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Amygdala - Britannica Online Encyclopedia
Amygdala - Britannica Online Encyclopedia
Amygdala
Amygdala, region of the brain primarily associated with
emotional processes. The name amygdala is derived from TABLE OF CONTENTS
the Greek word amygdale, meaning “almond,” owing to
Introduction
the structure’s almondlike shape. The amygdala is located
in the medial temporal lobe, just anterior to (in front of) Anatomy of the amygdala
the hippocampus. Similar to the hippocampus, the Function of the amygdala
amygdala is a paired structure, with one located in each Amygdala dysfunction
hemisphere of the brain. The amygdala is part of the
limbic system, a neural network that mediates many
aspects of emotion and memory. Although historically the amygdala was considered to
be involved primarily in fear and other emotions related to aversive (unpleasant) stimuli, it
is now known to be involved in positive emotions elicited by appetitive (rewarding)
stimuli.
The cortical and medial nuclei of the amygdala form the so-called cortico-medial group.
Olfactory (smell) information ows directly into the cortico-medial amygdala from the
olfactory bulb and pyriform cortex, both of which function in the sense of smell. The
intercalated masses are a ribbon of inhibitory neurons that gate information ow from the
basolateral complex to the central nucleus of the amygdala.
In addition to sensory input, the amygdala receives input from a number of cortical and
subcortical brain systems. Most prominently, the amygdala receives dense input from the
prefrontal cortex, especially from the anterior cingulate and orbitofrontal cortices. The
amygdala also receives prominent input from the insula and from the hippocampus and
rhinal (olfactory) cortices. Subcortical information ows to the amygdala from numerous
nuclei, including every neuromodulatory system.
Output from the amygdala can be directed to both subcortical and cortical brain
structures. The central nucleus is directed to numerous subcortical structures known to
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In the early part of the 20th century, psychologist Heinrich Klüver and neurosurgeon Paul
C. Bucy studied monkeys with lesions of the temporal lobe that included the amygdala
and observed changes in emotional, feeding, and sexual behaviour. Subsequent studies
established that the amygdala was a critical structure mediating those effects.
Pheromones and innately appetitive and aversive stimuli, including certain odours, tastes,
or sexual imagery, can produce physiological and behavioral expressions of emotional
state. For olfactory stimuli, the cortico-medial amygdala is known to mediate innate
emotional behaviour. For other innately reinforcing stimuli, including some drugs of
abuse, circuitry within the basolateral complex likely also contributes to emotional
responses.
Emotional learning most commonly has been studied in both animal models and
humans, using Pavlovian conditioning, in which an otherwise neutrally conditioned
stimulus is paired with an innately aversive unconditioned stimulus. This type of
paradigm, often referred to as fear conditioning, can result in robust learning, owing to
the convergence of sensory information about the conditioned stimulus and the
unconditioned stimulus. Neuromodulatory input may also contribute to this learning. As
an animal learns, the responses of amygdala neurons to conditioned stimuli change,
re ecting the learning process. Furthermore, the activation of neurons in the basolateral
amygdala can induce learning, suggesting that those neurons play a causal role in
emotional learning. After learning, input from the basolateral complex to the central
nucleus of the amygdala leads to the orchestration of a range of physiological and
behavioral responses that are correlated with emotional states. Measures of fear
conditioning include the cessation of movement (“freezing”), a defensive behaviour, and
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Although the study of the amygdala has been most extensively pursued by means of
aversive stimuli, there is substantial evidence that the amygdala is also involved in the
processing of rewarding stimuli and in appetitive learning. Within the amygdala neural
responses to conditioned stimuli change during appetitive learning, and many amygdala
neurons respond to different rewarding stimuli. The activation of amygdala neurons that
respond to a rewarding stimulus can induce both Pavlovian and instrumental learning
(learning in which behaviour is in uenced by consequences). A pathway from the
amygdala to the ventral striatum, which has been implicated in reward processing in
addiction, mediates learned approach behaviours (movements toward objects or other
individuals). However, amygdalar lesions often do not impair appetitive learning,
indicating that such learning is likely also supported by parallel neural pathways that do
not involve the amygdala.
Regulation of emotion
Emotional responses to sensory stimuli not only arise through innate mechanisms and
through learning but also can be altered by extinction and cognitive control mechanisms.
Both extinction and cognitive control involve interactions between the prefrontal cortex
and the amygdala. Extinction, which itself is a learning process, is induced by the repeated
presentation of a conditioned stimulus in the absence of a previously associated
unconditioned stimulus, resulting in the elimination of a previously elicited response.
Projections from the prefrontal cortex to the amygdala mediate extinction, with complex
circuitry involving the central nucleus, the basolateral complex, and the intercalated
masses playing a role in the modi cation of responses to previously conditioned stimuli.
The cognitive control of emotion is an important process to understand, given its critical
role in normal adaptive emotional behaviour. Human studies using functional magnetic
resonance imaging have implicated prefrontal-amygdala interactions in these processes,
though the precise mechanisms remain poorly understood, in part owing to the dif culty
in studying those processes in animal models.
disorder) can exhibit a de cit in identifying fearful facial expressions. That de cit appears
to be due to dif culties in directing attention to the eyes of others, which is important for
discerning fear. Consistent with that observation, amygdala neural activity can re ect the
emotional signi cance and location of visual stimuli. Substantial work also implicates a
role for the basolateral amygdala in modulating the formation of memories in relation to
emotional events. In addition, human neuroimaging studies suggest a role for the
amygdala in mediating the so-called framing effect during economic choices, which is
thought to re ect the effect of positive or negative emotion on decision making.
Amygdala dysfunction
Dysfunction within the amygdala and the neural circuits connecting the amygdala with a
variety of cortical and subcortical structures likely contributes to the pathophysiology
(disease-associated physiological processes) of a number of neuropsychiatric disorders.
However, the precise mechanisms responsible for those disorders remain poorly
understood. The anatomical interconnections between the amygdala and the prefrontal
cortex, which likely are critical for normal adaptive emotional behaviour, do not fully
develop until early adulthood. Many neuropsychiatric disorders emerge during or before
that time.
Work in animals and studies of clinical populations suggest a role for amygdalar
dysfunction in anxiety disorders, addiction, and complex neuropsychiatric disorders such
as autism, where clinical features include social, cognitive, and affective components. As
research on the amygdala and related structures advances, the precise disturbances in
circuit mechanisms that underlie those and other psychiatric disorders are likely to be
elucidated, opening the way to the development of new therapeutic interventions that
transform the treatment of psychiatric disorders.
C. Daniel Salzman
CITATION INFORMATION
ARTICLE TITLE: Amygdala
WEBSITE NAME: Encyclopaedia Britannica
PUBLISHER: Encyclopaedia Britannica, Inc.
DATE PUBLISHED: 27 February 2019
URL: https://www.britannica.com/science/amygdala
ACCESS DATE: December 15, 2019
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