional studies of Pavlovian conditioning, and
have provided insight into the brain mechanisms of fear acquisition as
well as avenues to reduce the intensity of fear memories. Rodents, such as
rats and mice, are popular choices for studying fear in nonhuman animals
because they are relatively easy to house and care for and have stereotyped
responses that can be easily quantified. Rodent fear can be measured in a
variety of ways, but one of the most popular methods is measuring freezing
behavior, a stereotypical behavioral response to fear in a number of species.
In addition to classical conditioning, many animal models of learning
use paradigms involving indirect measures of fear, such as conditioned
suppression or avoidance behavior. Owing to the focus on fear reduction
mechanisms in this essay, these paradigms will not be reviewed in further
detail. Research has also clearly demonstrated that fear can be acquired
through mechanisms other than classical conditioning, such as vicarious
learning (Askew & Field, 2008). Furthermore, as described by Mowrer’s
(1960) two-factor theory, after the fear is acquired through classical conditioning, it can be maintained by operant conditioning or, specifically, learned
avoidance. When the feared stimulus is confronted and the escape response
follows, escape is negatively reinforced by removal of the feared stimulus
and fear response. The frequency of the avoidance response then reduces
the opportunity for confrontation with the feared stimulus, a procedure that
is central to fear reduction (see the section titled “Procedural Models” for
further details).

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Appropriate fear responses are essential to survival, but this adaptive mechanism sometimes goes awry, and the associated memories are
extremely persistent. As such, reducing fear responses is often a difficult task
both in the laboratory and in clinical settings. Many aspects of animal models
of fear conditioning resemble pathological fear and anxiety conditions seen
in humans (Rosen & Schulkin, 1998; Wolpe, 1981; for review, see Delgado,
Olsson, & Phelps, 2006), so optimizing fear reduction in these models is
critical to our effort to understand and treat fear conditions in the clinic.
FOUNDATIONAL THEORIES OF FEAR REDUCTION
PROCEDURAL MODELS
Extinction. One of the most established approaches to reduce fear is through
extinction trials, as the procedure is called in the animal literature, or through
exposure therapy, as the procedure is called in the psychotherapy literature.
During extinction trials, repeated presentations of the CS in the absence of
the US lead to a progressive decrease in expression of fear of the stimulus
(Bouton & Bolles, 1979; Pavlov, 1927; Rescorla & Heth, 1975). For example, a
fear response to a tone, conditioned through repeated pairing with an electrical shock, can be extinguished by repeatedly presenting the tone without
the shock.
Unfortunately, as initially suggested by Pavlov, extinction procedures do
not seem to modify the original fear memory trace. Instead, extinction trials produce a new, separate, inhibitory memory that is stored in parallel to
the original fear memory (Bouton, 2002; Pavlov, 1927). This is evident at the
behavioral level when the fear response returns through the phenomena of
spontaneous recovery, reinstatement, and renewal. Spontaneous recovery is
brought about by the passage of time; reinstatement is return of fear following a stressful and triggering event; and renewal is the return of fear in
contexts other than the extinction context. Research on neural mechanisms
underlying extinction also suggests that the extinction memory is processed
differently than the original fear memory and serves to inhibit responding to
the original memory (for review, see Quirk, Garcia, & Gonzalex-Lima, 2006).
Reciprocal Inhibition and Counterconditioning. Wolpe (1954) proposed that
fear reduction observed during various psychotherapies could be explained
by the mechanism of reciprocal inhibition. Reciprocal inhibition suggests
that fear reduces when the presentation of a fear-provoking stimulus is
paired with a response that is physiologically incompatible with fear, such
as relaxation induced by a procedure such as progressive muscle relaxation
(Wolpe, 1961). This view was inspired by the law of reciprocal innervation
(Ciuffreda & Stark, 1975), which states that when one muscle is activated,

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

its opposite muscle relaxes automatically to allow for smooth flexing of the
limb. Wolpe (1968) noted that each pairing of the competing response with
the target stimulus would progressively weaken the relationship between
the stimulus and the fear response, resulting in the conditioned inhibition of
fear. This theory led to Wolpe’s development of systematic desensitization,
which consists of graduated, imaginal exposure to a feared stimulus while
maintaining a relaxed state. Wolpe (1968) used the term counterconditioning
interchangeably with reciprocal inhibition. However, others (e.g., Davison,
1968) suggest that counterconditioning is different because it does not
assume an underlying mechanism of physiological incompatibility; instead,
it simply states that through conditioning, the feared stimulus is gradually
paired with a new emotional state (e.g., pleasure, if the feared stimulus is
presented consistently with an enjoyable food; Jones, 1924).
Both of these models fell out of favor when evidence demonstrated that
procedures such as flooding and implosive therapy also led to fear reduction (e.g., Boulougouris, Marks & Marset, 1971; Emmelkamp, 1974; Keane,
Fairbank, Caddell, & Zimering, 1989). In contrast to systematic desensitization, flooding and implosive therapy are not graduated and do not involve
the practice of relaxation during exposure to the feared stimulus. Therefore,
the reciprocal inhibition and counterconditioning models cannot explain the
fear reduction observed after flooding and implosive therapy. Furthermore,
the mechanism of reciprocal inhibition cannot account for fear extinction
observed in animal models.
Habituation. It is important to note that in the literature at large, habituation
is sometimes referred to as a mechanism, and in other cases it is referred to as
an outcome—simply the observed reduction in fear response over. We will
focus our critique on habituation as a mechanism, defined by Harris (1943) as
“response decrement due to repeated stimulation” (p. 387). This theory posits
that repeated stimulation (i.e., repeated presentation of a feared stimulus) is
the central procedure necessary for fear reduction. Similar to reciprocal inhibition, this model was inspired by analogy to a physiological phenomenon.
Specifically, fear reduction is seen as analogous to the refractory period in
the nerve–muscle response, in which the nerve or the muscle is incapable of
response as a result of recent stimulation. The habituation model suggests
that the fear response cannot be maintained indefinitely, so after a prolonged
fear response during confrontation with the feared stimulus, the body will
eventually fatigue and the fear response will temporarily reduce as a result.
Although habituation provides an explanation for the recovery of fear that
can occur after the passage of time (Lader and Mathews, 1968), it cannot
explain the reduction in fear that can last for years after the completion of

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exposure therapy (e.g., Fava et al., 2001). In addition, using the habituation
model to explain long-term fear reduction directly contradicts the finding
that exposure treatment terminated after 50% reduction in fear is not less
effective than treatment terminated after 100% reduction in fear (Rachman,
Robinson, & Lopatka, 1987).
COGNITIVE MODELS
Self-Efficacy. Bandura (1977, 1983) proposed that a key mechanism of fear
reduction (and other psychological changes) across various psychological
treatments involves improvement in self-efficacy, defined as “the conviction that one can successfully execute the behavior required to produce
the [desired] outcomes” (1977, p. 193). Bandura posits that change in
self-efficacy can occur via performance accomplishments (e.g., exposure
therapy), vicarious experience (e.g., witnessing another person confront
the feared stimulus successfully), verbal persuasion (e.g., being told that
one has the skill set to achieve the desired outcome), or emotional arousal
(e.g., noticing that one is not physiologically aroused by a previously feared
situation; Bandura, 1977). As one example of data that corroborate this
theory, higher self-efficacy during confrontation with a feared stimulus
predicts greater approach, and lower subjective and physiological fear
response (e.g., Bandura, Reese & Adams, 1982). Self-efficacy has also been
extended beyond the beliefs about the ability to cope behaviorally, to beliefs
about the ability to cope with thoughts and feelings associated with fear
while in the presence of the feared stimulus (Valentiner, Telch, Petruzzi &
Bolte, 1996). Bandura (1997) provides a thorough review of the model and
the supporting data for self-efficacy theory.
Expectancy Theory and Prediction Error Theory. In his description of
expectancy theory, Reiss (1980) describes that the fear response is an
algebraic sum of danger expectancy (e.g., “the spider will probably bite
me”) and the product of anxiety expectancy (e.g., “being in a room with
a spider will probably make me feel anxious”) with anxiety sensitivity
(e.g., “the feeling of being anxious, itself, makes me anxious”). Note that
anxiety expectancy will have no impact on an individual’s fear response
if the individual does not find the experience of anxiety to be threatening.
On the basis of this model, the fear response should decrease under two
conditions: (i) when the danger expectancy decreases (e.g., someone expects
the spider to bite them, and it does not), and (ii) when the anxiety expectancy
decreases if some level of anxiety sensitivity is present (e.g., one finds the
experience of anxiety to be aversive, and is not as nervous as expected while

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

in the same room as a spider). Reiss (1991) later added other components
to the expectancy model, such as social evaluation expectancy (e.g., “they
will laugh at me when they see that I am anxious”) and social evaluation
sensitivity (e.g., “I will feel very embarrassed when they laugh at me”).
Expectancy theory is directly in line with the prediction error model initially proposed by Rescorla and Wagner (1972). The prediction error model
states that when the disparity between expectations and the occurrence of
events is greater, more learning will occur. For example, when a CS is presented without the US during extinction training, expectation is violated and
learning occurs. The prediction error theory would suggest that the most
learning occurs early in an extinction session, as the mismatch between what
is expected and what actually occurs attenuates across extinction trials.
Emotional Processing Theory. Emotional processing theory, as applied specifically to fear reduction by Foa and Kozak (1986), was based on the foundation
of Lang’s bioinformational theory (1977) and on Rachman’s (1980) proposal
of the emotional processing construct. In their explanation of emotional processing theory, Foa and Kozak acknowledge that some components of fear
memory are not consciously accessible. However, this theory clearly recognizes the role of conscious cognitive processes as mechanisms of change, and
is closely associated with psychotherapy research, and so has been grouped
with the cognitive models.
Foa and Kozak (1986) defined emotional processing as, “the modification
of memory structures that underlie emotions” (p. 20). Borrowing from the
bioinformational account of fear, they stated that fear structures involve
three basic representations: (i) characteristics of the feared stimulus; (ii)
response to the feared stimulus (including verbal, physiological, and behavioral responses); and (iii) interpretive meaning of both the stimulus and the
responses. They describe two key elements of a treatment that modifies the
pathological fear structure: (i) initial activation of the fear structure during
treatment, and (ii) confrontation with, and incorporation of, information
that is incompatible with the fear structure. Finally, they proposed three
signs that emotional processing is occurring (i) initial fear activation, (ii)
within-session habituation, and (iii) between-session habituation.
Foa, Huppert, and Cahill (2006) provided an update of emotional processing theory that incorporates recent research findings. In line with the
evidence for inhibitory learning (see the section titled “New Inhibitory
Learning” for a review), they described that modifying the fear structure
may involve the addition of new learning that completes with old learning,
rather than the elimination or replacement of previous associations in the
fear structure. Furthermore, they recognized that research to date does

Mechanisms of Fear Reduction

7

not provide strong support for the originally posited association between
within-session habituation and emotional processing. They accounted for
this finding by explaining that the critical mechanism of emotional processing is encountering disconfirming information. Therefore, within-session
habituation should only be important for individuals who hold the belief that
their anxiety will continue indefinitely until they escape the feared situation.
Emotional processing theory has been a heavily influential theory, in part,
because of its integrative nature. For example, the habituation, expectancy,
and prediction error models can all be incorporated into emotional processing theory, under the central concept of mechanisms by which disconfirming
information is encountered and/or incorporated. Despite its strengths, emotional processing theory has several areas for continued growth. A review
of the literature conducted by Craske et al. (2008) found that within-session
habituation is not indicative of emotional processing, and that initial fear
activation correlates with emotional processing in some studies but not
others. Foa, Huppert, and Cahill (2006) interpreted this type of evidence
to suggest that proposed correlates of emotional processing (e.g., within
session habituation) may not provide reliable evidence of the emotional
processing. As evidence contrary to the proposed theory begins to emerge,
clearly outlining central components of the theory that are falsifiable will be
crucial to the continued development of innovative and integrative theories
such as emotional processing.
NEUROBIOLOGICAL MODELS
New Inhibitory Learning. New inhibitory learning was proposed as a mechanism of fear reduction to explain the observation that extinguished fear can
later reemerge through processes such as spontaneous recovery, renewal, and
reinstatement. Essentially, extinction training is thought to produce a new
memory (of the feared stimulus as being safe), which acts to suppress the
fear response (Bouton & Swartzentruber, 1991). The original fear association
remains intact and can reemerge whenever the inhibitory memory fails to
activate. It is theorized that the new inhibitory memory is context specific,
so fear is more likely to emerge in contexts dissimilar to those of extinction
training. For example, if a patient successfully extinguished fear of tarantulas
during exposure therapy in their therapist’s office, the patient might experience a return of fear when encountering tarantulas outside the office because
the inhibitory memory might fail to activate. The persistence of the original association in combination with a new inhibitory memory explains why
extinguished fear might later reemerge. Today, this model of fear reduction is
widely accepted by researchers who work with fear models in humans and
other animals (Bouton, 2002; Craske et al., 2008; Foa, Huppert, & Cahill, 2006).

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

Fear Memory Unlearning/Erasure. In the context of psychotherapy, exposure
therapy (also called extinction training) is one of the most empirically
supported methods to reduce fear. However, as explained earlier, inhibitory
learning produced by extinction training is not equivalent to unlearning or
erasure of fear, so it is always possible that the fear response may reemerge
(Bouton, 2002). Other lines of research suggest that certain time windows
leave memories more susceptible to persistent (possibly permanent) disruption. For example, pharmacological agents applied shortly after learning
can prevent consolidation (i.e., strengthening/solidifying) of a fear memory.
Another such window of opportunity is during reconsolidation.
Reconsolidation is a mechanism by which a memory becomes susceptible
for disruption or updating every time it is retrieved. When memory reactivation experiments were in their infancy, the most prominent methods of inducing amnesia after a reactivation for previously learned fear events involved
administering electroconvulsive shock (ECS) or hypothermia after a reactivation of the memory (Mactutus, Riccio, & Ferek, 1979; Misanin, Miller, &
Lewis, 1968).
In 2000, Nader and colleagues performed an important study in which
they convincingly demonstrated that when a memory is retrieved, it enters
a reconsolidation period during which it requires new protein synthesis
before becoming re-encoded into long-term storage. When protein synthesis
is prevented through the infusion of a pharmacological agent, the freezing
response to the CS was drastically reduced the next day. Nader, Schafe
and Le Doux (2000) also showed that the amnesic effect is sensitive to
the time between reactivation and drug injection; 6 hours after retrieval,
the memory is no longer susceptible to pharmacological blockade. This
study reinvigorated a field that had been somewhat dormant for a number
of years. Since Nader et al.’s publication, the number of studies testing
reconsolidation blockade of fear memory has grown exponentially, and
researchers have tested a variety of potential pharmacological agents for this
use (e.g., Duvarci & Nader, 2004). Unlike inhibitory learning, reconsolidation
blockade does not seem to be susceptible to the return of fear in studies
using a number of pharmacological agents.
It is important to add that the strength or age of a memory can influence
whether a reconsolidation-based paradigm can effectively lead to fear reduction (for a review, see Alberini, 2005). Furthermore, although many drugs
are effective in reducing fear to a simple CS during reconsolidation in rodent
studies, those same drugs are often toxic to humans (propranolol being an
exception; Pitman et al., 2002). Therefore, pharmacological reconsolidation
blockade provides an excellent avenue for understanding the mechanisms
of fear memory reconsolidation and for developing animal models of fear
reduction; however, the ability to translate this into a clinical setting remains

Mechanisms of Fear Reduction

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questionable and not without risk (see the section titled “Cutting-Edge
Paradigms”).

COMMENTS ON REVIEWED MODELS
PROCEDURAL MODELS FOR FEAR REDUCTION ARE INSUFFICIENT
Procedural models for fear reduction are insufficient, because each procedure can be described on the level of neurobiological modeling, and
conscious cognitive mechanisms also play an important role. Conscious
cognitive processes probably include processes that are initiated by the
cortex, which may sometimes override more automatic processes, or work
in conjunction with unconscious/automatic processes. However, procedural
models provide an excellent foundation for the investigation of fear reduction mechanisms because they outline the situations in which changes in the
memory trace are most likely to occur. Procedural models can be viewed
as the context in which both unconscious and conscious pathways of fear
reduction operate.

WE ASSUME THERE ARE NEUROBIOLOGICAL MECHANISMS FOR THE COGNITIVE MODELS
DESCRIBED
In a sense, cognitive models could also be deemed insufficient because we
assume that changes in cognitive processes are mediated by neurobiological mechanisms, as with any psychological process. We predict that we will
understand more about the neurobiological models that underlie the changes
in cognitive processes over time, particularly as we develop more sophisticated, noninvasive tools to study neurobiological mechanisms. However, the
neurobiological models involved in updating of cognitive processes are probably so complex and individuated that they are unlikely to replace cognitive
models in a reductionistic manner. It may be more effective to conceptualize
each of these models as representing different levels of understanding or different levels of detail (e.g., understanding change in memory structures on a
macro vs micro level).
CUTTING-EDGE PARADIGMS
With extinction providing a practical but not necessarily permanently
effective method to reduce fear, and reconsolidation blockade providing an
effective but somewhat impractical method for targeting the original fear
memory (owing to the fact that many reconsolidation blocking drugs cannot
be used in humans), a more effective behavioral technique is much desired.

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

FEAR MEMORY UPDATING DURING RECONSOLIDATION
Monfils, Cowansage, Klann, and LeDoux (2009) addressed this issue by
combining the strengths of both reconsolidation and extinction methods into
a behavioral paradigm to permanently reduce fear. In this paradigm, they
found that using extinction training during the reconsolidation window
allows for a persistent updating of the memory and prevents the return of
fear. Similar to previous experiments that attempted to reduce fear after a
reactivation session, Monfils et al. (2009) found that the effectiveness of the
retrieval+extinction paradigm was restricted to a specific temporal range
between the retrieval and the extinction session. A number of additional
studies have since been published, most of which have replicated the
retrieval+extinction effect described by Monfils et al. (e.g., Clem & Huganir,
2010; Rao-Ruiz et al., 2011; but see Chan, Leung, Westbrook, & McNally,
2010). It should also be noted that extinction applied shortly after fear
conditioning (before consolidation) has also shown success in preventing
the return of fear (Myers, Ressler, & Davis, 2006; see Chang & Maren, 2009).
The retrieval+extinction technique allows for a behavioral paradigm to permanently attenuate fear expression to a conditioned CS in a manner that does
not involve drugs or surgery by slightly modifying the timing between the
first and the second presentation of the CS (e.g., conducting the retrieval
trial, which is the first CS presentation, between 10 min and 1 h prior to
extinction training). This method has also been successful in extinguishing
shock-conditioned fear in humans (Schiller et al., 2010). Owing to the fact that
the retrieval+extinction might prevent the return of fear using a protocol that
is methodologically similar to exposure therapy, there is significant enthusiasm from a number of clinicians in translating the initial findings into therapeutic avenues (see also Graff et al., 2014—an important recent study that
combines the retrieval+extinction approach with a pharmacological manipulation to successfully target older memories in rodents).
CONCLUSIONS AND FUTURE DIRECTIONS
Although some of the tools we have at our disposal are effective in decreasing fear responding, it is clear that they do not work in all cases, and even for
those in which they work, return of fear is often a concern. Moving forward,
we need to better identify the parameters in which various mechanisms operate. For example, under what conditions are inhibitory learning, reconsolidation update, or both operating as the mechanisms of fear reduction?
We should also seek to understand the influence of individual differences
on the mechanisms of fear reduction. This returns to the much-repeated
question, “What treatment works best for whom, and why?” but adds an
emphasis on the possible biomarkers and/or a priori neural states that could

Mechanisms of Fear Reduction

11

predispose an individual to responding optimally to one approach rather
than another.
Ultimately, to effectively agree on a theory of what models and/or mechanisms best underlie fear reduction, we will also need to agree on an acceptable determinant for the said reduction. One determinant, and arguably the
one that ultimately matters most, is subjective decrease in fear. Still, while
evidence suggests that more than one type of approach may be successful in
reducing fear, it is clear that early success of treatment (either within the treatment session or shortly after treatment) does not always reflect the long-term
outcome. As such, developing additional means (e.g., physiological, behavioral, neural, or otherwise) of identifying long-term predictors of fear reduction will be crucial.
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CYNTHIA L. LANCASTER SHORT BIOGRAPHY
Cynthia L. Lancaster received her bachelor’s degree from Trinity University, where she completed a study on the topic of mirror exposure for body
image dissatisfaction. She then worked as a research assistant at the University of Texas Health Science Center at San Antonio, primarily studying the
etiology and treatment of posttraumatic stress disorder in active duty military personnel. She is currently in the clinical psychology doctoral program
at the University of Texas at Austin, where she studies the mechanisms and
augmentation of exposure therapy for anxiety disorders.
MARIE-H. MONFILS SHORT BIOGRAPHY
Marie-H. Monfils is an assistant professor in the Department of Psychology
at the University of Texas at Austin. She received her PhD in behavioral neuroscience from the Canadian Centre for Behavioural Neuroscience, under
the supervision of Bryan Kolb and Jeffrey Kleim, and her master’s degree
from the University of Calgary with Cam Teskey. She conducted a postdoctoral fellowship at New York University in Joseph LeDoux’s laboratory. Her
laboratory is currently pursuing three research streams: (i) investigating postconsolidation manipulations that can persistently attenuate fear memories,
(ii) isolating the mechanisms that underlie social transmission of fear, and
(iii) examining the interactions between early experience and fear learning in
adulthood. More details about the Monfils Fear Memory Lab may be found at
http://homepage.psy.utexas.edu/HomePage/Group/MonfilsLAB/Site/
Monfils_Lab.html.
RELATED ESSAYS
What Is Neuroticism, and Can We Treat It? (Psychology), Amantia Ametaj
et al.
Aggression and Victimization (Psychology), Sheri Bauman and Aryn Taylor

Mechanisms of Fear Reduction

15

Delusions (Psychology), Max Coltheart
Depression (Psychology), Ian H. Gotlib and Daniella J. Furman
Positive Emotion Disturbance (Psychology), June Gruber and John Purcell
Mental Imagery in Psychological Disorders (Psychology), Emily A. Holmes
et al.
Normal Negative Emotions and Mental Disorders (Sociology), Allan V.
Horwitz
Dissociation and Dissociative Identity Disorder (DID) (Psychology), Rafaële
J. C. Huntjens and Martin J. Dorahy
Computer Technology and Children’s Mental Health (Psychology), Philip C.
Kendall et al.
Understanding Risk-Taking Behavior: Insights from Evolutionary Psychology (Psychology), Karin Machluf and David F. Bjorklund
Evolutionary Perspectives on Animal and Human Personality (Anthropology), Joseph H. Manson and Lynn A. Fairbanks
Disorders of Consciousness (Psychology), Martin M. Monti
Cognitive Remediation in Schizophrenia (Psychology), Clare Reeder and Til
Wykes
Cognitive Bias Modification in Mental (Psychology), Meg M. Reuland et al.
Clarifying the Nature and Structure of Personality Disorder (Psychology),
Takakuni Suzuki and Douglas B. Samuel
Rumination (Psychology), Edward R. Watkins
Emotion Regulation (Psychology), Paree Zarolia et al.



Mechanisms of Fear Reduction
CYNTHIA L. LANCASTER and MARIE-H. MONFILS

Abstract
Over the past century, numerous theories have been advanced toward a unified
account of fear reduction and have achieved various degrees of empirical support.
Here, we first provide a brief overview of the basic models that account for fear
acquisition, then we provide a review of several of the most prominent theories of
fear reduction, and finally, we describe important cutting-edge directions for future
research.

Although it is clear that fear reduction occurs across a broad range of
biological organisms (Harris, 1943), there is no single, widely accepted
theory for the mechanism of fear reduction. Over the past century, numerous theories have been advanced and have achieved various degrees of
empirical support. Here, we first provide a brief overview of the basic
models that account for fear acquisition, then we provide a review of several
of the most prominent theories of fear reduction, and finally, we describe
important cutting-edge directions for future research.
We have divided the theories into three broad categories: procedural
models, cognitive models, and neurobiological models. Procedural models,
as defined here, focus primarily on which particular procedures are seen
as most critical for achieving fear reduction. This perspective aligns well
with early work in behaviorism, a movement that focused on observable
procedures and responses. Cognitive models, as defined here, propose that
changes in conscious cognition play a key role in fear reduction. Note that
cognitive models imply the importance of cognitive change as a mechanism,
though cognitive change might be facilitated by behavioral methods (cf.,
Bandura, 1977). The perspective of cognitive models aligns closely with the
cognitive movement and more recent research in psychotherapy. Neurobiological models provide theories on the specific mechanisms of neural
plasticity and the changes of biological systems that are associated with
fear reduction. Behavioral neuroscience and nonhuman animal models of
Emerging Trends in the Social and Behavioral Sciences. Edited by Robert Scott and Stephen Kosslyn.
© 2015 John Wiley & Sons, Inc. ISBN 978-1-118-90077-2.

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

fear reduction have provided the foundation for the development of the
neurobiological models.
“Behavior therapists have had more success in developing clinical treatments
for phobia than in explaining how fear is learned and unlearned.”
—Reiss (1980, p. 380)

FEAR ACQUISITION
Pavlov’s (1927) model of classical conditioning is one of the most important
accounts of fear acquisition. According to this model, fear can be acquired
through pairing an initially neutral stimulus (conditioned stimulus (CS))
with another inherently aversive stimulus (unconditioned stimulus (US)).
For example, in the famous little Albert experiments, young Albert learned
to fear a white rat though classical conditioning (Watson & Rayner, 1920).
At first, Albert showed signs of interest in the rat, but after being repeatedly
presented with a loud noise, the presence of the rat alone elicited distress.
Albert had thus learned to fear the rat, and this fear response generalized
to similar stimuli. Since the little Albert experiments, extensive data have
been gathered through additional studies of Pavlovian conditioning, and
have provided insight into the brain mechanisms of fear acquisition as
well as avenues to reduce the intensity of fear memories. Rodents, such as
rats and mice, are popular choices for studying fear in nonhuman animals
because they are relatively easy to house and care for and have stereotyped
responses that can be easily quantified. Rodent fear can be measured in a
variety of ways, but one of the most popular methods is measuring freezing
behavior, a stereotypical behavioral response to fear in a number of species.
In addition to classical conditioning, many animal models of learning
use paradigms involving indirect measures of fear, such as conditioned
suppression or avoidance behavior. Owing to the focus on fear reduction
mechanisms in this essay, these paradigms will not be reviewed in further
detail. Research has also clearly demonstrated that fear can be acquired
through mechanisms other than classical conditioning, such as vicarious
learning (Askew & Field, 2008). Furthermore, as described by Mowrer’s
(1960) two-factor theory, after the fear is acquired through classical conditioning, it can be maintained by operant conditioning or, specifically, learned
avoidance. When the feared stimulus is confronted and the escape response
follows, escape is negatively reinforced by removal of the feared stimulus
and fear response. The frequency of the avoidance response then reduces
the opportunity for confrontation with the feared stimulus, a procedure that
is central to fear reduction (see the section titled “Procedural Models” for
further details).

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3

Appropriate fear responses are essential to survival, but this adaptive mechanism sometimes goes awry, and the associated memories are
extremely persistent. As such, reducing fear responses is often a difficult task
both in the laboratory and in clinical settings. Many aspects of animal models
of fear conditioning resemble pathological fear and anxiety conditions seen
in humans (Rosen & Schulkin, 1998; Wolpe, 1981; for review, see Delgado,
Olsson, & Phelps, 2006), so optimizing fear reduction in these models is
critical to our effort to understand and treat fear conditions in the clinic.
FOUNDATIONAL THEORIES OF FEAR REDUCTION
PROCEDURAL MODELS
Extinction. One of the most established approaches to reduce fear is through
extinction trials, as the procedure is called in the animal literature, or through
exposure therapy, as the procedure is called in the psychotherapy literature.
During extinction trials, repeated presentations of the CS in the absence of
the US lead to a progressive decrease in expression of fear of the stimulus
(Bouton & Bolles, 1979; Pavlov, 1927; Rescorla & Heth, 1975). For example, a
fear response to a tone, conditioned through repeated pairing with an electrical shock, can be extinguished by repeatedly presenting the tone without
the shock.
Unfortunately, as initially suggested by Pavlov, extinction procedures do
not seem to modify the original fear memory trace. Instead, extinction trials produce a new, separate, inhibitory memory that is stored in parallel to
the original fear memory (Bouton, 2002; Pavlov, 1927). This is evident at the
behavioral level when the fear response returns through the phenomena of
spontaneous recovery, reinstatement, and renewal. Spontaneous recovery is
brought about by the passage of time; reinstatement is return of fear following a stressful and triggering event; and renewal is the return of fear in
contexts other than the extinction context. Research on neural mechanisms
underlying extinction also suggests that the extinction memory is processed
differently than the original fear memory and serves to inhibit responding to
the original memory (for review, see Quirk, Garcia, & Gonzalex-Lima, 2006).
Reciprocal Inhibition and Counterconditioning. Wolpe (1954) proposed that
fear reduction observed during various psychotherapies could be explained
by the mechanism of reciprocal inhibition. Reciprocal inhibition suggests
that fear reduces when the presentation of a fear-provoking stimulus is
paired with a response that is physiologically incompatible with fear, such
as relaxation induced by a procedure such as progressive muscle relaxation
(Wolpe, 1961). This view was inspired by the law of reciprocal innervation
(Ciuffreda & Stark, 1975), which states that when one muscle is activated,

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its opposite muscle relaxes automatically to allow for smooth flexing of the
limb. Wolpe (1968) noted that each pairing of the competing response with
the target stimulus would progressively weaken the relationship between
the stimulus and the fear response, resulting in the conditioned inhibition of
fear. This theory led to Wolpe’s development of systematic desensitization,
which consists of graduated, imaginal exposure to a feared stimulus while
maintaining a relaxed state. Wolpe (1968) used the term counterconditioning
interchangeably with reciprocal inhibition. However, others (e.g., Davison,
1968) suggest that counterconditioning is different because it does not
assume an underlying mechanism of physiological incompatibility; instead,
it simply states that through conditioning, the feared stimulus is gradually
paired with a new emotional state (e.g., pleasure, if the feared stimulus is
presented consistently with an enjoyable food; Jones, 1924).
Both of these models fell out of favor when evidence demonstrated that
procedures such as flooding and implosive therapy also led to fear reduction (e.g., Boulougouris, Marks & Marset, 1971; Emmelkamp, 1974; Keane,
Fairbank, Caddell, & Zimering, 1989). In contrast to systematic desensitization, flooding and implosive therapy are not graduated and do not involve
the practice of relaxation during exposure to the feared stimulus. Therefore,
the reciprocal inhibition and counterconditioning models cannot explain the
fear reduction observed after flooding and implosive therapy. Furthermore,
the mechanism of reciprocal inhibition cannot account for fear extinction
observed in animal models.
Habituation. It is important to note that in the literature at large, habituation
is sometimes referred to as a mechanism, and in other cases it is referred to as
an outcome—simply the observed reduction in fear response over. We will
focus our critique on habituation as a mechanism, defined by Harris (1943) as
“response decrement due to repeated stimulation” (p. 387). This theory posits
that repeated stimulation (i.e., repeated presentation of a feared stimulus) is
the central procedure necessary for fear reduction. Similar to reciprocal inhibition, this model was inspired by analogy to a physiological phenomenon.
Specifically, fear reduction is seen as analogous to the refractory period in
the nerve–muscle response, in which the nerve or the muscle is incapable of
response as a result of recent stimulation. The habituation model suggests
that the fear response cannot be maintained indefinitely, so after a prolonged
fear response during confrontation with the feared stimulus, the body will
eventually fatigue and the fear response will temporarily reduce as a result.
Although habituation provides an explanation for the recovery of fear that
can occur after the passage of time (Lader and Mathews, 1968), it cannot
explain the reduction in fear that can last for years after the completion of

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exposure therapy (e.g., Fava et al., 2001). In addition, using the habituation
model to explain long-term fear reduction directly contradicts the finding
that exposure treatment terminated after 50% reduction in fear is not less
effective than treatment terminated after 100% reduction in fear (Rachman,
Robinson, & Lopatka, 1987).
COGNITIVE MODELS
Self-Efficacy. Bandura (1977, 1983) proposed that a key mechanism of fear
reduction (and other psychological changes) across various psychological
treatments involves improvement in self-efficacy, defined as “the conviction that one can successfully execute the behavior required to produce
the [desired] outcomes” (1977, p. 193). Bandura posits that change in
self-efficacy can occur via performance accomplishments (e.g., exposure
therapy), vicarious experience (e.g., witnessing another person confront
the feared stimulus successfully), verbal persuasion (e.g., being told that
one has the skill set to achieve the desired outcome), or emotional arousal
(e.g., noticing that one is not physiologically aroused by a previously feared
situation; Bandura, 1977). As one example of data that corroborate this
theory, higher self-efficacy during confrontation with a feared stimulus
predicts greater approach, and lower subjective and physiological fear
response (e.g., Bandura, Reese & Adams, 1982). Self-efficacy has also been
extended beyond the beliefs about the ability to cope behaviorally, to beliefs
about the ability to cope with thoughts and feelings associated with fear
while in the presence of the feared stimulus (Valentiner, Telch, Petruzzi &
Bolte, 1996). Bandura (1997) provides a thorough review of the model and
the supporting data for self-efficacy theory.
Expectancy Theory and Prediction Error Theory. In his description of
expectancy theory, Reiss (1980) describes that the fear response is an
algebraic sum of danger expectancy (e.g., “the spider will probably bite
me”) and the product of anxiety expectancy (e.g., “being in a room with
a spider will probably make me feel anxious”) with anxiety sensitivity
(e.g., “the feeling of being anxious, itself, makes me anxious”). Note that
anxiety expectancy will have no impact on an individual’s fear response
if the individual does not find the experience of anxiety to be threatening.
On the basis of this model, the fear response should decrease under two
conditions: (i) when the danger expectancy decreases (e.g., someone expects
the spider to bite them, and it does not), and (ii) when the anxiety expectancy
decreases if some level of anxiety sensitivity is present (e.g., one finds the
experience of anxiety to be aversive, and is not as nervous as expected while

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

in the same room as a spider). Reiss (1991) later added other components
to the expectancy model, such as social evaluation expectancy (e.g., “they
will laugh at me when they see that I am anxious”) and social evaluation
sensitivity (e.g., “I will feel very embarrassed when they laugh at me”).
Expectancy theory is directly in line with the prediction error model initially proposed by Rescorla and Wagner (1972). The prediction error model
states that when the disparity between expectations and the occurrence of
events is greater, more learning will occur. For example, when a CS is presented without the US during extinction training, expectation is violated and
learning occurs. The prediction error theory would suggest that the most
learning occurs early in an extinction session, as the mismatch between what
is expected and what actually occurs attenuates across extinction trials.
Emotional Processing Theory. Emotional processing theory, as applied specifically to fear reduction by Foa and Kozak (1986), was based on the foundation
of Lang’s bioinformational theory (1977) and on Rachman’s (1980) proposal
of the emotional processing construct. In their explanation of emotional processing theory, Foa and Kozak acknowledge that some components of fear
memory are not consciously accessible. However, this theory clearly recognizes the role of conscious cognitive processes as mechanisms of change, and
is closely associated with psychotherapy research, and so has been grouped
with the cognitive models.
Foa and Kozak (1986) defined emotional processing as, “the modification
of memory structures that underlie emotions” (p. 20). Borrowing from the
bioinformational account of fear, they stated that fear structures involve
three basic representations: (i) characteristics of the feared stimulus; (ii)
response to the feared stimulus (including verbal, physiological, and behavioral responses); and (iii) interpretive meaning of both the stimulus and the
responses. They describe two key elements of a treatment that modifies the
pathological fear structure: (i) initial activation of the fear structure during
treatment, and (ii) confrontation with, and incorporation of, information
that is incompatible with the fear structure. Finally, they proposed three
signs that emotional processing is occurring (i) initial fear activation, (ii)
within-session habituation, and (iii) between-session habituation.
Foa, Huppert, and Cahill (2006) provided an update of emotional processing theory that incorporates recent research findings. In line with the
evidence for inhibitory learning (see the section titled “New Inhibitory
Learning” for a review), they described that modifying the fear structure
may involve the addition of new learning that completes with old learning,
rather than the elimination or replacement of previous associations in the
fear structure. Furthermore, they recognized that research to date does

Mechanisms of Fear Reduction

7

not provide strong support for the originally posited association between
within-session habituation and emotional processing. They accounted for
this finding by explaining that the critical mechanism of emotional processing is encountering disconfirming information. Therefore, within-session
habituation should only be important for individuals who hold the belief that
their anxiety will continue indefinitely until they escape the feared situation.
Emotional processing theory has been a heavily influential theory, in part,
because of its integrative nature. For example, the habituation, expectancy,
and prediction error models can all be incorporated into emotional processing theory, under the central concept of mechanisms by which disconfirming
information is encountered and/or incorporated. Despite its strengths, emotional processing theory has several areas for continued growth. A review
of the literature conducted by Craske et al. (2008) found that within-session
habituation is not indicative of emotional processing, and that initial fear
activation correlates with emotional processing in some studies but not
others. Foa, Huppert, and Cahill (2006) interpreted this type of evidence
to suggest that proposed correlates of emotional processing (e.g., within
session habituation) may not provide reliable evidence of the emotional
processing. As evidence contrary to the proposed theory begins to emerge,
clearly outlining central components of the theory that are falsifiable will be
crucial to the continued development of innovative and integrative theories
such as emotional processing.
NEUROBIOLOGICAL MODELS
New Inhibitory Learning. New inhibitory learning was proposed as a mechanism of fear reduction to explain the observation that extinguished fear can
later reemerge through processes such as spontaneous recovery, renewal, and
reinstatement. Essentially, extinction training is thought to produce a new
memory (of the feared stimulus as being safe), which acts to suppress the
fear response (Bouton & Swartzentruber, 1991). The original fear association
remains intact and can reemerge whenever the inhibitory memory fails to
activate. It is theorized that the new inhibitory memory is context specific,
so fear is more likely to emerge in contexts dissimilar to those of extinction
training. For example, if a patient successfully extinguished fear of tarantulas
during exposure therapy in their therapist’s office, the patient might experience a return of fear when encountering tarantulas outside the office because
the inhibitory memory might fail to activate. The persistence of the original association in combination with a new inhibitory memory explains why
extinguished fear might later reemerge. Today, this model of fear reduction is
widely accepted by researchers who work with fear models in humans and
other animals (Bouton, 2002; Craske et al., 2008; Foa, Huppert, & Cahill, 2006).

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

Fear Memory Unlearning/Erasure. In the context of psychotherapy, exposure
therapy (also called extinction training) is one of the most empirically
supported methods to reduce fear. However, as explained earlier, inhibitory
learning produced by extinction training is not equivalent to unlearning or
erasure of fear, so it is always possible that the fear response may reemerge
(Bouton, 2002). Other lines of research suggest that certain time windows
leave memories more susceptible to persistent (possibly permanent) disruption. For example, pharmacological agents applied shortly after learning
can prevent consolidation (i.e., strengthening/solidifying) of a fear memory.
Another such window of opportunity is during reconsolidation.
Reconsolidation is a mechanism by which a memory becomes susceptible
for disruption or updating every time it is retrieved. When memory reactivation experiments were in their infancy, the most prominent methods of inducing amnesia after a reactivation for previously learned fear events involved
administering electroconvulsive shock (ECS) or hypothermia after a reactivation of the memory (Mactutus, Riccio, & Ferek, 1979; Misanin, Miller, &
Lewis, 1968).
In 2000, Nader and colleagues performed an important study in which
they convincingly demonstrated that when a memory is retrieved, it enters
a reconsolidation period during which it requires new protein synthesis
before becoming re-encoded into long-term storage. When protein synthesis
is prevented through the infusion of a pharmacological agent, the freezing
response to the CS was drastically reduced the next day. Nader, Schafe
and Le Doux (2000) also showed that the amnesic effect is sensitive to
the time between reactivation and drug injection; 6 hours after retrieval,
the memory is no longer susceptible to pharmacological blockade. This
study reinvigorated a field that had been somewhat dormant for a number
of years. Since Nader et al.’s publication, the number of studies testing
reconsolidation blockade of fear memory has grown exponentially, and
researchers have tested a variety of potential pharmacological agents for this
use (e.g., Duvarci & Nader, 2004). Unlike inhibitory learning, reconsolidation
blockade does not seem to be susceptible to the return of fear in studies
using a number of pharmacological agents.
It is important to add that the strength or age of a memory can influence
whether a reconsolidation-based paradigm can effectively lead to fear reduction (for a review, see Alberini, 2005). Furthermore, although many drugs
are effective in reducing fear to a simple CS during reconsolidation in rodent
studies, those same drugs are often toxic to humans (propranolol being an
exception; Pitman et al., 2002). Therefore, pharmacological reconsolidation
blockade provides an excellent avenue for understanding the mechanisms
of fear memory reconsolidation and for developing animal models of fear
reduction; however, the ability to translate this into a clinical setting remains

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9

questionable and not without risk (see the section titled “Cutting-Edge
Paradigms”).

COMMENTS ON REVIEWED MODELS
PROCEDURAL MODELS FOR FEAR REDUCTION ARE INSUFFICIENT
Procedural models for fear reduction are insufficient, because each procedure can be described on the level of neurobiological modeling, and
conscious cognitive mechanisms also play an important role. Conscious
cognitive processes probably include processes that are initiated by the
cortex, which may sometimes override more automatic processes, or work
in conjunction with unconscious/automatic processes. However, procedural
models provide an excellent foundation for the investigation of fear reduction mechanisms because they outline the situations in which changes in the
memory trace are most likely to occur. Procedural models can be viewed
as the context in which both unconscious and conscious pathways of fear
reduction operate.

WE ASSUME THERE ARE NEUROBIOLOGICAL MECHANISMS FOR THE COGNITIVE MODELS
DESCRIBED
In a sense, cognitive models could also be deemed insufficient because we
assume that changes in cognitive processes are mediated by neurobiological mechanisms, as with any psychological process. We predict that we will
understand more about the neurobiological models that underlie the changes
in cognitive processes over time, particularly as we develop more sophisticated, noninvasive tools to study neurobiological mechanisms. However, the
neurobiological models involved in updating of cognitive processes are probably so complex and individuated that they are unlikely to replace cognitive
models in a reductionistic manner. It may be more effective to conceptualize
each of these models as representing different levels of understanding or different levels of detail (e.g., understanding change in memory structures on a
macro vs micro level).
CUTTING-EDGE PARADIGMS
With extinction providing a practical but not necessarily permanently
effective method to reduce fear, and reconsolidation blockade providing an
effective but somewhat impractical method for targeting the original fear
memory (owing to the fact that many reconsolidation blocking drugs cannot
be used in humans), a more effective behavioral technique is much desired.

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FEAR MEMORY UPDATING DURING RECONSOLIDATION
Monfils, Cowansage, Klann, and LeDoux (2009) addressed this issue by
combining the strengths of both reconsolidation and extinction methods into
a behavioral paradigm to permanently reduce fear. In this paradigm, they
found that using extinction training during the reconsolidation window
allows for a persistent updating of the memory and prevents the return of
fear. Similar to previous experiments that attempted to reduce fear after a
reactivation session, Monfils et al. (2009) found that the effectiveness of the
retrieval+extinction paradigm was restricted to a specific temporal range
between the retrieval and the extinction session. A number of additional
studies have since been published, most of which have replicated the
retrieval+extinction effect described by Monfils et al. (e.g., Clem & Huganir,
2010; Rao-Ruiz et al., 2011; but see Chan, Leung, Westbrook, & McNally,
2010). It should also be noted that extinction applied shortly after fear
conditioning (before consolidation) has also shown success in preventing
the return of fear (Myers, Ressler, & Davis, 2006; see Chang & Maren, 2009).
The retrieval+extinction technique allows for a behavioral paradigm to permanently attenuate fear expression to a conditioned CS in a manner that does
not involve drugs or surgery by slightly modifying the timing between the
first and the second presentation of the CS (e.g., conducting the retrieval
trial, which is the first CS presentation, between 10 min and 1 h prior to
extinction training). This method has also been successful in extinguishing
shock-conditioned fear in humans (Schiller et al., 2010). Owing to the fact that
the retrieval+extinction might prevent the return of fear using a protocol that
is methodologically similar to exposure therapy, there is significant enthusiasm from a number of clinicians in translating the initial findings into therapeutic avenues (see also Graff et al., 2014—an important recent study that
combines the retrieval+extinction approach with a pharmacological manipulation to successfully target older memories in rodents).
CONCLUSIONS AND FUTURE DIRECTIONS
Although some of the tools we have at our disposal are effective in decreasing fear responding, it is clear that they do not work in all cases, and even for
those in which they work, return of fear is often a concern. Moving forward,
we need to better identify the parameters in which various mechanisms operate. For example, under what conditions are inhibitory learning, reconsolidation update, or both operating as the mechanisms of fear reduction?
We should also seek to understand the influence of individual differences
on the mechanisms of fear reduction. This returns to the much-repeated
question, “What treatment works best for whom, and why?” but adds an
emphasis on the possible biomarkers and/or a priori neural states that could

Mechanisms of Fear Reduction

11

predispose an individual to responding optimally to one approach rather
than another.
Ultimately, to effectively agree on a theory of what models and/or mechanisms best underlie fear reduction, we will also need to agree on an acceptable determinant for the said reduction. One determinant, and arguably the
one that ultimately matters most, is subjective decrease in fear. Still, while
evidence suggests that more than one type of approach may be successful in
reducing fear, it is clear that early success of treatment (either within the treatment session or shortly after treatment) does not always reflect the long-term
outcome. As such, developing additional means (e.g., physiological, behavioral, neural, or otherwise) of identifying long-term predictors of fear reduction will be crucial.
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CYNTHIA L. LANCASTER SHORT BIOGRAPHY
Cynthia L. Lancaster received her bachelor’s degree from Trinity University, where she completed a study on the topic of mirror exposure for body
image dissatisfaction. She then worked as a research assistant at the University of Texas Health Science Center at San Antonio, primarily studying the
etiology and treatment of posttraumatic stress disorder in active duty military personnel. She is currently in the clinical psychology doctoral program
at the University of Texas at Austin, where she studies the mechanisms and
augmentation of exposure therapy for anxiety disorders.
MARIE-H. MONFILS SHORT BIOGRAPHY
Marie-H. Monfils is an assistant professor in the Department of Psychology
at the University of Texas at Austin. She received her PhD in behavioral neuroscience from the Canadian Centre for Behavioural Neuroscience, under
the supervision of Bryan Kolb and Jeffrey Kleim, and her master’s degree
from the University of Calgary with Cam Teskey. She conducted a postdoctoral fellowship at New York University in Joseph LeDoux’s laboratory. Her
laboratory is currently pursuing three research streams: (i) investigating postconsolidation manipulations that can persistently attenuate fear memories,
(ii) isolating the mechanisms that underlie social transmission of fear, and
(iii) examining the interactions between early experience and fear learning in
adulthood. More details about the Monfils Fear Memory Lab may be found at
http://homepage.psy.utexas.edu/HomePage/Group/MonfilsLAB/Site/
Monfils_Lab.html.
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et al.
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Mechanisms of Fear Reduction

15

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J. C. Huntjens and Martin J. Dorahy
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Kendall et al.
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Mechanisms of Fear Reduction
CYNTHIA L. LANCASTER and MARIE-H. MONFILS

Abstract
Over the past century, numerous theories have been advanced toward a unified
account of fear reduction and have achieved various degrees of empirical support.
Here, we first provide a brief overview of the basic models that account for fear
acquisition, then we provide a review of several of the most prominent theories of
fear reduction, and finally, we describe important cutting-edge directions for future
research.

Although it is clear that fear reduction occurs across a broad range of
biological organisms (Harris, 1943), there is no single, widely accepted
theory for the mechanism of fear reduction. Over the past century, numerous theories have been advanced and have achieved various degrees of
empirical support. Here, we first provide a brief overview of the basic
models that account for fear acquisition, then we provide a review of several
of the most prominent theories of fear reduction, and finally, we describe
important cutting-edge directions for future research.
We have divided the theories into three broad categories: procedural
models, cognitive models, and neurobiological models. Procedural models,
as defined here, focus primarily on which particular procedures are seen
as most critical for achieving fear reduction. This perspective aligns well
with early work in behaviorism, a movement that focused on observable
procedures and responses. Cognitive models, as defined here, propose that
changes in conscious cognition play a key role in fear reduction. Note that
cognitive models imply the importance of cognitive change as a mechanism,
though cognitive change might be facilitated by behavioral methods (cf.,
Bandura, 1977). The perspective of cognitive models aligns closely with the
cognitive movement and more recent research in psychotherapy. Neurobiological models provide theories on the specific mechanisms of neural
plasticity and the changes of biological systems that are associated with
fear reduction. Behavioral neuroscience and nonhuman animal models of
Emerging Trends in the Social and Behavioral Sciences. Edited by Robert Scott and Stephen Kosslyn.
© 2015 John Wiley & Sons, Inc. ISBN 978-1-118-90077-2.

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

fear reduction have provided the foundation for the development of the
neurobiological models.
“Behavior therapists have had more success in developing clinical treatments
for phobia than in explaining how fear is learned and unlearned.”
—Reiss (1980, p. 380)

FEAR ACQUISITION
Pavlov’s (1927) model of classical conditioning is one of the most important
accounts of fear acquisition. According to this model, fear can be acquired
through pairing an initially neutral stimulus (conditioned stimulus (CS))
with another inherently aversive stimulus (unconditioned stimulus (US)).
For example, in the famous little Albert experiments, young Albert learned
to fear a white rat though classical conditioning (Watson & Rayner, 1920).
At first, Albert showed signs of interest in the rat, but after being repeatedly
presented with a loud noise, the presence of the rat alone elicited distress.
Albert had thus learned to fear the rat, and this fear response generalized
to similar stimuli. Since the little Albert experiments, extensive data have
been gathered through additional studies of Pavlovian conditioning, and
have provided insight into the brain mechanisms of fear acquisition as
well as avenues to reduce the intensity of fear memories. Rodents, such as
rats and mice, are popular choices for studying fear in nonhuman animals
because they are relatively easy to house and care for and have stereotyped
responses that can be easily quantified. Rodent fear can be measured in a
variety of ways, but one of the most popular methods is measuring freezing
behavior, a stereotypical behavioral response to fear in a number of species.
In addition to classical conditioning, many animal models of learning
use paradigms involving indirect measures of fear, such as conditioned
suppression or avoidance behavior. Owing to the focus on fear reduction
mechanisms in this essay, these paradigms will not be reviewed in further
detail. Research has also clearly demonstrated that fear can be acquired
through mechanisms other than classical conditioning, such as vicarious
learning (Askew & Field, 2008). Furthermore, as described by Mowrer’s
(1960) two-factor theory, after the fear is acquired through classical conditioning, it can be maintained by operant conditioning or, specifically, learned
avoidance. When the feared stimulus is confronted and the escape response
follows, escape is negatively reinforced by removal of the feared stimulus
and fear response. The frequency of the avoidance response then reduces
the opportunity for confrontation with the feared stimulus, a procedure that
is central to fear reduction (see the section titled “Procedural Models” for
further details).

Mechanisms of Fear Reduction

3

Appropriate fear responses are essential to survival, but this adaptive mechanism sometimes goes awry, and the associated memories are
extremely persistent. As such, reducing fear responses is often a difficult task
both in the laboratory and in clinical settings. Many aspects of animal models
of fear conditioning resemble pathological fear and anxiety conditions seen
in humans (Rosen & Schulkin, 1998; Wolpe, 1981; for review, see Delgado,
Olsson, & Phelps, 2006), so optimizing fear reduction in these models is
critical to our effort to understand and treat fear conditions in the clinic.
FOUNDATIONAL THEORIES OF FEAR REDUCTION
PROCEDURAL MODELS
Extinction. One of the most established approaches to reduce fear is through
extinction trials, as the procedure is called in the animal literature, or through
exposure therapy, as the procedure is called in the psychotherapy literature.
During extinction trials, repeated presentations of the CS in the absence of
the US lead to a progressive decrease in expression of fear of the stimulus
(Bouton & Bolles, 1979; Pavlov, 1927; Rescorla & Heth, 1975). For example, a
fear response to a tone, conditioned through repeated pairing with an electrical shock, can be extinguished by repeatedly presenting the tone without
the shock.
Unfortunately, as initially suggested by Pavlov, extinction procedures do
not seem to modify the original fear memory trace. Instead, extinction trials produce a new, separate, inhibitory memory that is stored in parallel to
the original fear memory (Bouton, 2002; Pavlov, 1927). This is evident at the
behavioral level when the fear response returns through the phenomena of
spontaneous recovery, reinstatement, and renewal. Spontaneous recovery is
brought about by the passage of time; reinstatement is return of fear following a stressful and triggering event; and renewal is the return of fear in
contexts other than the extinction context. Research on neural mechanisms
underlying extinction also suggests that the extinction memory is processed
differently than the original fear memory and serves to inhibit responding to
the original memory (for review, see Quirk, Garcia, & Gonzalex-Lima, 2006).
Reciprocal Inhibition and Counterconditioning. Wolpe (1954) proposed that
fear reduction observed during various psychotherapies could be explained
by the mechanism of reciprocal inhibition. Reciprocal inhibition suggests
that fear reduces when the presentation of a fear-provoking stimulus is
paired with a response that is physiologically incompatible with fear, such
as relaxation induced by a procedure such as progressive muscle relaxation
(Wolpe, 1961). This view was inspired by the law of reciprocal innervation
(Ciuffreda & Stark, 1975), which states that when one muscle is activated,

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

its opposite muscle relaxes automatically to allow for smooth flexing of the
limb. Wolpe (1968) noted that each pairing of the competing response with
the target stimulus would progressively weaken the relationship between
the stimulus and the fear response, resulting in the conditioned inhibition of
fear. This theory led to Wolpe’s development of systematic desensitization,
which consists of graduated, imaginal exposure to a feared stimulus while
maintaining a relaxed state. Wolpe (1968) used the term counterconditioning
interchangeably with reciprocal inhibition. However, others (e.g., Davison,
1968) suggest that counterconditioning is different because it does not
assume an underlying mechanism of physiological incompatibility; instead,
it simply states that through conditioning, the feared stimulus is gradually
paired with a new emotional state (e.g., pleasure, if the feared stimulus is
presented consistently with an enjoyable food; Jones, 1924).
Both of these models fell out of favor when evidence demonstrated that
procedures such as flooding and implosive therapy also led to fear reduction (e.g., Boulougouris, Marks & Marset, 1971; Emmelkamp, 1974; Keane,
Fairbank, Caddell, & Zimering, 1989). In contrast to systematic desensitization, flooding and implosive therapy are not graduated and do not involve
the practice of relaxation during exposure to the feared stimulus. Therefore,
the reciprocal inhibition and counterconditioning models cannot explain the
fear reduction observed after flooding and implosive therapy. Furthermore,
the mechanism of reciprocal inhibition cannot account for fear extinction
observed in animal models.
Habituation. It is important to note that in the literature at large, habituation
is sometimes referred to as a mechanism, and in other cases it is referred to as
an outcome—simply the observed reduction in fear response over. We will
focus our critique on habituation as a mechanism, defined by Harris (1943) as
“response decrement due to repeated stimulation” (p. 387). This theory posits
that repeated stimulation (i.e., repeated presentation of a feared stimulus) is
the central procedure necessary for fear reduction. Similar to reciprocal inhibition, this model was inspired by analogy to a physiological phenomenon.
Specifically, fear reduction is seen as analogous to the refractory period in
the nerve–muscle response, in which the nerve or the muscle is incapable of
response as a result of recent stimulation. The habituation model suggests
that the fear response cannot be maintained indefinitely, so after a prolonged
fear response during confrontation with the feared stimulus, the body will
eventually fatigue and the fear response will temporarily reduce as a result.
Although habituation provides an explanation for the recovery of fear that
can occur after the passage of time (Lader and Mathews, 1968), it cannot
explain the reduction in fear that can last for years after the completion of

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exposure therapy (e.g., Fava et al., 2001). In addition, using the habituation
model to explain long-term fear reduction directly contradicts the finding
that exposure treatment terminated after 50% reduction in fear is not less
effective than treatment terminated after 100% reduction in fear (Rachman,
Robinson, & Lopatka, 1987).
COGNITIVE MODELS
Self-Efficacy. Bandura (1977, 1983) proposed that a key mechanism of fear
reduction (and other psychological changes) across various psychological
treatments involves improvement in self-efficacy, defined as “the conviction that one can successfully execute the behavior required to produce
the [desired] outcomes” (1977, p. 193). Bandura posits that change in
self-efficacy can occur via performance accomplishments (e.g., exposure
therapy), vicarious experience (e.g., witnessing another person confront
the feared stimulus successfully), verbal persuasion (e.g., being told that
one has the skill set to achieve the desired outcome), or emotional arousal
(e.g., noticing that one is not physiologically aroused by a previously feared
situation; Bandura, 1977). As one example of data that corroborate this
theory, higher self-efficacy during confrontation with a feared stimulus
predicts greater approach, and lower subjective and physiological fear
response (e.g., Bandura, Reese & Adams, 1982). Self-efficacy has also been
extended beyond the beliefs about the ability to cope behaviorally, to beliefs
about the ability to cope with thoughts and feelings associated with fear
while in the presence of the feared stimulus (Valentiner, Telch, Petruzzi &
Bolte, 1996). Bandura (1997) provides a thorough review of the model and
the supporting data for self-efficacy theory.
Expectancy Theory and Prediction Error Theory. In his description of
expectancy theory, Reiss (1980) describes that the fear response is an
algebraic sum of danger expectancy (e.g., “the spider will probably bite
me”) and the product of anxiety expectancy (e.g., “being in a room with
a spider will probably make me feel anxious”) with anxiety sensitivity
(e.g., “the feeling of being anxious, itself, makes me anxious”). Note that
anxiety expectancy will have no impact on an individual’s fear response
if the individual does not find the experience of anxiety to be threatening.
On the basis of this model, the fear response should decrease under two
conditions: (i) when the danger expectancy decreases (e.g., someone expects
the spider to bite them, and it does not), and (ii) when the anxiety expectancy
decreases if some level of anxiety sensitivity is present (e.g., one finds the
experience of anxiety to be aversive, and is not as nervous as expected while

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

in the same room as a spider). Reiss (1991) later added other components
to the expectancy model, such as social evaluation expectancy (e.g., “they
will laugh at me when they see that I am anxious”) and social evaluation
sensitivity (e.g., “I will feel very embarrassed when they laugh at me”).
Expectancy theory is directly in line with the prediction error model initially proposed by Rescorla and Wagner (1972). The prediction error model
states that when the disparity between expectations and the occurrence of
events is greater, more learning will occur. For example, when a CS is presented without the US during extinction training, expectation is violated and
learning occurs. The prediction error theory would suggest that the most
learning occurs early in an extinction session, as the mismatch between what
is expected and what actually occurs attenuates across extinction trials.
Emotional Processing Theory. Emotional processing theory, as applied specifically to fear reduction by Foa and Kozak (1986), was based on the foundation
of Lang’s bioinformational theory (1977) and on Rachman’s (1980) proposal
of the emotional processing construct. In their explanation of emotional processing theory, Foa and Kozak acknowledge that some components of fear
memory are not consciously accessible. However, this theory clearly recognizes the role of conscious cognitive processes as mechanisms of change, and
is closely associated with psychotherapy research, and so has been grouped
with the cognitive models.
Foa and Kozak (1986) defined emotional processing as, “the modification
of memory structures that underlie emotions” (p. 20). Borrowing from the
bioinformational account of fear, they stated that fear structures involve
three basic representations: (i) characteristics of the feared stimulus; (ii)
response to the feared stimulus (including verbal, physiological, and behavioral responses); and (iii) interpretive meaning of both the stimulus and the
responses. They describe two key elements of a treatment that modifies the
pathological fear structure: (i) initial activation of the fear structure during
treatment, and (ii) confrontation with, and incorporation of, information
that is incompatible with the fear structure. Finally, they proposed three
signs that emotional processing is occurring (i) initial fear activation, (ii)
within-session habituation, and (iii) between-session habituation.
Foa, Huppert, and Cahill (2006) provided an update of emotional processing theory that incorporates recent research findings. In line with the
evidence for inhibitory learning (see the section titled “New Inhibitory
Learning” for a review), they described that modifying the fear structure
may involve the addition of new learning that completes with old learning,
rather than the elimination or replacement of previous associations in the
fear structure. Furthermore, they recognized that research to date does

Mechanisms of Fear Reduction

7

not provide strong support for the originally posited association between
within-session habituation and emotional processing. They accounted for
this finding by explaining that the critical mechanism of emotional processing is encountering disconfirming information. Therefore, within-session
habituation should only be important for individuals who hold the belief that
their anxiety will continue indefinitely until they escape the feared situation.
Emotional processing theory has been a heavily influential theory, in part,
because of its integrative nature. For example, the habituation, expectancy,
and prediction error models can all be incorporated into emotional processing theory, under the central concept of mechanisms by which disconfirming
information is encountered and/or incorporated. Despite its strengths, emotional processing theory has several areas for continued growth. A review
of the literature conducted by Craske et al. (2008) found that within-session
habituation is not indicative of emotional processing, and that initial fear
activation correlates with emotional processing in some studies but not
others. Foa, Huppert, and Cahill (2006) interpreted this type of evidence
to suggest that proposed correlates of emotional processing (e.g., within
session habituation) may not provide reliable evidence of the emotional
processing. As evidence contrary to the proposed theory begins to emerge,
clearly outlining central components of the theory that are falsifiable will be
crucial to the continued development of innovative and integrative theories
such as emotional processing.
NEUROBIOLOGICAL MODELS
New Inhibitory Learning. New inhibitory learning was proposed as a mechanism of fear reduction to explain the observation that extinguished fear can
later reemerge through processes such as spontaneous recovery, renewal, and
reinstatement. Essentially, extinction training is thought to produce a new
memory (of the feared stimulus as being safe), which acts to suppress the
fear response (Bouton & Swartzentruber, 1991). The original fear association
remains intact and can reemerge whenever the inhibitory memory fails to
activate. It is theorized that the new inhibitory memory is context specific,
so fear is more likely to emerge in contexts dissimilar to those of extinction
training. For example, if a patient successfully extinguished fear of tarantulas
during exposure therapy in their therapist’s office, the patient might experience a return of fear when encountering tarantulas outside the office because
the inhibitory memory might fail to activate. The persistence of the original association in combination with a new inhibitory memory explains why
extinguished fear might later reemerge. Today, this model of fear reduction is
widely accepted by researchers who work with fear models in humans and
other animals (Bouton, 2002; Craske et al., 2008; Foa, Huppert, & Cahill, 2006).

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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

Fear Memory Unlearning/Erasure. In the context of psychotherapy, exposure
therapy (also called extinction training) is one of the most empirically
supported methods to reduce fear. However, as explained earlier, inhibitory
learning produced by extinction training is not equivalent to unlearning or
erasure of fear, so it is always possible that the fear response may reemerge
(Bouton, 2002). Other lines of research suggest that certain time windows
leave memories more susceptible to persistent (possibly permanent) disruption. For example, pharmacological agents applied shortly after learning
can prevent consolidation (i.e., strengthening/solidifying) of a fear memory.
Another such window of opportunity is during reconsolidation.
Reconsolidation is a mechanism by which a memory becomes susceptible
for disruption or updating every time it is retrieved. When memory reactivation experiments were in their infancy, the most prominent methods of inducing amnesia after a reactivation for previously learned fear events involved
administering electroconvulsive shock (ECS) or hypothermia after a reactivation of the memory (Mactutus, Riccio, & Ferek, 1979; Misanin, Miller, &
Lewis, 1968).
In 2000, Nader and colleagues performed an important study in which
they convincingly demonstrated that when a memory is retrieved, it enters
a reconsolidation period during which it requires new protein synthesis
before becoming re-encoded into long-term storage. When protein synthesis
is prevented through the infusion of a pharmacological agent, the freezing
response to the CS was drastically reduced the next day. Nader, Schafe
and Le Doux (2000) also showed that the amnesic effect is sensitive to
the time between reactivation and drug injection; 6 hours after retrieval,
the memory is no longer susceptible to pharmacological blockade. This
study reinvigorated a field that had been somewhat dormant for a number
of years. Since Nader et al.’s publication, the number of studies testing
reconsolidation blockade of fear memory has grown exponentially, and
researchers have tested a variety of potential pharmacological agents for this
use (e.g., Duvarci & Nader, 2004). Unlike inhibitory learning, reconsolidation
blockade does not seem to be susceptible to the return of fear in studies
using a number of pharmacological agents.
It is important to add that the strength or age of a memory can influence
whether a reconsolidation-based paradigm can effectively lead to fear reduction (for a review, see Alberini, 2005). Furthermore, although many drugs
are effective in reducing fear to a simple CS during reconsolidation in rodent
studies, those same drugs are often toxic to humans (propranolol being an
exception; Pitman et al., 2002). Therefore, pharmacological reconsolidation
blockade provides an excellent avenue for understanding the mechanisms
of fear memory reconsolidation and for developing animal models of fear
reduction; however, the ability to translate this into a clinical setting remains

Mechanisms of Fear Reduction

9

questionable and not without risk (see the section titled “Cutting-Edge
Paradigms”).

COMMENTS ON REVIEWED MODELS
PROCEDURAL MODELS FOR FEAR REDUCTION ARE INSUFFICIENT
Procedural models for fear reduction are insufficient, because each procedure can be described on the level of neurobiological modeling, and
conscious cognitive mechanisms also play an important role. Conscious
cognitive processes probably include processes that are initiated by the
cortex, which may sometimes override more automatic processes, or work
in conjunction with unconscious/automatic processes. However, procedural
models provide an excellent foundation for the investigation of fear reduction mechanisms because they outline the situations in which changes in the
memory trace are most likely to occur. Procedural models can be viewed
as the context in which both unconscious and conscious pathways of fear
reduction operate.

WE ASSUME THERE ARE NEUROBIOLOGICAL MECHANISMS FOR THE COGNITIVE MODELS
DESCRIBED
In a sense, cognitive models could also be deemed insufficient because we
assume that changes in cognitive processes are mediated by neurobiological mechanisms, as with any psychological process. We predict that we will
understand more about the neurobiological models that underlie the changes
in cognitive processes over time, particularly as we develop more sophisticated, noninvasive tools to study neurobiological mechanisms. However, the
neurobiological models involved in updating of cognitive processes are probably so complex and individuated that they are unlikely to replace cognitive
models in a reductionistic manner. It may be more effective to conceptualize
each of these models as representing different levels of understanding or different levels of detail (e.g., understanding change in memory structures on a
macro vs micro level).
CUTTING-EDGE PARADIGMS
With extinction providing a practical but not necessarily permanently
effective method to reduce fear, and reconsolidation blockade providing an
effective but somewhat impractical method for targeting the original fear
memory (owing to the fact that many reconsolidation blocking drugs cannot
be used in humans), a more effective behavioral technique is much desired.

10

EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES

FEAR MEMORY UPDATING DURING RECONSOLIDATION
Monfils, Cowansage, Klann, and LeDoux (2009) addressed this issue by
combining the strengths of both reconsolidation and extinction methods into
a behavioral paradigm to permanently reduce fear. In this paradigm, they
found that using extinction training during the reconsolidation window
allows for a persistent updating of the memory and prevents the return of
fear. Similar to previous experiments that attempted to reduce fear after a
reactivation session, Monfils et al. (2009) found that the effectiveness of the
retrieval+extinction paradigm was restricted to a specific temporal range
between the retrieval and the extinction session. A number of additional
studies have since been published, most of which have replicated the
retrieval+extinction effect described by Monfils et al. (e.g., Clem & Huganir,
2010; Rao-Ruiz et al., 2011; but see Chan, Leung, Westbrook, & McNally,
2010). It should also be noted that extinction applied shortly after fear
conditioning (before consolidation) has also shown success in preventing
the return of fear (Myers, Ressler, & Davis, 2006; see Chang & Maren, 2009).
The retrieval+extinction technique allows for a behavioral paradigm to permanently attenuate fear expression to a conditioned CS in a manner that does
not involve drugs or surgery by slightly modifying the timing between the
first and the second presentation of the CS (e.g., conducting the retrieval
trial, which is the first CS presentation, between 10 min and 1 h prior to
extinction training). This method has also been successful in extinguishing
shock-conditioned fear in humans (Schiller et al., 2010). Owing to the fact that
the retrieval+extinction might prevent the return of fear using a protocol that
is methodologically similar to exposure therapy, there is significant enthusiasm from a number of clinicians in translating the initial findings into therapeutic avenues (see also Graff et al., 2014—an important recent study that
combines the retrieval+extinction approach with a pharmacological manipulation to successfully target older memories in rodents).
CONCLUSIONS AND FUTURE DIRECTIONS
Although some of the tools we have at our disposal are effective in decreasing fear responding, it is clear that they do not work in all cases, and even for
those in which they work, return of fear is often a concern. Moving forward,
we need to better identify the parameters in which various mechanisms operate. For example, under what conditions are inhibitory learning, reconsolidation update, or both operating as the mechanisms of fear reduction?
We should also seek to understand the influence of individual differences
on the mechanisms of fear reduction. This returns to the much-repeated
question, “What treatment works best for whom, and why?” but adds an
emphasis on the possible biomarkers and/or a priori neural states that could

Mechanisms of Fear Reduction

11

predispose an individual to responding optimally to one approach rather
than another.
Ultimately, to effectively agree on a theory of what models and/or mechanisms best underlie fear reduction, we will also need to agree on an acceptable determinant for the said reduction. One determinant, and arguably the
one that ultimately matters most, is subjective decrease in fear. Still, while
evidence suggests that more than one type of approach may be successful in
reducing fear, it is clear that early success of treatment (either within the treatment session or shortly after treatment) does not always reflect the long-term
outcome. As such, developing additional means (e.g., physiological, behavioral, neural, or otherwise) of identifying long-term predictors of fear reduction will be crucial.
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CYNTHIA L. LANCASTER SHORT BIOGRAPHY
Cynthia L. Lancaster received her bachelor’s degree from Trinity University, where she completed a study on the topic of mirror exposure for body
image dissatisfaction. She then worked as a research assistant at the University of Texas Health Science Center at San Antonio, primarily studying the
etiology and treatment of posttraumatic stress disorder in active duty military personnel. She is currently in the clinical psychology doctoral program
at the University of Texas at Austin, where she studies the mechanisms and
augmentation of exposure therapy for anxiety disorders.
MARIE-H. MONFILS SHORT BIOGRAPHY
Marie-H. Monfils is an assistant professor in the Department of Psychology
at the University of Texas at Austin. She received her PhD in behavioral neuroscience from the Canadian Centre for Behavioural Neuroscience, under
the supervision of Bryan Kolb and Jeffrey Kleim, and her master’s degree
from the University of Calgary with Cam Teskey. She conducted a postdoctoral fellowship at New York University in Joseph LeDoux’s laboratory. Her
laboratory is currently pursuing three research streams: (i) investigating postconsolidation manipulations that can persistently attenuate fear memories,
(ii) isolating the mechanisms that underlie social transmission of fear, and
(iii) examining the interactions between early experience and fear learning in
adulthood. More details about the Monfils Fear Memory Lab may be found at
http://homepage.psy.utexas.edu/HomePage/Group/MonfilsLAB/Site/
Monfils_Lab.html.
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Mechanisms of Fear Reduction