Fear and the Brain

Author(s): Jacek Debiec and Joseph LeDoux

Source: Social Research , WINTER 2004, Vol. 71, No. 4, FEAR: ITS POLITICAL USES &
ABUSES (WINTER 2004), pp. 807-818
Published by: The Johns Hopkins University Press

Stable URL: https://www.jstor.org/stable/40971979

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 Jacek Debiec and
Joseph LeDoux
Fear and the Brain

FEAR IS A NATURAL PART OF LIFE. IT OCCURS WHENEVER WE ARE THREATENED.

Threats come in many forms. A snake on the ground in front of yo

biologically prepared threat, and so is being face-to-face with an an
human. Evolution has put this kind of information into our brains
way of dealing with recurring and common themes. When we enc
ter them we have the familiar fight/flight response. But not all th
are genetically programmed. Most of the things that make us afrai
things we have learned about in our lives.
Biological research over the past two decades has made consid
able progress in understanding how the brain learns about danger.
of this work has been conducted in animals. For some people, word
"biological," "brain," and "animals" imply genetic predetermina
But this is not true. First of all, biological does not mean genetic. Nurtu
is just as much a part of biology as nature. The research we will des
in this paper in fact is all about how we learn to be afraid through
rience. Second, it is important to realize that the brain is a rich s
of information about human nature. By studying psychology thr
the brain, we can discover things about the mind that we cannot
by studying the mind alone. Third, much of the progress in unders
ing the brain basis of psychological functions has come from studi
animals . This is certainly true of fear. While animals are not people
brain and body of animals, like rats, respond similarly to the hum
brain and body when threatened. Muscles tense. Blood pressure ri
Stress hormones are released. This is all part of the physiological

social research Vol 71 : No 4 : Winter 2004 807

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tion of how to rapidly deal with a threat. These responses, however, can
also occur in anticipation of something that might happen - in which
case we tend to call it anxiety rather than fear.
What does the tension of muscles or the rise of blood pressure in
a rat have to do with fearful feelings in humans? Actually, quite a lot.
Every animal has to have the ability to detect and respond to threats.
Otherwise, it could not make it through the day. This is the job of the
brain's defense system. However, a subjective feeling of fear can only
occur in animals that have the capacity to be aware of their own brain's
activities. Fear, in other words, is the feeling that results when the
defense system is active in a brain that has the capacity for self-aware-
ness. This undoubtedly occurs in humans. Whether it occurs in other
creatures is not known, and may be unknowable. But if activation of
the defense system is a key component of the neural basis of fearful
feelings, and the defense system works similarly in rats and people,
then studies of the defense system in rats tells us about an important
system underlying human feelings of fear.
Even without this theoretical link to fearful feelings, studies of
fear behavior in rats are still important. This work, as we will see, has
identified a brain region called the amygdala that is essential for fear
learning in rats. This same region is known to be altered in fear disor-
ders in humans, including post-traumatic stress disorder (PTSD), panic
disorder, and phobia, as well as other conditions, including depression,
autism, and schizophrenia. We will summarize in this paper some of
what has been discovered about the defense system through studies of
fear learning in rats.

HOW IS FEAR LEARNING STUDIED IN RATS?

Much work on fear has involved fear conditioning, a variant on

conditioning procedures developed by Pavlov (1927). In fear condit
ing a relatively neutral event (a conditioned stimulus, CS), such as
or light, is paired with an aversive event (an unconditioned stimul
US), such as electric shock. After pairing with the US, the CS acquir
ability to elicit behavioral, autonomie, and endocrine responses. Th

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responses are expressed automatically in the presence of danger. Fear
conditioning occurs in a variety of species, ranging from flies, worms,
and snails to fish, reptiles, and birds to mammals, including people.
Several aspects of learned fear are important to keep in mind as
we explore the neural basis of this form of learning. First, fear condition-
ing occurs quickly. Quite often, a single CS-US pairing is sufficient to
establish a memory. In the wild, rapid identification of a threat followed
by efficient behaviors boosts chances of survival. Second, once acquired,
fear learning remains accessible throughout the life of an animal.
Survival is also enhanced if danger, once learned about, does not have to
be relearned. Third, defensive responses to stimuli previously associated
with physical harm sometimes weaken through experiences that show
that the stimulus is no longer harmful. However, the original learning
can often be recovered either spontaneously or as a result of stressful
events months or years after they have been weakened. Fourth, fear
motivates other kinds of behaviors, such as avoidance and approach.
Once these behaviors get ingrained, they become part of their own real-
ity, determining the behavioral patterns of an individual.

HOW DOES FEAR CONDITIONING WORK IN THE BRAIN?

The anatomical pathways underlying the acquisition of condit

fear have been extensively studied in recent years. Much of the ev
comes from studies involving the auditory modality (auditory
conditioning) in rats, which we will focus on here. Information a
the conditioned stimulus is transmitted through the sensory pat
to the thalamus and cortex, and from each of these brain region
the amygdala. These two independent sensory inputs into the am
dala are differentially involved in fear processing (LeDoux, 1996)
"low road" or thalamic pathway provides the amygdala with a rapi
imprecise representation of the sensory input, while the cortical
or "high road" conveys a more complex representation based on c
cal computations.
The amygdala (the Latin word for almond) was named after
almond-shape by the anatomist Burdach in 1819. It is located

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inside the temporal lobe and consists of several distinct groups of cells
organized in nuclei. Numerous studies have led to the conclusion that
damage to the amygdala interferes with the acquisition and expression
of conditioned fear. It does not matter what kind of stimulus you use
to turn the amygdala on, it does not matter what kind of response you
measure as fear response, and it does not matter what kind of animal
you do the experiment on, as long as that animal has an amygdala, the
amygdala is involved in fear processing. The regions of most relevance
to fear conditioning are the lateral (LA), basal (B), accessory basal (AB),
and central (CE) nuclei of the amygdala.
The LA is responsible for linking the information about the
neutral tone with that of the US (usually a mild shock to animal's feet),
which is conveyed through the nociceptive or pain pathways. The LA,
in turn, sends fibers to the CE, which projects to a variety of structures
in the brain controlling fear behaviors and accompanying autonomie
and endocrine responses. The CE also receives efferents from the basal
and accessory basal nuclei, which in turn receive inputs from LA. But
in addition to providing an additional link between LA and CE, these
receive inputs from higher cortical areas. For example, connections
from the hippocampus to B and AB may convey information about the
spatial context in which the CS and US occur.
A key aspect of memory formation during fear conditioning
involves the convergence of information about the auditory CS and the
nociceptive US in the LA. Through this pairing, the tone gains access to
the emotional response circuits controlled by CE.
Recent studies also provide some insight into the cellular and
molecular mechanisms underlying fear conditioning (for a summary
see LeDoux, 2002; Blair et al., 2001; Schafe et al., 2001; Maren, 2001).
When individual cells that process the CS are simultaneously activated
by the strong US, the processing of the CS in LA is modified in such a
way that it more effectively drives the output cells that control fear
responses. This plasticity of CS processing is triggered by the entry
of calcium into synapses on the distal dendrites of LA cells through
two sources: the NMDA class of glutamate receptors and voltage-gated

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calacium channels. The resulting elevation in calcium, in turn, leads
to the activation of certain protein kinases (especially calcium/calmdu-
lin kinase, mitogen activated kinase, and protein kinase A). These then
move into the cell nucleus and lead to gene expression and protein
synthesis. The proteins are then shipped back to the recently active
synapses, where they lead to a strengthening of the ability of the CS
inputs to activate those synapses. This process of memory formation is
commonly referred to as memory consolidation (McGaugh, 2000).
The traditional view of memory consolidation is based on the idea
of protein synthesis. In this model of learning, we store information
and then, each time we retrieve information, we are retrieving what we
initially learned. However, a new perspective of memory has emerged
from recent studies. According to these developments, whenever the
memory is retrieved it renders protein synthesis dependent again and
undergoes re -consolidation (Nader, Schafe, and LeDoux, 2000; Debiec,
LeDoux, and Nader, 2002). In this view, we learn, we store, we retrieve,
and when we retrieve the next time, we are not retrieving the original
experience - we are retrieving our last retrieval. In other words, upon
retrieval a new memory is formed. It has been proposed that the major
role of reconsolidation is to strengthen or to update the memory (Sara,
2000; Dudai, 2004). The discovery of these dynamic processes may help
to explain why the memory is vulnerable to the experience we have
in the meantime. Furthermore, it paves the way for selective memory
manipulation in patients suffering from debilitating, intrusive memo-
ries of trauma.

WHAT ARE THE IMPLICATIONS OF FEAR LEARNING IN THE

RAT BRAIN FOR NORMAL AND PATHOLOGICAL HUMAN
FEAR?

A growing number of studies have also suggested an importan

of the amygdala in human fear. Damage to areas of temporal
including the amygdala (LaBar et al., 1995) or to the amygdala
(Bechara et al., 1995) impairs fear conditioning in humans. B
imaging studies of the human brain demonstrate increased f

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tional activity of the amygdala during fear conditioning (LaBar et al.,
1998; Morris, Buchel, and Dolan, 2001). Recent work suggests that this
augmented firing correlates with activity in the thalamus but not the
cortex (Morris and Dolan, 2004; Pasley, Mayes, and Schultz, 2004). The
thalamic input into the amygdala thus appears to play an essential role
in fear processing in humans, as it does in animals. It has important
implications for our understanding of fear. While the "high" cortical
route is generally believed to be necessary for conscious identification
of the stimuli, the "low road" conveys rough information sufficient
and critical to trigger fear responses beyond the grasp of conscious
awareness. Imaging studies also reveal that subliminal presentations
of dreadful stimuli lead to stronger activations in the amygdala than
do explicit threads (Whalen et al., 1998).
While the amygdala is implied in fear learning and the stor-
age of implicit fear memory, the hippocampus is thought to be a part
of the system, which is responsible for the acquisition of declarative
memory in the human brain (Phelps, 2004). Thus, a person with selec-
tive damage to the amygdala and with an intact hippocampus fails to
acquire conditioned responses to fearful stimuli, but does learn the facts
about conditioning, while damage to the hippocampus alone impairs
explicit learning, but not implicit fear acquisition (Bechara et al., 1995).
Distinct systems in the human brain are involved in learning and stor-
age of declarative and implicit knowledge about dangerous events.
Furthermore, the underlying brain structures, the amygdala, and the
hippocampus differently respond to stress. Chronic exposure to stress
leads to the atrophy of hippocampal neurons (McEwen, 1999) and to
the hypertrophy of the amygdala (Vyas et al., 2002). These findings may
account for several behavioral manifestations. Individuals who suffered

from severe traumatic experiences can sometimes develop amnesia

for the event but at the same time they may have enhanced emotional
responsiveness to the trauma-related stimuli.
Clinical studies reveal the importance of the amygdala in
emotional life. Specifically, the amygdala has been implicated in several
fear disorders in humans, including PTSD, specific and social phobia,

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and panic disorder, as well as in major depression and schizophrenia
(Gorman et al, 2000; Pitman, Shin, and Rauch, 2001; Kent and Rauch,
2003). Therefore, it has been proposed that the neural circuits of normal
fear are malfunctional in fear disorders, and that similar malfunctions

may account for the overlapping symptoms and frequent comorbidity

of psychopathological conditions (Stahl, 2003).
However, the amygdala is not the only region involved in fear
regulation. Experiments in rats have implicated the medial prefrontal
cortex in extinguishing fear conditioning responses (Morgan, Romanski,
and LeDoux, 1993; Milad and Quirk, 2002). Based on animal models,
PTSD, a condition characterized by persistent, intrusive re-experiencing
of past traumatic events, has been considered to be a result of a failure
of cortical inhibition over the hyperactive amygdala (Shin et al., 2004).
Indeed, recent brain-imaging studies of PTSD subjects demonstrate
hyperactivity of the amygdala and hypoactivity of the medial prefron-
tal regions in response to fearful stimuli (Shin et al., 2004; Gilboa et
al. 2004). Stress-induced alterations in medial prefrontal cortex might
predispose certain individuals to learn fear in a way that is later diffi-
cult to extinguish (LeDoux, 2000).

CAN WE LEARN ABOUT THE POLITICAL USES OF FEAR

FROM STUDIES OF FEAR LEARNING IN THE BRAIN?

Politics involves social relations, authority, power, and decis

making. There is no question that fear can contribute to these phen
ena. Fear has been traditionally recognized as one of the fundame
forces that shape human life. According to Thomas Hobbes, fear a
shared emotion was even a grounding point for public life (Ho
1996). Hobbes believed that having control over human fears m
holding power in the society. Although Hobbesian philosophy has
critically revised (Blits, 1989), the intersections of fear and politics
remain a significant field of interest (Robin, 2004).
How then can brain studies contribute to our understanding
the political uses of fear? Although the humanities and natural scie
using different theoretical backgrounds and methodologies, an

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distinct levels of organization, there are some specific domains, where
different fields of study converge (Debiec and LeDoux, 2003). Fear and
fear-related phenomena constitute such a domain. We will summarize
some of the recent developments in brain sciences presented in this
discussion that might have implications for further studies of fear and
politics.
Experimental research depicts the predominant role of the
"lower," subcortical route in fear processing. As a result, initiation of
behavioral, autonomie, and endocrine responses associated with fear
precedes thoughts in threatening situations. This suggests that fear
and associated emotions by nature may affect our psychological and
social life before they can be consciously controlled. Moreover, the
anatomical and functional dissociation between implicit and explicit
fear learning, which involves different systems (implicit fear learning
involves the amygdala; explicit fear learning involves the hippocampus
and prefrontal cortex) explains how it is possible that in some cases
the way we rationalize our fears differs from what really causes us to
be afraid and to consciously experience fear. Such misattributions may
help relieve emotional arousal but at the same time can also distract
attention from actual sources of threat and harm.

Animal studies point to the persistent character of the memories

for fear as compared to other kinds of memories. Defensive reactions to
stimuli previously associated with physical threat, even if weakened by
experiences throughout life, can recover spontaneously or in the face
of stressful events. This may explain how dreadful events remain a part
of our selfhood. Past traumas experienced by individuals and groups are
a significant factor influencing current and future social interactions.
In this respect, history becomes an important aspect and a powerful
instrument in politics.
Recent studies of neural bases of memory show that retrieved
memories undergo reconsolidation and may be not only weakened by
pharmacological manipulations but also strengthened by personal expe-
rience. This suggests that instilling fear for political purposes can have
significant and lasting, perhaps traumatic, consequences. Fortunately,

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new ways of treatment of traumatic and other detrimental memories,
such as these occurring in PTSD, have been proposed (Nader, Schafe,
and LeDoux, 2000; Charney, 2004). Yet, ethical questions remain as to
how far we should go in interfering with past memories (Miller, 2004).
Scientific progress cannot proceed in a social vacuum.
Although Hobbes felt fear was a constituent element of social life,
one of the defined goals of public policy is to reduce fear (Weisburd and
Eck, 2004). Unfortunately, politicians do not always seek to achieve this
goal. Too often (recent times being a particularly germane instance), fear
is used to further political aims. Brain science tells us that fears, once
learned, are powerful forces in the brain, and should not be instilled
casually. As we learn more about the brain mechanisms of fear, we will
discover new ways of controlling and eliminating pathological fears.
Hopefully, we can find ways to use these ethically, and if so, that in
coming years we will not need to extensively use these new treatments
to ameliorate politically instilled fears.

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