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Biological Bases of Emotion
and Addiction
Learning Objectives
After completing this chapter, you should be able to:
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Explain the three components of emotion.
Contrast the James-Lange, Cannon-Bard, and Schachter-Singer theories of emotion.
Identify the regions of the brain that have been implicated in the regulation of emotions.
List four differences between positive and negative emotions.
Describe how fear and rage are produced and controlled in the brain.
Explain how serotonin, norepinephrine, dopamine, and testosterone influence aggression.
Name at least three aggressive and anxiety disorders, and explain how each is treated.
Draw a diagram that illustrates the role of various neurotransmitters in producing feelings of pleasure,
according to the cascade theory of reward.
Define reward deficiency syndrome and describe how it is related to addiction.
Compare and contrast psychological and physical dependence.
Explain the role of dopamine in addiction.
Describe the three stages of addiction according to the hedonic homeostatic dysregulation model.
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Section 11.1 Emotion
CHAPTER 11
While picnicking with a companion, Walter is suddenly overcome by a strange feeling. He imagines
seeing two large, white male dogs fighting, but he is puzzled because he knows only one such dog is
really present. Intrigued, he chases them, but the dogs run away and vanish “into nothing” as they
jump over a river. In their place Walter sees a fisherman in waders holding out a fly rod. Suddenly,
Walter charges the man—a total stranger toward whom he harbored no ill feelings—and pushes him
underwater, saying, “I’ll teach you how to fish like a bear.” The man, in his 40s, finds a rock and tries
to hit Walter in the face. Meanwhile, Walter’s picnic companion arrives, grabs his head, and shouts,
“No! No! Don’t do it!” But Walter, seemingly emotionless, bites her finger and holds the man under
until he drowns. He then tries to drown his companion, too, but he suddenly comes to his senses and
lets her go (LoPiccolo, 1996, p. 52).
Walter was a handsome man in his early 20s at the time of this homicide. People who knew Walter
called him mild mannered and a social loner. His police report indicated that he had no criminal
record and no history of violence. A forensic psychiatrist was called in to examine Walter because
the homicide he committed was so bizarre. Most homicides, approximately 90% of them, are committed by a murderer who has a motive and a plan. Most murderers feel strong emotions such as
rage, greed, or jealousy when they commit their murders. But Walter had no motive, no plan, and
no feelings of emotion as he drowned the stranger who happened to be fishing nearby. What caused
Walter to commit murder?
To understand the answer to this question, you will need to learn how emotions are produced and
controlled by the brain. In this chapter we will examine the biological basis of emotions. We will
also take a look at addictions because these behaviors use many of the same brain structures and
mechanisms as emotional behavior does. Let’s begin by defining emotion.
11.1 Emotion
W
e talk about emotions all the time. I’m so happy to see you! Dad was thrilled when he
found his watch. Polly was very angry at the interruption. Jamil was sad when the trip was
over. Tika loved the gift you bought her. Kevin got scared when the trees began to fall over. Each
of these statements describes a feeling or emotional reaction to a stimulus. For example, seeing someone you love causes happiness, finding a lost watch produces pleasure, an interruption
causes anger, and so forth. An emotion doesn’t occur on its own. A stimulus is needed to initiate
the reaction we call an emotion.
An emotion is a complicated response to a particular stimulus. The formal definition of an
emotion has three components: An emotion is a cognitive experience that is accompanied by
an affective reaction and a characteristic physiological response. That is, an emotion involves
thought processes (cognitive experience), alterations in mood (affective reaction), and a bodily
reaction (physiological response). When you are experiencing an emotion, you are consciously
aware that the emotion is occurring as you are thinking about the stimulus and your response to
that stimulus. Your mood changes when you experience an emotion, becoming more positive or
negative. This affective component of emotion is referred to as feeling (Panksepp, 1989).
In addition, the sympathetic nervous system is activated when you experience an emotion. Recall
from Chapter 2 that the sympathetic nervous system produces a number of changes in your body
when it is activated: Your pupils dilate, your heart beats faster, your breathing rate speeds up, you
begin to sweat, your saliva becomes thicker, your blood leaves your gut and flows to your muscles,
and so forth. These physiological responses accompany all emotional states.
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Section 11.1 Emotion
CHAPTER 11
Expression of emotions appears to be universal across all cultures. Regardless of the culture in
which an individual is raised, similar facial expressions are used to communicate emotion. Figure
11.1 illustrates a series of faces expressing various emotions. See if you can determine the emotion being expressed in each photograph. When you experience an emotion, the somatic nervous
system reflexively initiates contraction of certain muscles in your face by way of cranial nerve VII,
the facial nerve, which innervates the muscles of facial expression. For example, when you are
happy, muscles in your face contract to pull the corners of your mouth up and back. These muscle
contractions are produced reflexively in response to certain stimuli.
Figure 11.1: Facial expression of emotion
No matter what culture one is from, human beings appear to show particular emotions in similar facial
expressions.
Cordelia Molloy/Science Source
When we think about emotions, they seem to fall into one of two categories: positive emotions
and negative emotions. Positive emotions make us feel better, and they tend to draw us toward
the eliciting stimulus. In contrast, negative emotions are accompanied by feelings of anxiety,
depression, or hostility, and they tend to make us avoid the eliciting stimulus. Emotions organize
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Section 11.1 Emotion
CHAPTER 11
our behavior in such a way as to motivate us to approach pleasant stimuli (as in the case of positive emotions) or avoid unpleasant or noxious stimuli (as in the case of negative emotions). Thus,
emotions are important for our survival.
In general, emotions such as happiness, love, and euphoria are considered positive emotions.
Anger, hatred, disgust, and fear are considered negative emotions. These negative emotions
have also been called emotions of self-preservation because they function to produce defensive responses by an individual to an arousing stimulus. For example, when I picked up what I
thought was a dead snake from my driveway one day, the snake’s tail began to move. In response,
I reflexively dropped the snake and ran down the driveway away from the snake. Thus, I displayed
self-preservation as I dashed away from the snake that was still very much alive. In 1927 Walter
Cannon referred to these negative emotional reactions as fight-or-flight responses. Emotions of
self-preservation produce either fight behavior, in which an individual strikes out at a threatening stimulus in an attempt to eliminate it, or flight behavior, in which the individual runs from the
emotion-inducing stimulus (as I did from the snake).
Both positive and negative emotions are associated with activation of the sympathetic nervous
system. Whether you are in love or so angry that you could scream, your body has the same
reaction: dilation of the pupils, increased heart rate and sweating, cessation of peristalsis in
the gut. Investigators who study emotions do not agree as to whether each emotion produces
a specific pattern of physiological responses (Ekman, 1992; Ortony & Turner, 1990). Later in this
chapter, we will discuss how activation of the sympathetic nervous system occurs. Before we
get to that discussion, I want you to consider how emotions are generated and experienced. A
number of investigators have proposed theories to explain how emotions arise. Let’s examine
the best known of these theories.
James-Lange Theory
William James and Carl Lange published separate papers at about the same time—James in the
United States and Lange in Europe—that detailed the same explanation of emotion (James, 1890;
Lange & James, 1922). Today we call that explanation the James-Lange theory of emotion, in honor
of the two psychologists who proposed it. According to the James-Lange theory, a stimulus produces a physiological response, and the physiological response produces an emotion (Figure 11.2).
The classic example goes like this: You are walking in the woods and meet a bear. Seeing the bear
makes your heart pound, and you run away. Running away with a pounding heart causes you to feel
afraid. That is, according to the James-Lange theory of emotion, you feel afraid after you experience
the physiological responses produced by the sympathetic and somatic nervous systems.
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CHAPTER 11
Section 11.1 Emotion
Figure 11.2: Major theories of emotion
According to these major theories, a stimulus creates an emotional reaction that is then represented in
a physical response.
James-Lange Theory:
See bear
Run away, heart pounding
Experience emotion (fear)
Experience emotion (fear)
Run away, heart pounding
Cannon-Bard Theory:
See bear
Schachter-Singer Theory:
See bear
Cognitive appraisal of event.
“This is a bear. Bears are scary.”
Experience emotion (fear)
Run away, heart pounding
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Cognitive appraisal of bodily
response. “My heart is pounding.
I’m running away like crazy.”
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Section 11.1 Emotion
CHAPTER 11
Cannon-Bard Theory
You may recall Walter Cannon’s name from Chapter 9, when we examined stomach contractions
and the initiation of eating. (Cannon was the psychologist who had his grad student swallow the
balloon that was inflated in the stomach.) Cannon is also well known for his theory on emotion.
In 1927 Walter Cannon and his student, Phil Bard, wrote a paper that refuted the James-Lange
theory of emotion and proposed an alternative theory, known as the Cannon-Bard theory of
emotion (Cannon, 1927). According to the Cannon-Bard theory, a stimulus causes an emotion,
which then produces physiological changes. That is, the Cannon-Bard theory maintains that a
stimulus is directly followed by an emotional reaction, which then elicits a bodily response
(Figure 11.2). For example, if you meet a bear in the woods, you feel fear (an emotion) and run
away. According to the Cannon-Bard theory, you run away because you feel afraid.
Schachter-Singer Theory
At Columbia University, Stanley Schachter and his student, Jerome Singer, designed an ingenious
experiment to test whether the James-Lange or the Cannon-Bard theory is correct (Schachter
& Singer, 1962). In their experiment, they had three groups of male participants, who were told
that the study involved testing the effects of vitamin A on vision. The first group was administered
an injection of epinephrine but was uninformed about its effect (Epi-Uninformed group). The participants in this group were told that they had been injected with vitamin A but that it would have
no side effects. Recall from Chapter 3 that epinephrine is a powerful stimulant of the sympathetic
nervous system. The second group also received epinephrine but was told that the “vitamin A”
injection would cause them to feel shaky and excited (Epi-Informed group). The third group
received an injection of saline (salt water) and was told that the vitamin A shot would have no side
effects (Placebo group). Thus, the Epi-Uninformed group experienced physiological arousal but
had no explanation for that arousal, the Epi-Informed group experienced physiological arousal
and knew that the injection produced that arousal, and the Placebo group experienced no physiological arousal.
Following the injection, each participant was placed individually in
a room where a confederate was
completing a survey. (A confederate is a person who is paid to act
like a participant in the study.) The
participant was asked to complete
the same survey while he waited
for the “vitamin A” to be absorbed
into his bloodstream. As the participant completed the survey, the
confederate began to act either
euphoric or angry. In the euphoria
condition, the confederate began
laughing at the questions on the
survey and folded the pages into
paper airplanes, which he sailed
across the room. In the anger condition, the confederate became
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iStockphoto/Thinkstock
Photo 11.1 The Schachter-Singer theory of emotion predicts
that smiling will occur before the experience of happiness but
that happiness will be experienced only if the smiling person
can attribute the smile to some appropriate stimulus.
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Section 11.1 Emotion
CHAPTER 11
angry over the questions in the survey and wadded each page into a ball, which he angrily threw
across the room. Schachter and Singer were interested in observing how the participants reacted
when the confederate began to display emotion.
As Schachter and Singer predicted, the participants in the Epi-Uninformed group displayed
emotional behavior when exposed to a confederate who was displaying emotional behavior.
For example, those in the euphoria condition were observed to laugh and make airplanes with
the confederate, whereas those in the anger condition tore up their surveys in anger. These
participants in the Epi-Uninformed group experienced physiological arousal due to the injection of epinephrine, but they attributed this arousal to an emotional state, euphoria or anger,
depending on the behavior of the confederate.
On the other hand, subjects in the Epi-Informed and Placebo groups did not display emotional
behavior. Those participants in the Epi-Informed group experienced physiological arousal, but
they attributed that arousal to the drug that was injected because they were informed of the
true effects of the drug. Those in the Placebo group did not display emotional behavior because
they did not experience physiological arousal. Thus, according to the Schachter-Singer theory
of emotion, in order to experience an emotion, an individual needs to experience physiological
arousal and has to attribute the physiological arousal to an appropriate stimulus (Figure 11.2).
Vascular Theory of Emotion
A more recent theory of emotion was described by Zajonc, Murphy, and Inglehart in 1989. As
its name implies (vascular refers to blood vessels), the vascular theory of emotion is based on
changes in blood flow through particular blood vessels in the face. Facial blood vessels drain into
the cavernous sinus, a large venous pool of blood that collects at the base of the skull before
being carried back to the heart (Figure 11.3). The cavernous sinus is central to the vascular theory of emotion because blood draining from the superficial layers of the face is cooler than core
body temperature and thus cools the brain. A number of studies conducted by Zajonc and others
have demonstrated that increasing the temperature of the brain (just a few tenths of a degree)
produces negative emotions like anger and sadness, whereas cooling the brain produces feelings
of happiness (Zajonc, Murphy, & Inglehart, 1989). These minute changes in brain temperature
are believed to alter the activity of enzymes and neurotransmitters in the brain, which could
affect the experience of emotion.
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CHAPTER 11
Section 11.1 Emotion
Figure 11.3: Vascular theory of emotion
Figure A labels the many parts that are involved in emotional expression. Figure B illustrates the physical
reactions to positive emotions and what leads to smiling. Figure C illustrates the physical reactions to
negative emotions and what leads to frowning and crying.
B. Cool blood from the superficial
layer of the face (skin, muscle) drains
into cavernous sinus, cooling the brain.
A.
Frontopolar branch
Anterior cerebral artery
Cavernous sinus
Veins that drain blood
from the face to the
cavernous sinus
C. Cool blood pools in the face and
does not drain into cavernous
sinus, warming the brain.
Internal carotid artery
External jugular vein
According to the vascular theory of emotion, muscular contractions that produce smiling cause
blood to drain rapidly from the face into the cavernous sinus, which lowers the temperature of the
brain, producing a positive emotion (Figure 11.3). For example, when human participants hold a
pencil in their teeth, blood drains out of the face into the cavernous sinus, and after several minutes, a feeling of happiness or well-being is induced (McIntosh, Zajonc, Vig, & Emerick, 1997). Hold
a pencil in your mouth behind your canine teeth and look at yourself in the mirror. You will appear
to be smiling. Thus, smiling causes blood to drain from your face into the cavernous sinus, cooling
your brain and producing a positive emotion. In contrast, when participants hold a pencil with
their lips only, producing a frown, their mood declines, and they report feeling sad or unhappy
(Figure 11.3). Muscle contractions that produce a frown cause blood to pool in the face, rather
than drain into the brain, which increases the temperature of the brain.
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Section 11.2 Emotional Pathways in the Central Nervous System
CHAPTER 11
The vascular theory of emotion may explain why facial expression of emotions appears to be universal across all cultures. Because smiling causes blood to drain from the face and frowning causes
blood to pool in the face, these facial expressions are directly implicated in the control of brain
temperature. However, it is unclear whether smiling occurs before or after the experience of a
happy emotion in a natural setting, as when someone gives you an unexpected gift. In the laboratory, Zajonc proposed that smiling precedes the experience of the emotion because smiling lowers
the temperature of the brain and, consequently, stimulates those areas of the brain that cause us
to feel a positive emotion (McIntosh et al., 1997, Zajonc, Murphy, & Inglehart, 1989).
The James-Lange theory would also predict that smiling (the physiological response) precedes the
experience of happiness. The Cannon-Bard theory requires that happiness (the emotion) be felt
first, followed by smiling. In contrast, the Schachter-Singer theory predicts that smiling will occur
before the experience of happiness but that happiness will be experienced only if the smiling
person can attribute the smile to some appropriate stimulus. That is, if the individual could not
explain why he or she were smiling, or if the individual were to reason, “I’m not really smiling, I’m
holding a pencil in my teeth,” the Schachter-Singer theory of emotion would lead us to predict that
happiness would not be experienced. Thus, each theory of emotion that we have examined in this
section would lead us to a different interpretation of smiling behavior.
11.2 Emotional Pathways in the Central Nervous System
T
he theories presented in the previous section all emphasize physiological factors that produce
emotions. These physiological factors are associated with activation of certain regions of the
central and peripheral nervous systems. Thus far, you have learned that activation of two divisions of the peripheral nervous system, the sympathetic and somatic nervous systems, produces
the physical reactions that we associate with emotions. In this section we will examine the brain
regions that initiate and control the experience of emotion.
The Locus Coeruleus
The locus coeruleus is a hindbrain structure that contains neurons that produce norepinephrine, the neurotransmitter responsible for heightened arousal and vigilance. The locus coeruleus
receives inputs from many areas of the brain, including the hypothalamus (Figure 11.4). Excitation of the locus coeruleus activates the sympathetic nervous system, stimulating the release of
norepinephrine throughout the brain and the release of epinephrine from the adrenal glands
(Bremner, Krystal, Southwick, & Charney, 1996; Krukoff & Shan, 2001). In turn, the release of epinephrine produces the physical changes that we associate with emotions, such as increased heart
and respiration rates, pupil dilation, increased sweating, and changes in blood flow.
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CHAPTER 11
Section 11.2 Emotional Pathways in the Central Nervous System
Figure 11.4: The locus coeruleus
The locus coeruleus receives information about the internal state of the body from all parts of the brain,
including the hypothalamus. Excitation of the locus coeruleus activates the sympathetic nervous system,
stimulating the release of norepinephrine throughout the brain and the release of epinephrine from the
adrenal gland.
Thalamus
Cerebral cortex
Hypothalamus
Cerebellar
cortex
Amygdala
Hippocampus
Locus
coeruleus
To spinal cord
The Limbic System
Early investigators who studied emotion attempted to identify the brain structures responsible
for the experience of emotion. Cannon (1927) proposed that the thalamus initiates emotions,
although Bard, his former student, disagreed and suggested that the hypothalamus produces
emotions, based on his research involving hypothalamic lesions in rats (Bard, 1934). As a result
of a large body of research in animals, Papez (1937) and Yakovlev (1948) identified two separate
circuits in the forebrain that they concluded are responsible for generating emotions. However, in
1949 Paul MacLean used the term limbic system to refer to the two circuits (that is, the Papez and
Yakovlev circuits) that are involved in emotion. Limbic system is a term that most scholars continue
to use today.
The structures that make up the limbic system are located beneath the cerebral cortex, in the
white matter of the cerebrum. They include the hippocampus, the septum and its adjacent neighbor, the nucleus accumbens, and the amygdala. Many investigators also consider the olfactory
bulb to be a part of the limbic system, based on research studying rats, although it’s not clear that
the sense of smell plays an important role in human experience of emotion.
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Section 11.2 Emotional Pathways in the Central Nervous System
In addition, parts of the prefrontal cortex, the cingulate gyrus, the hypothalamus, the thalamus,
and the midbrain are also considered to be part of the limbic system (Figure 11.5). PET studies of
human participants who were exposed to different stimuli such as films, pictures, and emotional
memories that produced feelings of happiness, sadness, or disgust revealed that the thalamus,
hypothalamus, midbrain, and prefrontal cortex are all activated when an individual is experiencing positive or negative emotions (Lane et al., 1996, 1997). The amygdala, too, is activated by
positive and negative stimuli (Sergerie, Chochol, & Armony, 2008). However, the amygdala is more
likely to be activated when an individual is experiencing fear or disgust, compared to happiness
(Costafreda, Brammer, David, & Fu, 2008).
Figure 11.5: The limbic system
Figure A shows the major structures of the limbic system. Figure B shows the limbic system situated in
the human brain.
A.
Anterior
nucleus of
thalamus
Corpus
callosum
B.
Brain
stem
Corpus
callosum
Frontal
lobe
Septum
Nucleus
accumbens
Hypothalamus
Olfactory lobe
Hypothalamus
Stria
terminalis
Amygdala
Hippocampus
Amygdala
Substantia
Hippocampus
Hippocampus
nigra
Ventral tegmental
region
The Cerebral Cortex
Whereas early theorists in the first half of the 20th century focused on the role of subcortical
structures in the expression of emotions, investigators over the past 3 decades have come to
recognize the important role that the cerebral cortex plays in the experience of emotions. Modern techniques such as electroencephalography and brain imaging have demonstrated that many
regions of the cerebral cortex interact with subcortical areas to enable us to experience emotions.
For example, the understanding and expression of emotion appear to be processed in the right
hemisphere (Heller, Nitschke, & Miller, 1998). In contrast, both hemispheres are involved in the
feeling of emotion.
A variety of research methodologies have demonstrated that the left frontal lobe is active when
a person is feeling a positive emotion, whereas the frontal regions of the right hemisphere are
more active when a person is experiencing a negative emotion (Davidson, 1992). Patients with
lesions in the left hemisphere often show signs of anxiety or sadness following a stroke or surgery
(Barker-Collo, 2007; Gianotti, 1972; Goldstein, 1948; Palese et al., 2008; Salo, Niemelä, Joukamaa,
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Section 11.3 Negative Emotions
CHAPTER 11
& Koivukangas, 2002). In contrast, euphoria often results in patients with right hemisphere lesions
(Babinski, 1914; Denny-Brown, Meyers, & Horenstein, 1952; Gianotti, 1972; Heller et al., 1998).
When a short-acting barbiturate that anesthetizes (or turns off) the brain is injected into the left
carotid artery, anesthetizing the left hemisphere, patients exhibit sadness or anxiety. Injection of
barbiturate into the right carotid artery, which produces short-term anesthesia of the right cerebral hemisphere, induces euphoria in the affected patient (Rossi & Rosadini, 1967).
Wendy Heller (1994) reasoned that hemispheric differences in processing emotions would be
reflected in the way people represent emotion in drawings. That is, she hypothesized that sad
images would be drawn on the left side of a piece of paper because sad emotions activate the
right hemisphere more, which should direct the eyes to the left. She also hypothesized that happy
images would be displaced to the right side of a page due to the higher level of activation of the
left hemisphere by positive emotions. She asked 200 children between the ages of 5 and 12 to
draw a picture of something that made them happy and another picture showing something that
made them sad. As Heller predicted, sad images were drawn left of center, and happy images
were drawn right of center (Heller, 1994).
The Medial Forebrain Bundle and Periventricular Circuits
Two different circuits in the brain are implicated in the regulation of positive and negative emotions. Positive emotions are associated with stimulation of the medial forebrain bundle, a bundle
of axons that courses through the center of the forebrain. In contrast, negative emotions, or
emotions of self-preservation, are associated with activation of the amygdala and periventricular
circuit that passes through the thalamus, hypothalamus, and midbrain. On the basis of his and
others’ research on emotion, Jaak Panksepp has proposed that a separate circuit exists for each
emotion (Panksepp, 1989, 1992, 2011): the medial forebrain bundle for positive emotions and
the periventricular circuit for negative emotions.
Because different areas of the brain are activated by different emotions, we will consider the brain
mechanisms involved in regulating negative and positive emotions separately. In the next section,
we will examine the brain mechanisms involved in the production and regulation of the emotions
of self-preservation, that is, the fight-or-flight emotions.
11.3 Negative Emotions
T
he emotions of self-preservation motivate an individual to deal with an unpleasant or aversive
stimulus by eliminating it or avoiding it. Thus, rage and fear are two prime examples of negative emotions. We will focus our discussion on these two emotions in this section. The amygdala
plays an important role in regulating the expression of rage and fear. For example, rage is often
expressed as aggression, an emotional response that involves attacking a noxious stimulus. Before
moving to a discussion of rage, aggression, and fear, let’s examine the role of the amygdala in the
generation of negative emotions.
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Section 11.3 Negative Emotions
CHAPTER 11
The Role of the Amygdala
When we consider negative emotions, the role of the amygdala cannot be ignored. The amygdala
is an almond-shaped structure located in the temporal lobe, adjacent to the hippocampus. The
amygdala appears to be activated preferentially by negative emotions (Costafreda et al., 2008).
In addition, recent research has demonstrated that the amygdala plays an important role in emotional learning, memory, emotion and social behavior, and inhibition and regulation of emotion
(Phelps & LeDoux, 2005).
Bilateral damage to the part of the temporal lobe that contains the amygdala produces a bizarre
disorder known as Kluver-Bucy syndrome. This syndrome was originally described by Kluver and
Bucy in their classical studies of bilateral lesions of the anterior temporal lobe (Kluver & Bucy,
1937). Monkeys with bilateral damage to their temporal lobes, which included damage to the
amygdala on both sides of the brain, exhibited a loss of fear of their human handlers, a lack of
emotional responsiveness, increased and inappropriate sexual behavior, and indiscriminate eating and mouthing of items that are inedible or were previously rejected. This loss of emotionality
led a number of investigators to propose that the amygdala plays an important role in emotion
(LeDoux, 1992). However, monkeys and people with Kluver-Bucy syndrome have an impaired
ability to make discriminations and to associate stimuli with rewards, which tells us that the
amygdala is also important in processes that involve learning about consequences. The alterations in emotionality and in eating and sexual behavior seen in Kluver-Bucy syndrome may reflect
an impairment in the ability to link stimuli with reward and punishment (Olson, Page, Moore,
Chatterjee, & Verfaillie, 2006; Rolls, 1992).
The role of the amygdala in humans for the expression of emotions may actually be limited,
compared to its central role in other animals (Halgren, 1992). However, we cannot deny that the
amygdala plays some role in human emotions because the rare cases of Kluver-Bucy syndrome
indicate that damage to the amygdala disrupts emotional responsiveness. In addition, stimulation
of the amygdala in human patients produces fits of uncontrolled rage or feelings of fear (Charney,
Deutch, Southwick, & Krystal, 1995; Mark & Ervin, 1975), and PET studies have demonstrated that
the amygdala is activated when a person is experiencing fear (Costafreda et al., 2008; Phelps et
al., 2001).
Studies of patients with another extremely rare condition, called Urbach-Wiethe disease, have
demonstrated that the amygdala also plays an important role in emotional memories. UrbachWiethe disease involves bilateral brain damage that is limited to the amygdala. Compared to
healthy controls, patients with this disorder have markedly impaired memories for emotionally
arousing events (Markowitsch et al., 1994). For example, individuals with Urbach-Wiethe disease
had difficulty remembering an emotionally arousing story that was presented to them, whereas
they had no problem remembering a neutral story (Adolphs, Cahill, Schul, & Babinsky, 1997). In a
study that compared one 30-year-old woman with Urbach-Wiethe disease to 12 brain-damaged
patients and 7 healthy controls, the woman with bilateral amygdaloid damage was unable to recognize fear in facial expressions and also had difficulty judging other emotional facial expressions
(Adolphs, Tranel, Damasio, & Damasio, 1994). Another patient with Urbach-Wiethe disease could
not recognize vocal expressions of fears, although he was able to recognize vocal expressions of
joy, anger, and sadness (Ghika-Schmid et al., 1997). Thus, the amygdala appears to be involved in
the recognition of emotions in human facial and vocal expressions.
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Section 11.3 Negative Emotions
Recent research has indicated that impairment of the amygdala may be related to antisocial behavior in children and adults. Individuals with abnormal amygdala function demonstrate impaired
emotional processing with respect to guilt and remorse (Blair, 2010; Gao, Glenn, Schug, Yang, &
Raine, 2009; Harenski, Harenski, Shane, & Kiehl, 2010).
In summary, the amygdala appears to stimulate the behavioral response to emotionally arousing
stimuli. The amygdala also plays an important role in learning about consequences and in forming
memories involving emotional events. However, cognitive processes directed by the prefrontal
cortex are vital in the expression of human emotions. For example, whether an individual reacts
with fear or aggression to a noxious stimulus such as a snake or stinging insect is largely a product
of the individual’s memory, reasoning, and decision-making processes, which are controlled by
the prefrontal cortex (Halgren, 1992; LeDoux, 1992).
Rage and Aggression
Human aggression is usually associated with rage, which causes individuals to lash out physically
or verbally at others. Most of us, at one time or another, have experienced this emotion. However,
some people have uncontrollable bouts of aggressive behavior, in which they strike out at loved
ones for little or no reason. Study of these individuals has aided our understanding of the mechanisms underlying rage and aggression.
Head trauma is associated with increased levels of aggression (Kavoussi, Armstad, & Coccaro,
1997). Approximately 70% of patients with brain lesions due to head injury show aggression and
increased irritability. Men who batter their spouses are significantly more likely to have suffered
head trauma in the past, compared to other men. Abnormal CT scans and EEG recordings in the
temporal lobes are most commonly associated with episodic aggression, in which an individual
has bouts of aggressive behavior. Lesions in the prefrontal cortex are also associated with
increased physical and verbal aggression.
Pixland/Thinkstock
Photo 11.2 Many people have trouble controlling their negative
emotions and can be very aggressive.
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Individuals with temporal lobe
seizures will sometimes exhibit
aggression with little or no provocation (Gloor, 1992; Mark & Ervin,
1975). As with other forms of
epileptic seizures, patients with
temporal lobe epilepsy will often
experience an aura, or altered
perceptual episode, immediately
before the seizure. They may also
show a sudden change in mood or
thought, or they may experience
physiological symptoms such as
stomach upset, nausea, or pain.
An individual with temporal lobe
epilepsy will often exhibit vacant
staring and lip smacking or chewing movements at the onset of the
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seizure. As the seizure progresses, the individual will become aggressive, striking out at the nearest individual or object. Vernon Mark and Frank Ervin (1975) reported the case of one patient,
a quiet, reserved 34-year-old engineer, who experienced episodic bouts of aggression due to
temporal lobe seizures:
The assault against his wife characteristically began after a complaint of severe
abdominal or facial pain. During the ensuing conversation, he would seize upon
some innocuous remark and interpret it as an insult. At first, he would try to
ignore what she had said, but could not help brooding; and the more he thought
about it, the surer he felt that his wife no longer loved him and was “carrying on
with a neighbor.” Eventually he would reproach his wife for these faults, and she
would hotly deny them. Her denials were enough to set him off into a frenzy of
violence. He would sometimes pick his wife up and throw her against the wall; he
did this to her even when she was pregnant. He did the same thing to his children.
These periods of rage usually lasted for 5 to 6 minutes, after which he would be
overcome with remorse and grief and sob as uncontrollably as he had raged. He
would then go to sleep for a half-hour or so and wake up feeling refreshed and
eager to work. (pp. 93–94)
This patient was treated with antiepileptic medications, which are used to treat seizures, but these
did not stop the seizures and bouts of aggression. Typically, antiepileptic medications are the first
line of treatment in patients with temporal lobe epilepsy, and they are often successful in halting
the attacks. Stereotaxic surgery was performed on the patient whose case was just described, and
small bilateral lesions were made in the amygdala. Following surgery, this patient never had an
episode of aggression again. Because antiepileptic medications are usually successful in controlling temporal lobe seizures, surgery is rarely performed. However, surgery may be indicated when
medication does not work in preventing seizures.
It may be that Walter, whose case was described at the beginning of this chapter, also suffered
an epileptic seizure in his limbic system at the time that he drowned the unsuspecting fisherman (LoPiccolo, 1996). He first experienced visual hallucinations of two dogs fighting, and
hallucinations and confused thinking often precede a temporal lobe seizure. After he began
his aggressive attack, no amount of reasoning or pleading could make him stop. In humans the
frontal lobes generally function to hold emotions and emotional behavior in check. In Walter
and others experiencing seizures in the limbic system, the electrical storm produced by the
seizures appears to disrupt the usual communications between the frontal lobes and the limbic
system, allowing the limbic system to produce unchecked aggressive behavior. However, we
are still far from understanding how the frontal lobes control the limbic system and how the
limbic system generates aggression.
Although the brain mechanisms that mediate aggression in people are not well understood, we
do know quite a bit about the effects of neurotransmitters and certain hormones on aggression.
Serotonin, norepinephrine, dopamine, and certain hormones such as testosterone play an important role in controlling aggression. Let’s examine the relation of each of these neurochemicals
with aggressive behavior.
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Serotonin
Research with cats, rats, and mice, as well as humans, has demonstrated that serotonin plays
a central role in the inhibition of aggression (Kavoussi et al., 1997). Low levels of serotonin are
associated with aggressive behavior in every species studied. People who have histories of uncontrolled aggressive behavior have low levels of the serotonin metabolite 5-hydroxyindolacetic acid
(5-HIAA) in their cerebral spinal fluid (Asberg, Traskman, & Thoren, 1976; Brown, Kent, Bryant, &
Gevedon, 1989; Linnoila, De Jong, & Virkkunen, 1989). Suicide (aggression toward oneself) is also
associated with low levels of serotonin or 5-HIAA (Lee et al., 2009; Loefberg et al., 1998; Mann,
Arango, & Underwood, 1990: Raedler, 2011; Roy, De Wong, & Linnoila, 1989). Genetic mutations
that produce a faulty enzyme or a missing 5-HT receptor, resulting in a disturbance in serotonin
function, have been related to increased aggression in mice and humans (Kavoussi et al., 1997).
In addition, drugs that increase serotonin activity in the brain have been demonstrated to reduce
aggressive behavior.
Norepinephrine
High levels of norepinephrine activity in rats, mice, monkeys, and humans are associated with
increased aggression. For example, human subjects who were chronic “Ecstasy” users had significantly more aggressive responses and higher norepinephrine blood levels than control subjects
in an experiment designed to elicit aggression (Gerra et al., 2001). In addition, increased levels
of norepinephrine receptor binding have been measured in people who died as a result of violent suicide, compared with those who died in accidents (Arango, Underwood, & Mann, 1992).
Increased norepinephrine activity in the brain is also related to an increase in externally directed
aggression (Siever & Davis, 1991; Yanowitch & Coccaro, 2011). Further evidence for the role of
norepinephrine in aggression comes from studies that demonstrate that drugs that block norepinephrine receptors reduce aggressive behavior (Kavoussi et al., 1997).
Dopamine
Increased dopamine activity causes animals to respond aggressively to environmental stimuli.
This increase in dopamine activity may be the result of supersensitive dopamine receptors, which
have a greater-than-normal response to dopamine (Winchel & Stanley, 1991). Tranquilizers that
reduce dopamine activity in the brain are used to control aggression in agitated patients (Citrome
& Volavka, 2011; Fava, 1997).
Testosterone
Testosterone appears to be associated with aggressive behavior, although the nature of that
association is unclear (Kavoussi et al., 1997). For example, fighting among male animals increases
following puberty, when testosterone levels are higher. Studies comparing men who commit
violent crimes to those who commit nonviolent crimes revealed that violent offenders have
significantly higher testosterone levels. However, whereas drugs that block androgen activity
are useful in treating paraphilias, as you will learn in Chapter 12, these antiandrogens are not
effective in reducing aggressive behavior. Thus, testosterone may facilitate aggressive behavior,
but it does not appear to control aggression.
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Section 11.3 Negative Emotions
Table 11.1 summarizes the effects of neurotransmitters and hormones on aggressive behavior.
Table 11.1: Effects of neurotransmitters and hormones on aggression
Neurotransmier
Serotonin
serotonin
aggression;
serotonin
aggression
Norepinephrine
norepinephrine
aggression;
norepinephrine
aggression
Dopamine
dopamine
aggression;
dopamine
aggression
Hormones
Testosterone
Arginine-vasopressin
may facilitate aggression
arginine-vasopressin
aggression
Fear
Ned Kalin and Steven Shelton at the University of Wisconsin have been studying the development
of fear in infant rhesus monkeys in order to understand the brain mechanisms that underlie this
complex emotion. These investigators have found that young monkeys make three different fear
responses when they are separated from their mothers. When frightened, the infants cry to their
mothers, making cooing sounds, or they sit very still (freeze) to avoid detection by a predator, or
they make a threatening face, baring their teeth and growling (Kalin & Shelton, 1989). The fear
response that the baby monkeys make depends on the environmental stimuli. That is, if they are
separated from their mothers and left alone, they coo. If they are separated from their mothers
and can see a human who does not make eye contact with them, the infants will freeze to avoid
detection. If a human stares at them when they are separated from their mothers, the young
monkeys make threatening, hostile gestures toward the human. Thus, fear responses, even of
very young monkeys, are quite complicated, which makes identifying their biological underpinnings difficult.
Three structures in the forebrain work together to regulate the expression of fear: the prefrontal
cortex, the amygdala, and the hypothalamus (Bakshi, Shelton, & Kalin, 2000; Kalin, 1993; Kalin,
Shelton, Davidson, & Kelley, 2001). The prefrontal cortex interprets the meaning of environmental
stimuli and organizes the fear response to those stimuli. The amygdala initiates the fear response,
including stimulating the sympathetic nervous system and arousing motor systems. The third
structure, the hypothalamus, activates the body’s stress responses, which permits the body to
defend itself. You will learn more about the body’s stress responses in Chapter 12. In the meantime you should understand that the hypothalamus activates the pituitary gland, which in turn
stimulates the adrenal gland to release hormones, called steroids, that alter the responses of the
cardiovascular, nervous, and immune systems to the fearful stimulus.
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Investigators are just beginning to understand the relationship between neurotransmitters
and fear. Kalin and his colleagues have determined that two neurotransmitter pathways, those
involving endogenous opiates and those involving receptors for GABA, are associated with fear
responses. Recall from Chapter 3 that benzodiazepines are minor tranquilizers that bind with particular sites on GABA receptors. Benzodiazepines are antianxiety agents that produce a feeling of
calm. A decrease in activity in the endogenous opiate pathway causes increased cooing behavior
but has no effect on freezing or threatening behavior when an individual is afraid (Kalin, 1993;
Bakshi et al., 1999; Kalin et al., 2008). As you might expect, an increase in activity in endogenous
opiate receptors (for example, produced by an injection of morphine) decreases cooing behavior
but again has no effect on defensive responses. In contrast, increased activity at GABA receptors
has no effect on cooing, but it does decrease freezing and threatening behaviors in response to a
fearful stimulus. Thus, endorphins appear to mediate crying behavior when an individual is afraid,
and GABA mediates freezing and threatening behaviors.
Disorders Associated with Negative Emotions
Negative emotions are accompanied by defensive fight-or-flight reactions. Let’s consider what
would happen if one of these reactions went awry, as in the case when an individual experiences
too much fight (that is, excessive aggression) or too much flight (excessive anxiety).
Aggressive Disorders
Pathologic anger and aggression are associated with a number of brain disorders, which are listed
in Table 11.2. Typically, treatment of these disorders is the physician’s primary goal. Sometimes
the treatment, as for bipolar disorder or seizure disorder, will prevent the occurrence of attacks
of aggression. However, when the medication given to treat the primary disorder does not stop
aggressive behavior, additional medications are administered. Recall that low levels of serotonin
and high levels of norepinephrine are implicated in aggressive behavior. Therefore, drugs that
increase serotonin activity, such as serotonin specific reuptake inhibitors, and those that decrease
norepinephrine activity, such as medications that block norepinephrine receptors (for example,
adrenergic beta-blockers) are prescribed to control aggression and violent behavior (Fava, 1997).
Table 11.2: Brain disorders associated with pathologic aggression
Dementia
Korsakoff’s syndrome
Autism
Drug or alcohol withdrawal
Huntington’s disease
Brain tumors
Seizure disorder
Premenstrual dysphoric disorder
Brain injury
Mental retardation
Drug or alcohol intoxication
Attention deficit disorder
Source: Fava, M. (1997). Psychopharmacologic treatment of pathologic aggression. Psychiatric
Clinic North America, 20(2), 427–451.
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The diagnosis of intermittent explosive disorder is given when the pathologic aggression is not
associated with another brain disorder. According to the Diagnostic and Statistical Manual of the
American Psychiatric Association (DSM-IV), intermittent explosive disorder is characterized by
episodes of uncontrolled, aggressive outbursts that result in assaults causing personal injury or
destruction of property (American Psychiatric Association, 1994). The cause of this disorder is
unknown. Treatment of intermittent explosive disorder usually involves counseling or psychotherapy, in addition to administration of drugs such as serotonin reuptake inhibitors, beta-blockers, or
tranquilizers that decrease dopamine activity.
Self-mutilation, or an act of deliberate harm to one’s own body, occurs in a number of populations,
including mentally retarded people, psychotic patients, individuals in prisons, and people with
personality disorders such as borderline personality disorder. Typically, this self-injurious behavior
is done without the aid of another person, and the injury results in tissue damage (Winchel &
Stanley, 1991). Like other acts of aggression, self-mutilation is associated with low levels of serotonin and high levels of dopamine activity. This disorder is difficult to treat successfully, especially
when it occurs in people with personality disorders.
Anxiety Disorders
Uncontrolled bouts of fear and overactivation of the fear system have been implicated in the
development of anxiety disorders. Anxiety is sometimes difficult to distinguish from fear. Freud,
for example, did not make a distinction between fear and anxiety in his writings. Most authors
base their distinctions on the stimuli that arouse fear versus anxiety and the responses to these
stimuli. For example, fear might be described as a realistic, defensive response to a threatening
stimulus that is present, whereas anxiety might be described as an overly fearful response made
to a stimulus that most would not consider threatening or to a threatening stimulus that is not
present and perhaps unlikely to occur. Anxiety also has a cognitive component that is missing in a
fear response. This cognitive component involves an awareness of the changes occurring in the
body, such as pounding heart, dizziness, and visual blurring (Craig, Brown, & Baum, 1995).
We have all experienced anxiety at
one time or another, because anxiety serves to alert us to future or
impending danger and allows us to
prepare for this danger. (Fear, on
the other hand, alerts us to danger
that is present and must be dealt
with immediately.) However, anxiety becomes pathologic when it
disrupts normal behavior. That is,
when an individual makes repeated
inappropriate responses to some
unknown or unreal threat, an anxiety disorder is present. A number
of anxiety disorders have been
identified, including generalized
anxiety disorder, panic disorder,
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Wavebreak Media/Thinkstock
Photo 11.3 Anxiety becomes pathologic when it disrupts normal behavior.
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phobias, obsessive-compulsive disorder, and post-traumatic stress disorder. We will examine
post-traumatic stress disorder in detail in Chapter 12. In the meantime let’s look at the remaining
types of anxiety disorders and discuss the biological basis of each.
Generalized anxiety disorder is a syndrome characterized by excessive apprehension about
unknown future events. The affected individual will report feeling a sense of impending doom, as if
something terrible is going to happen. These feelings are accompanied by persistent, bothersome
physical symptoms such as trembling or twitching, shortness of breath, pounding or palpitating
heart, profuse sweating, nausea, or difficulty concentrating. These symptoms are all associated
with activation of the sympathetic nervous system.
Panic disorder is characterized by bouts of intense fear or terror that are unpredictable and seem
to occur “out of the blue.” That is, the onset of panic attacks does not appear to correlate with
environmental stimuli. The attacks can be so severe and incapacitating that affected individuals
may be unable to leave their homes and may feel as if they are going to die or going crazy. A person
with panic disorder experiences symptoms of autonomic arousal during a panic attack, including
trembling, dizziness, chest pains, breathing difficulties, increased heart rate, or faintness. Some
investigators have suggested that panic attacks take place because of an instability in the brain’s
fight-or-flight mechanism, which produces bouts of unprovoked autonomic arousal and an intense
desire to escape or flee (Deakin, 1998).
Many individuals with panic disorder become anxious when exercising, which indicates an
abnormality in lactate metabolism that affects acid-base balance. In fact, an injection of sodium
lactate produces panic attacks in 50% to 70% of individuals with panic disorder and in less than
10% of people without the disorder (Leibowitz et al., 1998; Pohl et al., 1988). The mechanism
that produces panic attacks is unclear, although lactate may cause hyperventilation, which in
turn induces a panic attack (Stein & Uhde, 1995). It may be that people with panic disorder are
especially sensitive to carbon dioxide levels in their blood and that changes in carbon dioxide
levels produce hyperventilation, which elicits a panic attack.
Panic disorder can also be accompanied by phobias, particularly agoraphobia. Phobias are intense
fears generated by stimuli that most people do not consider to be overly threatening. Three
classes of phobias have been distinguished: agoraphobia, social phobias, and specific phobias.
Agoraphobia refers to a disorder in which affected individuals feel tremendous anxiety when they
are in places or situations where they can’t easily escape or be helped, such as riding in a jet or
standing in the line at the grocery store. Some people with panic disorder come to fear these situations, especially if they experience a panic attack while in the situations, and will avoid them. In
fact, some people with agoraphobia are so anxious that they cannot leave their homes, even if
accompanied by a loved one whom they trust.
Social phobias are characterized by an overwhelming fear of being in situations in which one
might be evaluated or scrutinized by others. In contrast, specific phobias are unreasonable,
excessive fears of a particular object or situation, such as needles. As with other anxiety disorders, phobias are accompanied by symptoms of autonomic arousal, including dizziness, nausea
and other gastrointestinal symptoms, chest pain and heart palpitations, and loss of bladder or
bowel control.
Obsessive-compulsive disorders are characterized by repetitive thoughts, or obsessions, that
intrude into a person’s consciousness and ritualized behaviors that are performed repeatedly (compulsions). These obsessions and compulsions disrupt the affected individual’s normal activities.
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For example, a person with obsessive-compulsive disorder may have to wash his hands dozens of
times a day, or else he feels extremely anxious. Another person with obsessive-compulsive disorder may have a difficult time leaving for work in the morning because she has to keep checking
to make sure the appliances are unplugged. Still another may feel compelled to keep thinking the
same words over and over in order to feel secure. Although the individual is aware that the behavior is senseless and disruptive, that individual cannot stop performing it without experiencing a
great deal of anxiety and apprehension (see the “Case Study”).
Case Study: Obsessive-Compulsive Disorder
Ted was a college sophomore on academic probation
when he first visited the university counselor. He had
just failed another test in his American history class,
and he knew he needed help. Before he left for his
appointment with the counselor, Ted vacuumed his
apartment. He started to go out the door when he
noticed a piece of fuzz on the carpet. Without hesitation, he got the vacuum back out and went over the
entire carpet in his three-room apartment again, this
Jupiterimages/Pixland/Thinkstock
time moving all the furniture, including the couch and
Photo 11.4 A common compulsion in
heavy dresser. Then Ted found a crumb on the carpet in
obsessive-compulsive disorder is to
the hallway. He knew he had to go, but he felt he must
constantly clean.
vacuum the apartment one more time to make sure it
was really clean. Finally, he went out the door, 10 minutes late for his appointment.
The counselor seemed very friendly and warm, which put Ted at ease. His problem was quite embarrassing, but he found it was easy to tell the counselor about how crazy he felt. Ted told her that he
was afraid he was going to flunk out of school. The counselor asked him about his study habits. That
was the problem, Ted admitted. He tried to study, but he couldn’t study unless the apartment was
“in order.” Ted explained that he couldn’t study unless the carpet was immaculately clean. He couldn’t
bear to have even a speck of dust on the floor, so he vacuumed the rug over and over.
After he was certain that the carpet was clean, he set up his desk to study. Ted owned about 50 pens,
which he arranged by color and size on top of his desk. The pens had to be lined up straight, in a row.
If one pen looked crooked, he had to start all over again, lining up the pens carefully, all parallel, all
in a row. This process often took over an hour. If a pen happened to fall on the floor, Ted got out the
vacuum cleaner to vacuum the area where the pen dropped. When the pens were lined up to his satisfaction, he next arranged the books on his desk, again by size and color. Ted felt that the books had to
be perfectly straight and lined up parallel with his pens. By the time he got around to studying, it was
usually after 10:00 p.m., which left him little time to study.
The counselor listened carefully and seemed to understand his dilemma. She talked to him about
obsessive-compulsive behaviors, and Ted had to admit that it sounded like his problem in a nutshell.
He agreed to see the counselor on a weekly basis to learn to control his compulsions. In addition, the
counselor arranged for Ted to begin taking a selective serotonin reuptake inhibitor. The SSRI made him
feel less anxious when he sat down to study. If the urge to vacuum came over him, Ted found that he
could ignore it and focus on his studying. In his sessions with the counselor, Ted learned to identify his
compulsions when they occurred, and he began to relabel those troubling thoughts and urges and thus
gained control over them.
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CHAPTER 11
Treatment of Anxiety Disorders
Because activation of the sympathetic nervous system is implicated in all forms of anxiety disorders, drugs that decrease activity of the sympathetic nervous system would be expected to
alleviate the symptoms of these disorders (Charney, Bremner, & Redmond, 1995). Some forms of
social anxiety are treated successfully with beta-blockers, which decrease activity at epinephrine
and norepinephrine receptors. However, one of the most effective treatments for anxiety disorders is imipramine, a drug that blocks the reuptake of catecholamines and therefore increases
norepinephrine activity. Likewise, buspirone (trade name Buspar), which acts as both an agonist
and antagonist of dopamine as well as an agonist of serotonin, is effective in treating anxiety
(Ballenger, 2001; Goldberg & Finnerty, 1979; Paul & Skolnick, 1982; Taylor et al., 1982).
Benzodiazepines are widely used for the control of anxiety. As you learned earlier in this chapter,
benzodiazepines alleviate freezing and other defensive behaviors in baby monkeys. By binding
with sites on GABA receptors, benzodiazepines augment the inhibiting activity of GABA throughout the brain. Investigators are uncertain about where the antianxiety actions of GABA occur
in the brain, but benzodiazepines are unquestionably successful in reducing anxiety in people
(Malizia, Coupland, & Nutt, 1995). It is interesting that alcohol, which also binds with GABA
receptors, has an anxiolytic, or anxiety-reducing, effect on people, too. This demonstrates that
GABA must be an important mediator of anxiety.
However, the symptoms of obsessive-compulsive disorder are not alleviated by benzodiazepines.
Although individuals with this disorder experience a great deal of anxiety, this anxiety is not
reduced by benzodiazepines. Instead, people with obsessive-compulsive disorder get the most
relief with a special class of antidepressants that increases serotonin activity in the brain, known
as selective serotonin reuptake inhibitors. Brain activity in a patient with severe obsessivecompulsive disorder changes following administration of an SSRI. In contrast, antidepressants
that block the reuptake of norepinephrine, such as desipramine, do not reduce obsessivecompulsive symptoms. Thus, obsessive-compulsive behaviors appear to be related to decreased
serotonin activity in the brain (Baumgarten & Grozdanovic, 1998).
11.4 Positive Emotions
E
uphoria, happiness, being in love, joy—these positive emotions are all associated with stimulation of the mesolimbic dopamine pathway. This pathway extends from the midbrain to
the nucleus accumbens in the forebrain (Figure 11.6). It has projections to the limbic system
and the prefrontal cortex, which allow it to communicate with a large group of structures that
regulate emotional behavior. In the diencephalon this pathway of dopamine fibers is known as
the medial forebrain bundle.
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Section 11.4 Positive Emotions
Figure 11.6: The mesolimbic dopamine pathway
Positive emotions are associated with the stimulation of the mesolimbic dopamine pathway.
Corpus callosum
Basal
ganglia
Ventral tegmental area
and substantia nigra
Frontal
lobe
Prefrontal
cortex
Nucleus
accumbens
Cerebellum
Hypothalamus
Amygdala
Mesolimbic
pathway
Brain
stem
Spinal cord
Research involving the medial forebrain bundle led to the accidental discovery of this pleasure
system. In 1954 James Olds and Peter Milner at McGill University were conducting a study of
the brain’s alerting system in rats. Electrodes were mistakenly inserted in the medial forebrain
bundle, and then electrical stimulation was passed down the electrodes into the brains of the rats.
Careful observation of the rats that received electrical stimulation of the medial forebrain bundle
revealed that the rats found the brain stimulation to be rewarding. When a lever was placed in the
cage and the rats were trained to press the lever for stimulation of the medial forebrain bundle,
the rats pressed the lever almost continuously, up to 5,000 times per hour. This indicated that the
rats found this brain stimulation to be very pleasurable because a rat will normally make 300 to
500 bar presses per hour for food reinforcement.
Microscopic examination of the brains of Olds and Milner’s rat revealed that the electrodes
that produced pleasure were located in the medial forebrain bundle in the hypothalamus (Olds
& Milner, 1954). Since that time, investigators have found that pleasurable brain stimulation
can be produced in a number of brain regions, from the midbrain to the forebrain, that contain
dopamine fibers (Wise & Rompre, 1989). Electrical stimulation of these brain regions in humans
has produced two types of sensations: either an intense feeling of sexual arousal (“as if I’m
about to have an orgasm”) or a feeling of lightheadedness that erased negative thoughts (Hall,
Bloom, & Olds, 1977; Olds & Olds, 1969). Thus, pleasure in the human brain is linked to this
dopamine pathway.
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Section 11.4 Positive Emotions
In addition to dopamine, other neurotransmitters are involved in the generation of pleasurable feelings, including serotonin, endorphin, and GABA. The cascade theory of reward has
been proposed to explain how these neurotransmitters work together to produce feelings of
pleasure or well-being (Blum, Cull, Braverman, & Comings, 1996; Blum et al., 1997). According
to this theory, pleasurable feelings arise when dopamine is released and binds with neurons in
the nucleus accumbens and hippocampus. However, the cascade begins in the hypothalamus,
where serotonin is released by excitatory neurons (Figure 11.7). The release of serotonin causes
endorphins to be released in the midbrain, which inhibits the release of GABA. Normally, GABA
inhibits the release of dopamine. But when endorphins inhibit the release of GABA, no GABA
is present in the midbrain to inhibit the release of dopamine. Therefore, dopamine neurons
in the midbrain are permitted to fire, and they release dopamine at their axonal endplates in
the nucleus accumbens and hippocampus, producing a feeling of well-being or pleasure. Many
different stimuli can cause the release of dopamine in the nucleus accumbens and hippocampus, including food and water reward, gratifying social experiences, and drugs such as alcohol,
cocaine, nicotine, and opiates.
Figure 11.7: The cascade theory of reward
The reward cascade begins with the release of serotonin by neurons in the hypothalamus. The release
of serotonin stimulates the release of endorphins in the midbrain, which inhibits the release of GABA,
allowing dopamine to be released in the nucleus accumbens and hippocampus.
Hypothalamus
Serotonin
Endorphin
Ventral
tegmental
region
Substantia
nigra
GABA
Dopamine
Amygdala
Dopamine
Nucleus
accumbens
Hippocampus
D2 receptor
Dopamine
Reward
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D2 receptor
Dopamine
Reward
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Please remember that the cascade theory of reward is just that: a theory. Although there is considerable experimental evidence that supports this theory, pleasurable feelings may not arise
from the mechanism just described. The idea that dopamine is responsible for the experience
of pleasure and reward is accepted by most investigators, but some investigators believe that
dopamine does not produce feelings of pleasure. Instead, these investigators believe that dopamine functions to draw attention to important stimuli (Gray, Young, & Joseph, 1997; Sarter &
Bruno, 1997; Wickelgren, 1997). That is, the release of dopamine in the nucleus accumbens may
influence processing in the prefrontal cortex that motivates an individual to pay more attention
to certain stimuli and to be more aware of sensory stimulation from these stimuli.
Although the exact brain mechanisms underlying positive emotions are not known, there is no
denying that we have the ability to experience a range of pleasurable feelings. Whether we are
sharing a laugh with friends, glowing from praise for a job well done, or smiling into the eyes of
a loved one, certain brain regions are activated, and certain brain chemicals are released. Most
current evidence from lesioning, stimulation, and recording experiments indicates that dopamine
plays an important role in most, if not all, rewarding experiences (Koob & Le Moal, 1997; Wise &
Rompre, 1989). In addition, PET studies have demonstrated that activation of dopamine receptors
is important for the experience of pleasure (Volkow, Fowler, & Wang, 1999a; Volkow et al., 1999b).
Functional imaging studies of human brains have also increased our understanding of positive
emotion by revealing which brain structures are active during rewarding episodes. For example,
in one PET study (Thut et al., 1997), cerebral blood flow was measured in human participants
performing a task during two conditions: one in which they were rewarded by a simple “okay”
and the other in which they were rewarded with money. Money reward, which presumably provided more pleasure, was associated with significantly higher levels of activation in the prefrontal
cortex. With respect to subcortical structures, a functional MRI study revealed that certain subcortical structures—namely, the nucleus accumbens and amygdala—are activated by pleasurable
rewards in human participants (Breiter & Rosen, 1999). A more recent functional MRI study indicated that winning a competitive tournament was associated with activation of the left amygdala
and losing was associated with activation of the right amygdala (Zalla et al., 2000). Recall that
earlier in this chapter you learned that the left hemisphere is active during positive emotions
and that the right hemisphere is more active during negative emotions. The findings of Zalla and
his colleagues reflect the hemispheric asymmetry associated with the processing of positive and
negative emotions.
Disorders Associated with Positive Emotions
Disorders associated with positive emotions may present as too much positive emotion, as in
the case of mania, or too little, as in the case of depression. In some cases an individual may
not be able to recognize or experience pleasure, as sometimes happens in schizophrenia. One
or more monoamines (serotonin, norepinephrine, or dopamine) have been implicated in these
disorders. We will discuss these disorders and their biological bases in detail in Chapter 12.
In some individuals the reward system can fail to function properly, as in the reward deficiency
syndrome. This disorder is characterized by decreased activity of neurons in the nucleus accumbens and hippocampus, which produces dysphoria (the opposite of euphoria), negative emotions,
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Section 11.5 Addiction
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and cravings for substances that can increase dopamine activity. Recall that a variety of substances
can induce the release of dopamine in the nucleus accumbens and hippocampus, including food,
sex, and drugs. People with reward deficiency syndrome may overeat, take drugs, or engage in
risky behaviors, like gambling or unsafe sex, in order to increase dopamine activity in their brains
and thus enhance their feeling of well-being. For example, recent research has linked cigarette
smoking and nicotine addiction with reward deficiency syndrome (Lerman et al., 1999).
Kenneth Blum and his colleagues (Blum, Cull, Braverman, & Comings, 1996; Blum et al., 1997;
Blum et al., 2000) have determined that a variant of a specific gene, called the A1 allele, in some
individuals is associated with reward deficiency syndrome. In these individuals the A1 allele codes
for an inactive dopamine D2 receptor, which is less likely to bind with dopamine and severely
reduces excitation of neurons in the nucleus accumbens and hippocampus. Thus, a decrease in
the activity of dopamine D2 receptors can produce the symptoms of reward deficiency syndrome.
A person who abuses a drug over a long period of time can also experience a decrease in the
availability of dopamine D2 receptors (Lee, Parish, Tomas, & Horne, 2011; Volkow et al., 1993).
For example, chronic exposure to cocaine is associated with a decrease in dopamine D2 receptors in the brain. This decrease in dopamine D2 receptors is believed to produce craving for the
drug. Thus, people with reward deficiency syndrome will experience dysphoria and cravings due
to decreased dopamine activity in the limbic system. Blum suggests that these cravings can lead
to a variety of problem behaviors, including compulsive overeating, substance abuse, or addiction.
11.5 Addiction
P
eople talk about addictions nearly every day. Someone may say, “He’s a real alcoholic,” or
“She’s trying to kick her nicotine addiction.” Others speak of being a “chocoholic” or a “workaholic.” Still others complain of their addiction to shopping or to exercise. What does it mean
to be an addict? Can a person truly be addicted to chocolate or exercise? In this section we will
examine the nature of addiction. In addition, we will look at how an addiction develops and how
it is treated.
Definition of Addiction
An addiction is a disorder in which the affected person loses control over his or her intake of a
particular substance and demonstrates psychological dependence and physical dependence on
the substance. An addicted individual craves the abused substance when it is not available for
consumption. This craving is called psychological dependence. The abused substance also causes
physical dependence, a state characterized by severe physical withdrawal symptoms such as
tremors, seizures, hallucinations, or nausea when the individual abstains from taking the substance. Different abused substances are associated with specific withdrawal symptoms. The “For
Further Thought” box describes the withdrawal symptoms of chronic alcoholics who stop drinking
for more than a few hours.
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For Further Thought: Withdrawal from Alcohol
When a person abuses alcohol for a long period of
time, changes take place in that person’s brain that
lead to physical dependence. People who are physically dependent on alcohol will develop withdrawal
symptoms when they stop drinking for even a few
hours, and these symptoms can be fatal. Every year,
thousands of people die due to alcohol withdrawal.
Three phases of alcohol withdrawal have been identified, based on their time of onset after a person has
stopped drinking.
Creatas Images/Creatas/Thinkstock
Phase I occurs within a few hours after drinking has Photo 11.5 Headaches are part of Phase I
stopped. In Phase I a person develops uncontrollable alcohol withdrawal.
shakes, profuse sweating, and feelings of agitation
and weakness. That person may also complain of headache, nausea, vomiting, and abdominal cramps.
If the abstaining individual goes more than a few hours without alcohol, auditory and visual hallucinations may be experienced. A person in Phase I also feels an overwhelming urge to resume drinking,
and many alcoholics begin drinking again when Phase I withdrawal symptoms occur, avoiding the more
severe and life-threatening withdrawal symptoms associated with Phases II and III.
Phase II occurs within 24 hours of abstaining from alcohol, grand mal seizures, in which a person loses
consciousness, are seen in this phase. Some people in this phase of alcohol withdrawal will have only
one seizure, whereas some suffer severe seizures that continue without interruption until treated by
a medical professional. Other alcoholics who abstain from alcohol do not have any seizures at all in
Phase II.
Phase III occurs after 30 or more hours of abstention from alcohol. In this stage the individual is
extremely agitated and confused, is disoriented for time and place, and suffers from frightening hallucinations. Very often, the alcoholic in Phase III of withdrawal will feel as if bugs are crawling on his
or her skin and clothing, or the individual will experience visual hallucinations of bugs or small animals
crawling about. Physically, the person may have an extremely high fever and tachycardia (abnormally
rapid heart rate). This phase may last for 3 or 4 days if untreated and is often referred to as delirium
tremens (DTs). This is the stage during which an alcoholic in withdrawal is most likely to die, due to
very high fever, heart failure, or self-injury resulting from delusions and hallucinations. Initial treatment for alcohol withdrawal normally includes antiseizure medications, including antianxiety agents
such as benzodiazepines, and drugs to treat fever, dehydration, and other physical symptoms, as well
as supportive psychotherapy.
Many investigators and clinicians disagree over the exact definition of addiction. Most require
both psychological dependence and physical dependence in their definition. However, this very
stringent definition creates problems when some drugs are considered. For example, there is
convincing evidence that marijuana produces psychological dependence. But withdrawal symptoms are not observed when a person stops using marijuana, because tetrahydrocannabinol
is absorbed by fat cells in the body and remains in the body for several weeks after a person
abstains. Thus, physical dependence is not seen in chronic marijuana users who stop smoking.
For this reason, some authorities claim that marijuana is not addicting.
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By the same token, because physical withdrawal symptoms are not apparent when a compulsive
shopper refrains from shopping or a compulsive gambler refrains from gambling, most investigators and clinicians assert that an individual cannot really be addicted to shopping or gambling.
The term dependence is used instead to characterize these compulsive behaviors, as in shopping
dependence or gambling dependence. The same is true for compulsive exercising, which is referred
to as exercise dependence (Cockerill & Riddington, 1996). People who engage in obligatory exercise spend most of their waking hours either exercising or planning their next run or next weighttraining session—that is, thinking about their next opportunity to exercise even when they are not
actually exercising, often at a great cost to their family life or career. However, even though some
people will organize their lives around these compulsive activities (shopping, gambling, exercising), with devastating effects on family and work, there is little consensus as to whether these
behaviors constitute addictions.
Role of Neurotransmitters in Addiction
Drugs that are frequently abused, such as alcohol, cocaine, or opiates (for example, morphine or
heroin), induce release of dopamine in the limbic system when ingested (Koob & Bloom, 1988;
Ortiz, Fitzgerald, Lane, Terwilliger, & Nesder, 1996; Sell et al., 1999; Volkow et al., 1999a). Nicotine
and tetrahydrocannabinol (the active ingredient in marijuana) also induce release of dopamine
in the nucleus accumbens (Chen, Parades, Lowinson, & Gardner, 1991; Tanda, Pontieri, Frau, &
Di Chiara, 1997). Thus, addictive substances produce the same effects as pleasurable emotions in
the brain. Ingvar and associates (1998) conducted PET scans on 13 male, nonalcoholic participants
to localize the brain areas that are activated by consumption of moderate doses of alcohol. The
alcohol ingested produced inebriation and a feeling of enhanced well-being in the subjects, and it
increased brain activity in the temporal lobe, where the hippocampus and amygdala are located,
and in the septum and nucleus accumbens (Ingvar et al., 1998). That is, a moderate amount of
alcohol selectively activates the brain structures associated with reward and positive emotions.
Like positive emotions, alcohol has been demonstrated to activate the reward cascade that you
learned about in the preceding section (Koob & Bloom, 1988). Alcohol stimulates the release
of serotonin, which activates the release of endorphins and ultimately results in the release of
dopamine in the nucleus accumbens. Consequently, drugs that increase the activity of serotonin,
endorphins, or dopamine in the brain will decrease craving for alcohol in alcoholic individuals and
will prevent relapse in recovered alcoholics (Johnson & Ait-Daoud, 1999; Verheul, van den Brink,
& Geerlings, 1999).
Addictive drugs also have biological effects similar to positive emotions in that they are associated with stimulation of D2 dopamine receptors. For example, research with rats has demonstrated that D2 receptor activity is related to alcohol intake in rats, increasing alcohol
intake in alcoholic rats when D2 activity is low and reducing alcohol intake when D2 activity is
high (Dyr, McBride, Lumeng, Li, & Murphy, 1993; McBride, Chernet, Dyr, Lumeng, & Li, 1993).
The aberrant A1 allele, which we discussed in conjunction with reward deficiency syndrome,
is found in most people who have a severe form of alcoholism (Blum et al., 1997). This means
that the D2 receptor activity is drastically reduced in most human alcoholics. Similarly, Nora
Volkow and her colleagues (1999a, 1999b) have conducted PET studies that have revealed
that low levels of D2 receptors are associated with a liking for and abuse of cocaine and
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Section 11.5 Addiction
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other psychostimulant drugs (Volkow et al., 1999a, 1999b). Thus, a number of investigators have
suggested that reduced dopamine D2 receptor activity leads to compulsive drug abuse and addiction (Blum, Cull, Braverman, & Comings, 1996; Blum et al., 1997, 2000; Blum, Yijun, Shriner, &
Gold, 2011; Volkow et al., 1999a, 1999b). The reduction in D2 receptor activity results in decreased
activation of the nucleus accumbens and hippocampus, producing dysphoria, craving for the
abused substance, and compulsive self-administration of the drug.
To summarize, substances that are associated with addiction induce the release of dopamine in
the limbic system and activate the pleasure-reward system associated with positive emotions.
Hence, self-administration of the substance makes the individual feel good. Addiction appears
to be related to low levels of D2 dopamine receptor activity. Some individuals are born with the
abnormal A1 allele, which produces D2 receptors that are defective and less active than normal
D2 receptors. These individuals with abnormal D2 receptors appear to be prone to develop addictions. However, chronic drug use can alter brain function, changing brain metabolism, receptor
function, gene expression, and responsiveness to drug-related cues in the environment (Leshner,
1997). All addictive substances share common effects on the brain that reflect an underlying
mechanism associated with all addictions.
The Development of an Addiction
When a person begins to use a drug, that drug use is sporadic and voluntary. But after an addiction develops, the addicted individual is compelled to seek out the drug and consume it. This
compulsive drug use is the hallmark of addiction. Addicts lose control over their drug intake. They
have a difficult time thinking of anything but acquiring the drug, and they will forsake all kinds of
social obligations (including family life and work) in order to obtain and use the drug. We still do
not know for sure how an addiction develops, but research in this area has given us some clues.
Most people who use drugs do not become addicts. Genetics, stress, life circumstances, and drug
availability all determine who develops an addiction and who does not. George Koob and Michel
Le Moal (1997) have proposed a model of hedonic homeostatic dysregulation, involving alterations in the reward pathway, to explain how an addiction develops. This model explains not only
how drug addiction occurs but also how other compulsive behaviors like binge eating and compulsive gambling develop. According to this model, addiction is a downward spiraling process that
proceeds from an initial failure in self-regulation to a large-scale breakdown in self-regulation
(Figure 11.8). The mesolimbic dopamine system is central to this model because addicting drugs
produce their rewarding effects through the release of dopamine by neurons in this system.
The hedonic homeostatic dysregulation model is based on the three stages of the addiction
cycle: preoccupation-anticipation, binge-intoxication, and withdrawal-negative affect. That is,
an addict (or a person developing an addiction) is always in one of these stages. The addict is
either (1) preoccupied with procuring the drug and anticipating its ingestion (preoccupationanticipation), (2) ingesting the drug in an uncontrolled manner and reeling from the effects of
the drug (binge-intoxication), or (3) abstaining from the drug and feeling miserable (withdrawalnegative affect). As the individual spirals downward into addiction, these stages are repeated,
each time altering the function of the brain a bit more (Koob & LeMoal, 1997).
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Section 11.5 Addiction
Figure 11.8: The hedonic homeostatic dysregulation model
According to this model, what contributes to addiction?
Dopamine
Opioid peptides
Stress hormones
Preoccupationanticipation
Withdrawal–
negative affect
Dopam
ine
iO
Oppioid
peptides
Dopamine
Opioid peptides
Stress
es
hormon
Bingeintoxication
Spiraling distress
Addiction
Treatment for Addiction
Initially, treatment for addiction is focused on treating the withdrawal symptoms associated with
drug abstinence. In many cases these withdrawal symptoms can be life-threatening, as you learned
in the “For Further Thought” box. However, long after the symptoms of physical dependence have
disappeared, psychological dependence continues to be a problem. A number of pharmacological
treatments have been developed to ease cravings and other aspects of psychological dependence.
Pharmacological treatment of addiction involves restoring neurotransmitter levels that have been
altered by the addiction. Drugs that increase dopamine function, particularly those that increase
D2 receptor function, can be used to help the addicted person remain abstinent (Koob & Le Moal,
1997). In addition, drugs that increase endorphin or serotonin activity are helpful in preventing
relapse and maintaining abstinence. Antianxiety agents, which increase GABA activity, are also
used to help reduce the symptoms, associated with the withdrawal-negative affect phase, that the
abstaining addict experiences. Drugs that antagonize the effect of glutamate, such as acamprosate, have been shown to be effective in reducing craving and compulsive drug-seeking in addicts
(Wickelgren, 1998).
Addiction is a disorder that is long-term and prone to relapse. Typically, a recovering addict will
have periods of abstinence interrupted by relapses characterized by compulsive drug-seeking and
use. Some investigators question whether a cure for addiction is possible, given the chronic nature
of the disorder (Leshner, 1997). Treating a chronic disorder like an addiction is difficult, due to the
many structural, functional, cellular, and biochemical changes in the brain that have occurred as a
result of the addiction. In addition, social and other environmental stimuli act as cues that prompt
the addictive behavior (Siegel, 1979; Siegel, Baptista, Kim, McDonald, & Weiss-Kelly, 2000). For
example, a person who is trying to quit smoking will find it extremely difficult to refuse a cigarette
at a party, especially if he or she has been drinking. Treatment for addiction involves changing the
way an individual thinks about and responds to environmental cues, in addition to compensating
for altered brain function caused by the addiction.
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Section 11.6 Chapter Summary
CHAPTER 11
In this chapter we have examined the biological basis of emotion and addiction. Negative emotions are associated with activation of the periventricular gray areas of the hypothalamus and
midbrain, whereas positive emotions are associated with the stimulation of the hippocampus.
Addiction appears to involve these same brain structures. During the preoccupation-anticipation
and binge-intoxication stages of the addiction cycle, the nucleus accumbens and periventricular and periaqueductal gray areas are activated. During the withdrawal-negative affect stage, the
periventricular area in the hypothalamus stimulates the release of stress hormones. We will examine how stress hormones affect the brain and behavior in Chapter 13.
11.6 Chapter Summary
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Emotion
An emotion is a complicated response to a stimulus, involving an alteration of mood,
cognition, and physiology, including activation of the sympathetic nervous system.
According to the James-Lange theory of emotion, a stimulus produces a physiological
response, which in turn produces an emotion.
According to the Cannon-Bard theory of emotion, a stimulus produces an emotion, which
in turn produces a physiological response.
According to the Schachter-Singer theory of emotion, an individual must experience physiological arousal and have an appropriate cognitive attribution in order to experience an
emotion.
According to Zajonc’s vascular theory of emotion, smiling causes blood to drain rapidly
from the face, cooling the blood in the cavernous sinus, which produces a positive emotion. In contrast, frowning causes blood to pool in the face, which increases the temperature of the brain and produces a negative emotion.
Emotional Pathways in the Central Nervous System
Particular regions of the brain have also been implicated in the regulation of emotions,
including the locus coeruleus, the limbic system, the cerebral cortex, the medial forebrain
bundle, and periventricular circuits.
Neurons in the locus coeruleus release norepinephrine and activate the sympathetic
nervous system in response to an emotional stimulus.
The term limbic system is used to refer to both the Papez circuit and Yakovlev’s circuit.
The left frontal lobe is activated during positive emotions, and the right frontal lobe is
activated during negative emotions.
Positive emotions are also associated with a bundle of axons that run through the center
of the forebrain called the medial forebrain bundle. Activation of the periventricular gray
regions is associated with negative emotions.
Negative Emotions
The amygdala relays information about sensory stimuli to different parts of the brain,
including the frontal lobe and periventricular gray area, which produces defensive
reactions.
Bilateral damage to the medial temporal lobe produces Kluver-Bucy syndrome, a disorder
in which affected individuals exhibit a loss of emotionality and an impaired ability to associate stimuli with consequences. Individuals with Urbach-Wiethe disease, which is caused
by bilateral damage limited to the amygdala, have difficulty remembering emotionally
arousing events.
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Questions for Thought
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CHAPTER 11
Head trauma is associated with increased levels of aggression. Individuals with temporal
lobe seizures may exhibit aggression with very little or no provocation.
Various neurotransmitters and hormones, including serotonin, norepinephrine, dopamine, and testosterone, are implicated in the control of aggression. Low levels of serotonin
and high levels of norepinephrine or dopamine are associated with aggressive behavior.
The prefrontal cortex, the amygdala, and the hypothalamus work together to control the
expression of fear. Endogenous opiates and GABA appear to be important in fear reactions.
Disorders associated with negative emotions include aggressive and anxiety disorders.
Treatment of these disorders involves blocking norepinephrine activity or increasing serotonin activity.
Positive Emotions
Positive emotions are associated with stimulation of the mesolimbic dopamine pathway,
known as the medial forebrain bundle in the diencephalon. Stimulation of the medial
forebrain bundle is rewarding, and rats will press a bar continuously for it.
According to the cascade theory of reward, feelings of pleasure arise when dopamine
binds with receptors in the hippocampus and nucleus accumbens. According to this
theory, release of serotonin by neurons in the hypothalamus causes endorphins to be
released in the midbrain, which inhibits the release of GABA, producing an increased
release of dopamine in the forebrain.
Reward deficiency syndrome has been linked to various addictions and is characterized by
feelings of dysphoria and craving, which are associated with decreased activity of neurons
in the hippocampus and nucleus accumbens.
A variant of a gene, called the A1 allele, codes for an inactive D2 dopamine receptor and
may be associated with reward deficiency syndrome.
Addiction
Addiction involves psychological and physical dependence on a substance that results in
a loss of control over its intake and has been linked to alterations in dopamine, serotonin,
and endorphin activity in the brain.
Reduced D2 receptor activity has also been associated with drug abuse and addiction.
Drugs that are frequently abused stimulate the release of dopamine in the limbic system.
Addictive drugs are also associated with stimulation of D2 dopamine receptor.
The hedonic homeostatic dysregulation model has been proposed to explain how an
addiction develops. According to this theory, an addict is always in one of three stages:
preoccupation-anticipation, binge-intoxication, or withdrawal-negative affect.
Treatments for addiction include pharmacological agents that increase dopamine, endorphin, or serotonin function, as well as psychotherapy.
Questions for Thought
1. Which plays the most important role in the experience of emotion: the peripheral nervous
system, the limbic system, or the cerebral cortex? Why?
2. Which brain mechanisms are shared by fear and anxiety?
3. Why do some people develop an alcohol addiction whereas others develop an addiction
for cocaine or heroin?
4. What is the difference between the James-Lange and the Cannon-Bard theories of
emotion?
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Key Terms
CHAPTER 11
5. Which emotions are associated with the medial forebrain bundle? Which are associated
with the periventricular circuits?
6. How is the D2 receptor implicated in addiction?
7. Describe the three stages of the hedonic homeostatic dysregulation model.
Web Links
The Mental Health America website provides information on anxiety disorders, including phobias, obsessive-compulsive disorder (OCD), and post-traumatic stress disorder (PTSD).
http://www.nmha.org
The National Institute of Drug Abuse offers many resources on the relationship between drug
addiction and the brain, especially the effects of drugs on brain chemistry and, ultimately,
human behavior.
http://www.drugabuse.gov/
Key Terms
A1 allele A variant of a specific gene that is
associated with reward deficiency syndrome.
addiction A disorder in which the affected
person loses control over intake of a particular
substance and demonstrates craving and physical dependence with withdrawal symptoms.
anxiety disorders Disorders characterized by
uncontrolled bouts of fear or overactivation of
the fear system.
Cannon-Bard theory of emotion A theory of
emotion that states that a stimulus causes an
emotion, which then produces physiological
changes.
cascade theory of reward A theory that states
that feelings of pleasure arise when dopamine
binds with receptors in the hippocampus
and nucleus accumbens; release of serotonin by neurons in the hypothalamus causes
endorphins to be released in the midbrain,
which inhibits the release of GABA, producing an increased release of dopamine in the
forebrain.
cavernous sinus A large venous pool of blood
that collects at the base of the skull before
being carried back to the heart.
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emotion A cognitive experience that is accompanied by an affective reaction and
a characteristic physiological response.
endogenous opiates Chemicals produced
inside the body that bind to opiate receptors
in the brain and mimic the analgesic effects of
morphine.
fight-or-flight responses Reactions to a
threatening stimulus that produce either fight
behavior, in which an individual strikes out at
the stimulus in an attempt to eliminate it, or
flight behavior, in which the individual runs
from the stimulus.
generalized anxiety disorder A syndrome
characterized by excessive apprehension about
unknown future events.
hedonic homeostatic dysregulation A model
that explains the development of addiction,
in which an addict is always in one of three
stages: preoccupation-anticipation, bingeintoxication, or withdrawal-negative affect.
intermittent explosive disorder A disorder
characterized by episodes of uncontrolled,
aggressive outbursts that result in assaults causing personal injury or property damage.
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Key Terms
James-Lange theory of emotion A theory of
emotion that states that a stimulus produces a
physiological response, which in turn produces
an emotion.
Kluver-Bucy syndrome A disorder caused by
bilateral damage to the anterior temporal lobe
that is characterized by a loss of fear, a lack
of emotional responsiveness, inappropriate
sexual behavior, and indiscriminate mouthing
of inedible items.
locus coeruleus A hindbrain structure that
produces norepinephrine and regulates
arousal.
medial forebrain bundle A bundle of neurons that courses through the center of the
forebrain, which is associated with positive
emotions.
CHAPTER 11
phobias Intense fears generated by specific
stimuli.
physical dependence A state characterized by
severe withdrawal symptoms when an individual abstains from taking an abused substance.
psychological dependence A craving or discomfort experienced when a substance is not
available for consumption.
reward deficiency syndrome A disorder in
which the reward system fails to function
properly; it is characterized by decreased
activity of neurons in the nucleus accumbens
and hippocampus, which produces dysphoria
(the opposite of euphoria), negative emotions,
and cravings for substances that can increase
dopamine activity.
mesolimbic dopamine pathway A pathway
that extends from the midbrain to the nucleus
accumbens in the forebrain; it is associated
with the regulation of emotional behavior.
Schachter-Singer theory of emotion
A theory of emotion that states that an individual must experience physiological arousal and
have an appropriate cognitive attribution in
order to experience an emotion.
nucleus accumbens A forebrain nucleus
where dopamine is released, producing pleasurable feelings.
steroids Hormones that alter the responses
of the cardiovascular, nervous, and immune
systems to the fearful stimulus.
obsessive-compulsive disorders Anxiety
disorders, associated with decreased serotonin
levels in the brain, that are characterized by
repetitive thoughts and ritualized behaviors
that are performed repeatedly.
temporal lobe seizures Epileptic seizures
caused by damage to the temporal lobes,
which produces aggressive behaviors with little
or no provocation.
panic disorder A disorder characterized by
bouts of intense fear or terror that are unpredictable and seem to occur “out of the blue.”
periventricular circuit A region of the brain
that passes through the thalamus, hypothalamus, and midbrain and is associated with
negative emotions.
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vascular theory of emotion A theory of emotion that states that smiling causes blood to
drain rapidly from the face, cooling the blood
in the cavernous sinus, which produces a
positive emotion. In contrast, frowning causes
blood to pool in the face, which increases the
temperature of the brain and produces a negative emotion.
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iStockphoto/Thinkstock
12
Images.com/Corbis
Disordered Behavior and
Stress Syndromes
Learning Objectives
After completing this chapter, you should be able to:
• Give examples of several stressors and describe how the locus coeruleus and HPA axis react to these stressors.
• Explain how the brain prepares the body to respond to stress, by describing changes in blood flow, breathing
rate, alertness, sleep, eating, growth, and reproduction.
• Draw a diagram of the HPA axis.
• Discuss how the dexamethasone suppression test can be used to diagnose depression.
• Explain the difference between habituation and sensitization.
• Name several disorders associated with stress.
• List the symptoms of major depressive disorder and relate these to brain functions.
• Giv...