Through various animal species have
different behavioural responses to danger, the central
role of the amygdala in the fear response seems to have been
very well preserved in all of them. The earliest experiments,
in which the amygdala was removed, demonstrated that its absence
interfered tremendously with an animal’s ability to assess
danger. Later experiments, in which electrical stimuli were
applied to the amygdala, repeatedly generated the same well-known
defence reactions (bodily changes, inhibition, flight, defensive
attack) in several different species of mammals.
As with the hippocampus, most of the
neural pathways that enter the amygdala are paired with other
pathways that exit it. One of these output pathways is the ventral
amygdalofugal pathway, which plays an important role
in associative learning–of a conditioned fear, for
example. The gratifying or aversive nature of a stimulus
is associated by connections of this pathway to the nucleus
accumbens, which plays a recognized role in the brain’s
pleasure circuits. The other main destinations of this
pathway are the ventral striatum, the septum, the hypothalamus,
the nuclei of the brainstem, and certain parts of the cortex
(orbitofrontal, piriform, cingulate, etc.).
pathway emerging from the amygdala is the stria terminalis,
which is to the amygdala as the
fornix is to the hippocampus. Like the fornix, the stria
terminalis projects only to sub-cortical structures such as the
hypothalamus and the septum. The hypothalamus and the septum
also receive projections from the amygdala by another route–the
ventral amygdalofugal pathway–as well as from the hippocampus.
Moreover, the hippocampus and the amygdala are located beside
and have many connections with each other.
The basal ganglia, a group of sub-cortical
nuclei, are another area of the brain that seems to be closely involved
in voluntary emotional activity. The basal ganglia are known to be
involved in controlling movement, and their interaction with the
amygdala supports this active, voluntary component of the behavioural
expression of emotion.
Meanwhile, the automatic bodily responses involved
in emotions such as fear are controlled mainly by the outputs of
the amygdala to the nuclei of the sympathetic nervous system in the
brainstem and to the hypothalamus, which itself controls the hormonal
secretions of the pituitary gland.
The outputs of the amygdala
provide a good idea of what is necessary for the experience
of an emotion such as fear. The connections from the amygdala
to the cortex can influence attention to and perception and
memory of dangerous situations. The amygdala can also influence
the cortex indirectly, through its connections to the attention
system in the brainstem. Other parts of the brainstem trigger
the cascade of physiological reactions associated with fear
that send feedback to the brain. When this feedback is combined
memory with the other “ingredients” just described,
it produces the feeling of experiencing an emotion.
Because both of these systems are activated
by the same memory indexes, we do not realize that they are
actually specialized. But certain experiments and pathological
case studies have highlighted their independence.
For example, one woman had suffered
such severe damage to her hippocampi that she could not recognize
her doctor, even though she saw him every day. Every day,
they shook hands and introduced themselves as if for the
first time. One day, to test a hunch, the doctor placed a
thumbtack in the palm of his hand before extending it to
his patient. When she saw it, she pulled her hand back suddenly.
The next day, when she and the doctor were about to shake
hands again, she pulled her hand back at the last minute.
When the doctor asked her why she had done so, the only explanation
she could give was that she had experienced a sudden sense
THE TWO PATHWAYS
When the brain receives a sensory stimulus
indicating a danger, it is routed first to the thalamus. From there,
the information is sent out over two parallel pathways: the thalamo-amygdala
pathway (the “short route”) and the thalamo-cortico-amygdala
pathway (the “long route”). The short route conveys
a fast, rough impression of the situation, because it is a sub-cortical
pathway in which no cognition is involved. This pathway activates
the amygdala which, through its central
nucleus, generates emotional responses before any perceptual
integration has even occurred and before the mind can form a complete
representation of the stimulus.
First, the various modalities of
the perceived object are processed by the primary sensory
cortex. Then the unimodal associative cortex provides the
amygdala with a representation of the object. At an even
higher level of analysis, the polymodal associative cortex
conceptualizes the object and also informs the amygdala
about it. This elaborate representation of the object is
then compared with the contents of explicit memory by means
of the hippocampus, which also communicates closely with
The hippocampus is the structure that supports
memory required to learn about the dangerousness of an object
or situation in the first place. The hippocampus is also especially
sensitive to the encoding of the context associated with an aversive
experience. It is because of the hippocampus that not only can
a stimulus become a source of conditioned fear, but so can all
the objects surrounding it and the situation or location in which
The imminent presence of a danger then
performs the task of activating the amygdala, whose discharge
patterns in turn activate the efferent structures responsible
for physical manifestations of fear, such as increased heart
rate and blood pressure, sweaty hands, dry mouth, and tense muscles.
The parallel operation of our explicit (hippocampal)
and implicit (amygdalic) memory systems explains why
we do not remember traumas experienced very early in our
lives. At that age, the hippocampus is still immature, while
the amygdala is already able to record unconscious memories.
Early childhood traumas can disturb the mental and behavioural
functions of adults by mechanisms that they cannot access