1 and 2

Images.com/Corbis

Learning Objectives

After completing this chapter, you should be able to:

• 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.

11

Biological Bases of Emotion and Addiction

Visuals Unlimited, Inc./Science VU/ Visuals Unlimited/Getty Images

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CHAPTER 11Section 11.1 Emotion

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 com- mitted 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

We 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, see- ing 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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CHAPTER 11Section 11.1 Emotion

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 emo- tion 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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CHAPTER 11Section 11.1 Emotion

our behavior in such a way as to motivate us to approach pleasant stimuli (as in the case of posi- tive 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 defen- sive 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 threaten- ing 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 pro- duces 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 11Section 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.

See bear

James-Lange Theory:

Run away, heart pounding Experience emotion (fear)

See bear

Cannon-Bard Theory:

Experience emotion (fear) Run away, heart pounding

See bear

Schachter-Singer Theory:

Cognitive appraisal of event. “This is a bear. Bears are scary.”

Run away, heart pounding Cognitive appraisal of bodily response. “My heart is pounding.

I’m running away like crazy.”

Experience emotion (fear)

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CHAPTER 11Section 11.1 Emotion

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 par- ticipants 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 physi- ological arousal.

Following the injection, each par- ticipant was placed individually in a room where a confederate was completing a survey. (A confeder- ate 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 par- ticipant 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 con- dition, the confederate became

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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CHAPTER 11Section 11.1 Emotion

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 injec- tion 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 the- ory 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 11Section 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.

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 min- utes, 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.

Veins that drain blood from the face to the cavernous sinus

Anterior cerebral artery

Frontopolar branch

External jugular vein

Internal carotid artery

Cavernous sinus

B. Cool blood from the superficial layer of the face (skin, muscle) drains into cavernous sinus, cooling the brain.

C. Cool blood pools in the face and does not drain into cavernous sinus, warming the brain.

A.

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CHAPTER 11Section 11.2 Emotional Pathways in the Central Nervous System

The vascular theory of emotion may explain why facial expression of emotions appears to be uni- versal 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 labora- tory, 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

The 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 divi- sions 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 norepineph- rine, 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). Excita- tion 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 epi- nephrine 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 11Section 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.

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 neigh- bor, 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.

Thalamus

Locus coeruleus

Cerebellar cortex

To spinal cord

Hippocampus

Hypothalamus

Amygdala

Cerebral cortex

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CHAPTER 11Section 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 experienc- ing 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.

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. Mod- ern 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,

Frontal lobe

Anterior nucleus of thalamus

Septum

Olfactory lobe

Amygdala Hippocampus

Stria terminalis

Brain stem

Corpus callosum

Amygdala

Substantia nigra Ventral tegmental

region

Hypothalamus

Hypothalamus

Nucleus accumbens

HippocampusHippocampus

Corpus callosum

A. B.

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CHAPTER 11Section 11.3 Negative Emotions

& 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 cere- bral 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 emo- tions. 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

The 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 nega- tive 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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CHAPTER 11Section 11.3 Negative Emotions

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 emo- tional 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 eat- ing 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 altera- tions 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. Urbach- Wiethe 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 rec- ognize 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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CHAPTER 11Section 11.3 Negative Emotions

Recent research has indicated that impairment of the amygdala may be related to antisocial behav- ior 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 mecha- nisms 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.

Individuals with temporal lobe seizures will sometimes exhibit aggression with little or no provo- cation (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 chew- ing movements at the onset of the

Pixland/Thinkstock

Photo 11.2 Many people have trouble controlling their negative emotions and can be very aggressive.

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CHAPTER 11Section 11.3 Negative Emotions

seizure. As the seizure progresses, the individual will become aggressive, striking out at the near- est 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 control- ling 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 fisher- man (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 impor- tant role in controlling aggression. Let’s examine the relation of each of these neurochemicals with aggressive behavior.

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CHAPTER 11Section 11.3 Negative Emotions

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 uncon- trolled 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 signifi- cantly 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 vio- lent 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 norepi- nephrine 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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CHAPTER 11Section 11.3 Negative Emotions

Serotonin

Norepinephrine

Dopamine

Testosterone may facilitate aggression

Arginine-vasopressin arginine-vasopressin aggression

Neurotransmi�er

Hormones

dopamine aggression; dopamine aggression

serotonin aggression

norepinephrine aggressionnorepinephrine aggression;

serotonin aggression;

Table 11.1 summarizes the effects of neurotransmitters and hormones on aggressive behavior.

Table 11.1: Effects of neurotransmitters and hormones on 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 underpin- nings 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 mean- time 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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CHAPTER 11Section 11.3 Negative Emotions

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 par- ticular 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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CHAPTER 11Section 11.3 Negative Emotions

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 psychother- apy, 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 sero- tonin 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 anxi- ety 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, anxi- ety becomes pathologic when it disrupts normal behavior. That is, when an individual makes repeated inappropriate responses to some unknown or unreal threat, an anxi- ety disorder is present. A number of anxiety disorders have been identified, including generalized anxiety disorder, panic disorder,

Wavebreak Media/Thinkstock

Photo 11.3 Anxiety becomes pathologic when it disrupts nor- mal behavior.

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CHAPTER 11Section 11.3 Negative Emotions

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 situ- ations, 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 disor- ders, 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 (com- pulsions). These obsessions and compulsions disrupt the affected individual’s normal activities.

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CHAPTER 11Section 11.3 Negative Emotions

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 hesita- tion, he got the vacuum back out and went over the entire carpet in his three-room apartment again, this time moving all the furniture, including the couch and heavy dresser. Then Ted found a crumb on the carpet in the hallway. He knew he had to go, but he felt he must 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 embar- rassing, 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 satis- faction, 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.

Jupiterimages/Pixland/Thinkstock

Photo 11.4 A common compulsion in obsessive-compulsive disorder is to constantly clean.

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 disor- der 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 behav- ior is senseless and disruptive, that individual cannot stop performing it without experiencing a great deal of anxiety and apprehension (see the “Case Study”).

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CHAPTER 11Section 11.4 Positive Emotions

Treatment of Anxiety Disorders Because activation of the sympathetic nervous system is implicated in all forms of anxiety dis- orders, 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 dis- orders 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 through- out 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 obsessive- compulsive disorder changes following administration of an SSRI. In contrast, antidepressants that block the reuptake of norepinephrine, such as desipramine, do not reduce obsessive- compulsive symptoms. Thus, obsessive-compulsive behaviors appear to be related to decreased serotonin activity in the brain (Baumgarten & Grozdanovic, 1998).

11.4 Positive Emotions

Euphoria, happiness, being in love, joy—these positive emotions are all associated with stim-ulation 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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CHAPTER 11Section 11.4 Positive Emotions

Figure 11.6: The mesolimbic dopamine pathway

Positive emotions are associated with the stim ulation of the mesolimbic dopamine pathway.

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.

Corpus callosum

Brain stem

Cerebellum

Ventral tegmental area and substantia nigra

Spinal cord

Mesolimbic pathway

Hypothalamus

Nucleus accumbens

Amygdala

Frontal lobe

Prefrontal cortex

Basal ganglia

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CHAPTER 11Section 11.4 Positive Emotions

In addition to dopamine, other neurotransmitters are involved in the generation of pleasur- able 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 hippocam- pus, 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

Dopamine

Dopamine Dopamine

Reward Reward

Dopamine

D2 receptorD2 receptor

Ventral tegmental

region

Nucleus accumbens

Substantia nigra

Amygdala

Hippocampus

GABA

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CHAPTER 11Section 11.4 Positive Emotions

Please remember that the cascade theory of reward is just that: a theory. Although there is con- siderable 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 dopa- mine 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 pro- vided 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 sub- cortical structures—namely, the nucleus accumbens and amygdala—are activated by pleasurable rewards in human participants (Breiter & Rosen, 1999). A more recent functional MRI study indi- cated 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 accum- bens and hippocampus, which produces dysphoria (the opposite of euphoria), negative emotions,

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CHAPTER 11Section 11.5 Addiction

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 D

2 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 D

2 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 D

2 receptors (Lee, Parish, Tomas, & Horne, 2011; Volkow et al., 1993).

For example, chronic exposure to cocaine is associated with a decrease in dopamine D 2 recep-

tors in the brain. This decrease in dopamine D 2 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

People 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 “work- aholic.” 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 sub- stance. 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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CHAPTER 11Section 11.5 Addiction

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 physi- cally 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 identi- fied, based on their time of onset after a person has stopped drinking.

Phase I occurs within a few hours after drinking has stopped. In Phase I a person develops uncontrollable 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 hallucina- tions 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 hal- lucinations. 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 treat- ment 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.

Creatas Images/Creatas/Thinkstock

Photo 11.5 Headaches are part of Phase I alcohol withdrawal.

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 symp- toms 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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CHAPTER 11Section 11.5 Addiction

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 investiga- tors 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 exer- cise spend most of their waking hours either exercising or planning their next run or next weight- training 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, exercis- ing), 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 asso- ciated with stimulation of D

2 dopamine receptors. For example, research with rats has dem-

onstrated that D 2 receptor activity is related to alcohol intake in rats, increasing alcohol

intake in alcoholic rats when D 2 activity is low and reducing alcohol intake when D

2 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 D

2 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 D

2 receptors are associated with a liking for and abuse of cocaine and

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CHAPTER 11Section 11.5 Addiction

other psychostimulant drugs (Volkow et al., 1999a, 1999b). Thus, a number of investigators have suggested that reduced dopamine D

2 receptor activity leads to compulsive drug abuse and addic-

tion (Blum, Cull, Braverman, & Comings, 1996; Blum et al., 1997, 2000; Blum, Yijun, Shriner, & Gold, 2011; Volkow et al., 1999a, 1999b). The reduction in D

2 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 D

2 dopamine receptor activity. Some individuals are born with the

abnormal A1 allele, which produces D 2 receptors that are defective and less active than normal

D 2 receptors. These individuals with abnormal D

2 receptors appear to be prone to develop addic-

tions. 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 addic- tion 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 altera- tions 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 com- pulsive 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 (preoccupation- anticipation), (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 (withdrawal- negative 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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CHAPTER 11Section 11.5 Addiction

Figure 11.8: The hedonic homeostatic dysregulation model

According to this model, what contributes to 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 D

2 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 acampro- sate, 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.

Preoccupation- anticipation

Binge- intoxication

Withdrawal– negative affect

Dopamine peptides horm ones

iOpoid Stre ss

Opioid Stre ss

Dopamine

Opioid peptides

Stress hormones

Dopamine

Opioid peptides

Stress hormones

Dopamine

Opioid peptides

Dopamine

Opioid peptides

Dopamine peptides horm ones

Spiraling distress

Addiction

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CHAPTER 11Section 11.6 Chapter Summary

In this chapter we have examined the biological basis of emotion and addiction. Negative emo- tions 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 periventricu- lar 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 exam- ine how stress hormones affect the brain and behavior in Chapter 13.

11.6 Chapter Summary 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 phys- iological 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 emo- tion. In contrast, frowning causes blood to pool in the face, which increases the tempera- ture 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 asso- ciate 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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CHAPTER 11Questions for Thought

• 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, dopa- mine, 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 sero- tonin 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 D 2 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 D 2 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 D

2 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, endor- phin, 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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CHAPTER 11Key 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 phys- ical 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 sero- tonin by neurons in the hypothalamus causes endorphins to be released in the midbrain, which inhibits the release of GABA, produc- ing 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.

emotion A cognitive experience that is accom- panied 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, binge- intoxication, or withdrawal-negative affect.

intermittent explosive disorder A disorder characterized by episodes of uncontrolled, aggressive outbursts that result in assaults caus- ing personal injury or property damage.

5. Which emotions are associated with the medial forebrain bundle? Which are associated with the periventricular circuits?

6. How is the D 2 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 pho- bias, 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

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CHAPTER 11Key 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 neu- rons that courses through the center of the forebrain, which is associated with positive emotions.

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.

nucleus accumbens A forebrain nucleus where dopamine is released, producing plea- surable feelings.

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.

panic disorder A disorder characterized by bouts of intense fear or terror that are unpre- dictable and seem to occur “out of the blue.”

periventricular circuit A region of the brain that passes through the thalamus, hypothala- mus, and midbrain and is associated with negative emotions.

phobias Intense fears generated by specific stimuli.

physical dependence A state characterized by severe withdrawal symptoms when an individ- ual abstains from taking an abused substance.

psychological dependence A craving or dis- comfort 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.

Schachter-Singer theory of emotion A theory of emotion that states that an individ- ual must experience physiological arousal and have an appropriate cognitive attribution in order to experience an emotion.

steroids Hormones that alter the responses of the cardiovascular, nervous, and immune systems to the fearful stimulus.

temporal lobe seizures Epileptic seizures caused by damage to the temporal lobes, which produces aggressive behaviors with little or no provocation.

vascular theory of emotion A theory of emo- tion 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 nega- tive emotion.

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