Aggression and Testosterone

Pinel, J. P. (2010). Biopsychology, 8th Edition [VitalSource Bookshelf version]. Retrieved from

Please use this book in the paper many times



Biopsychology of Emotion, Stress, and Health Fear, the Dark Side of Emotion

17.1 Biopsychology of Emotion: Introduction

17.2 Fear, Defense, and Aggression

17.3 Neural Mechanisms of Fear Conditioning

17.4 Stress and Health

17.5 Brain Mechanisms of Human Emotion

This chapter about the biopsychology of emotion, stress, and health begins with a historical introduction to the biopsychology of emotion and then focuses in the next two sections on the dark end of the emotional spectrum: fear. Biopsychological research on emotions has concentrated on fear not because biopsy-chologists are a scary bunch, but because fear has three important qualities: It is the easiest emotion to infer from behavior in various species; it plays an important adaptive function in motivating the avoidance of threatening situations; and chronic fear induces stress. In the final two sections of the chapter, you will learn how stress increases susceptibility to illness and how some brain structures have been implicated in human emotion.

17.1 Biopsychology of Emotion: Introduction

To introduce the biopsychology of emotion, this section reviews several classic early discoveries and then discusses the role of the autonomic nervous system in emotional experience and the facial expression of emotion.

Early Landmarks in the Biopsychological Investigation of Emotion

This subsection describes, in chronological sequence, six early landmarks in the biopsychological investigation of emotion. It begins with the 1848 case of Phineas Gage.

The Mind-Blowing Case of Phineas Gage

In 1848, Phineas Gage, a 25-year-old construction foreman for the Rutland and Burlington Railroad, was the victim of a tragic accident. In order to lay new tracks, the terrain had to be leveled, and Gage was in charge of the blasting. His task involved drilling holes in the rock, pouring some gun powder into each hole, covering it with sand, and tamping the material down with a large tamping iron before detonating it with a fuse. On the fateful day, the gunpowder exploded while Gage was tamping it, launching the 3-cm-thick, 90-cm-long tamping iron through his face, skull, and brain and out the other side.

Clinical Implications

Amazingly, Gage survived his accident, but he survived it a changed man. Before the accident, Gage had been a responsible, intelligent, socially well-adapted person, who was well liked by his friends and fellow workers. Once recovered, he appeared to be as able-bodied and intellectually capable as before, but his personality and emotional life had totally changed. Formerly a religious, respectful, reliable man, Gage became irreverent and impulsive. In particular, his abundant profanity offended many. He became so unreliable and undependable that he soon lost his job, and was never again able to hold a responsible position.

Gage became itinerant, roaming the country for a dozen years until his death in San Francisco. His bizarre accident and apparently successful recovery made headlines around the world, but his death went largely unnoticed and unacknowledged.

Gage was buried next to the offending tamping iron. Five years later, neurologist John Harlow was granted permission from Gage’s family to exhume the body and tamping iron to study them. Since then, Gage’s skull and the tamping iron have been on display in the Warren Anatomical Medical Museum at Harvard University.

FIGURE 17.1 A reconstruction of the brain injury of Phineas Gage. The damage focused on the medial prefrontal lobes. (Based on Damasio et al., 1994.)

In 1994, Damasio and her colleagues brought the power of computerized reconstruction to bear on Gage’s classic case. They began by taking an X-ray of the skull and measuring it precisely, paying particular attention to the position of the entry and exit holes. From these measurements, they reconstructed the accident and determined the likely region of Gage’s brain damage (see Figure 17.1). It was apparent that the damage to Gage’s brain affected both medial prefrontal lobes, which we now know are involved in planning and emotion (see Machado & Bachevalier, 2006; Vogt, 2005).

Darwin’s Theory of the Evolution of Emotion

The first major event in the study of the biopsychology of emotion was the publication in 1872 of Darwin’s book The Expression of Emotions in Man and Animals. In it, Darwin argued, largely on the basis of anecdotal evidence, that particular emotional responses, such as human facial expressions, tend to accompany the same emotional states in all members of a species.

Evolutionary Perspective

Darwin believed that expressions of emotion, like other behaviors, are products of evolution; he therefore tried to understand them by comparing them in different species. From such interspecies comparisons, Darwin developed a theory of the evolution of emotional expression that was composed of three main ideas:

• Expressions of emotion evolve from behaviors that indicate what an animal is likely to do next.

• If the signals provided by such behaviors benefit the animal that displays them, they will evolve in ways that enhance their communicative function, and their original function may be lost.

• Opposite messages are often signaled by opposite movements and postures, an idea called the principle of antithesis.

Consider how Darwin’s theory accounts for the evolution of threat displays. Originally, facing one’s enemies, rising up, and exposing one’s weapons were the components of the early stages of combat. But once enemies began to recognize these behaviors as signals of impending aggression, a survival advantage accrued to attackers that could communicate their aggression most effectively and intimidate their victims without actually fighting. As a result, elaborate threat displays evolved, and actual combat declined.

To be most effective, signals of aggression and submission must be clearly distinguishable; thus, they tended to evolve in opposite directions. For example, gulls signal aggression by pointing their beaks at one another and submission by pointing their beaks away from one another; primates signal aggression by staring and submission by averting their gaze. Figure 17.2 reproduces the woodcuts Darwin used in his 1872 book to illustrate this principle of antithesis in dogs.

James-Lange and Cannon-Bard Theories

The first physiological theory of emotion was proposed independently by James and Lange in 1884. According to the James-Lange theory, emotion-inducing sensory stimuli are received and interpreted by the cortex, which triggers changes in the visceral organs via the autonomic nervous system and in the skeletal muscles via the somatic nervous system. Then, the autonomic and somatic responses trigger the experience of emotion in the brain. In effect, what the James-Lange theory did was to reverse the usual common-sense way of thinking about the causal relation between the experience of emotion and its expression. James and Lange argued that the autonomic activity and behavior that are triggered by the emotional event (e.g., rapid heartbeat and running away) produce the feeling of emotion, not vice versa.

FIGURE 17.2 Two woodcuts from Darwin’s 1872 book, The Expression of Emotions in Man and Animals, that he used to illustrate the principle of antithesis. The aggressive posture of dogs features ears forward, back up, hair up, and tail up; the submissive posture features ears back, back down, hair down, and tail down.

Around 1915, Cannon proposed an alternative to the James-Lange theory of emotion, and it was subsequently extended and promoted by Bard. According to the Cannon-Bard theory, emotional stimuli have two independent excitatory effects: They excite both the feeling of emotion in the brain and the expression of emotion in the autonomic and somatic nervous systems. That is, the Cannon-Bard theory, in contrast to the James-Lange theory, views emotional experience and emotional expression as parallel processes that have no direct causal relation.

The James-Lange and Cannon-Bard theories make different predictions about the role of feedback from autonomic and somatic nervous system activity in emotional experience. According to the James-Lange theory, emotional experience depends entirely on feedback from autonomic and somatic nervous system activity; according to the Cannon-Bard theory, emotional experience is totally independent of such feedback. Both extreme positions have proved to be incorrect. On the one hand, it seems that the autonomic and somatic feedback is not necessary for the experience of emotion: Human patients whose autonomic and somatic feedback has been largely eliminated by a broken neck are capable of a full range of emotional experiences (e.g., Lowe & Carroll, 1985). On the other hand, there have been numerous reports—some of which you will soon encounter—that autonomic and somatic responses to emotional stimuli can influence emotional experience.

Failure to find unqualified support for either the James-Lange or the Cannon-Bard theory led to the modern biopsychological view. According to this view, each of the three principal factors in an emotional response—the perception of the emotion-inducing stimulus, the autonomic and somatic responses to the stimulus, and the experience of the emotion—can influence the other two (see Figure 17.3).

Sham Rage

In the late 1920s, Bard (1929) discovered that decorticate cats—cats whose cortex has been removed—respond aggressively to the slightest provocation: After a light touch, they arch their backs, erect their hair, growl, hiss, and expose their teeth.

FIGURE 17.3 Four ways of thinking about the relations among the perception of emotion-inducing stimuli, the autonomic and somatic responses to the stimuli, and the emotional experience.

The aggressive responses of decorticate animals are abnormal in two respects: They are inappropriately severe, and they are not directed at particular targets. Bard referred to the exaggerated, poorly directed aggressive responses of decorticate animals as sham rage.

Sham rage can be elicited in cats whose cerebral hemispheres have been removed down to, but not including, the hypothalamus; but it cannot be elicited if the hypothalamus is also removed. On the basis of this observation, Bard concluded that the hypothalamus is critical for the expression of aggressive responses and that the function of the cortex is to inhibit and direct these responses.

Limbic System and Emotion

In 1937, Papez (pronounced “Payps”) proposed that emotional expression is controlled by several interconnected nuclei and tracts that ring the thalamus. Figure 17.4 illustrates some of the key structures in this circuit, now known as the limbic system (limbic means “border”): the amygdala, mammillary body, hippocampus, fornix, cortex of the cingulate gyrus, septum, olfactory bulb, and hypothalamus. Papez proposed that emotional states are expressed through the action of the other structures of the circuit on the hypothalamus and that they are experienced through their action on the cortex. Papez’s theory of emotion was revised and expanded by Paul MacLean in 1952 and became the influential limbic system theory of emotion.

Kluver-Bucy Syndrome

In 1939, Kluver and Bucy observed a striking syndrome (pattern of behavior) in monkeys whose anterior temporal lobes had been removed. This syndrome, which is commonly referred to as the Kluver-Bucy syndrome, includes the following behaviors: the consumption of almost anything that is edible, increased sexual activity often directed at inappropriate objects, a tendency to repeatedly investigate familiar objects, a tendency to investigate objects with the mouth, and a lack of fear. Monkeys that could not be handled before surgery were transformed by bilateral anterior temporal lobectomy into tame subjects that showed no fear whatsoever—even in response to snakes, which terrify normal monkeys. In primates, most of the symptoms of the Kluver-Bucy syndrome appear to result from damage to the amygdala (see Phelps, 2006), a structure that has played a major role in research on emotion, as you will learn later in this chapter.

Evolutionary Perspective

The Kluver-Bucy syndrome has been observed in several species. Following is a description of the syndrome in a human patient with a brain infection.

FIGURE 17.4 The location of the major limbic system structures. In general, they are arrayed near the midline in a ring around the thalamus. (See also Figure 3.28 on page 70.)

A Human Case of Kluver-Bucy Syndrome

He exhibited a flat affect, and although originally restless, ultimately became remarkably placid. He appeared indifferent to people or situations. He spent much time gazing at the television, but never learned to turn it on; when the set was off, he tended to watch reflections of others in the room on the glass screen. On occasion he became facetious, smiling inappropriately and mimicking the gestures and actions of others. Once initiating an imitative series, he would perseverate copying all movements made by another for extended periods of time. . . . He engaged in oral exploration of all objects within his grasp, appearing unable to gain information via tactile or visual means alone. All objects that he could lift were placed in his mouth and sucked or chewed. . . .

Clinical Implications

Although vigorously heterosexual prior to his illness, he was observed in hospital to make advances toward other male patients. . . . [H]e never made advances toward women, and, in fact, his apparent reversal of sexual polarity prompted his fiancée to sever their relationship. (Marlowe, Mancall, & Thomas, 1985, pp. 55–56)

The six early landmarks in the study of brain mechanisms of emotion just reviewed are listed in Table 17.1.

Emotions and the Autonomic Nervous System

Research on the role of the autonomic nervous system (ANS) in emotion has focused on two issues: the degree to which specific patterns of ANS activity are associated with specific emotions and the effectiveness of ANS measures in polygraphy (lie detection).

Emotional Specificity of the Autonomic Nervous System

The James-Lange and Cannon-Bard theories differ in their views of the emotional specificity of the autonomic nervous system. The James-Lange theory says that different emotional stimuli induce different patterns of ANS activity and that these different patterns produce different emotional experiences. In contrast, the Cannon-Bard theory claims that all emotional stimuli produce the same general pattern of sympathetic activation, which prepares the organism for action (i.e., increased heart rate, increased blood pressure, pupil dilation, increased flow of blood to the muscles, increased respiration, and increased release of epinephrine and norepinephrine from the adrenal medulla).

TABLE 17.1 Biopsychological Investigation of Emotion: Six Early Landmarks



Case of Phineas Gage


Darwin’s theory of the evolution of emotion


James-Lange and Cannon-Bard theories

about 1900

Discovery of sham rage


Discovery of Kluver-Bucy syndrome


Limbic system theory of emotion


The experimental evidence suggests that the specificity of ANS reactions lies somewhere between the extremes of total specificity and total generality (Levenson, 1994). There is ample evidence that not all emotions are associated with the same pattern of ANS activity (see Ax, 1955); however, there is insufficient evidence to make a strong case for the view that each emotion is characterized by a different pattern of ANS activity.


Polygraphy is a method of interrogation that employs autonomic nervous system indexes of emotion to infer the truthfulness of the subject’s responses. Polygraph tests administered by skilled examiners can be useful additions to normal interrogation procedures, but they are far from infallible.

The main problem in evaluating the effectiveness of polygraphy is that it is rarely possible in real-life situations to know for certain whether a suspect is guilty or innocent. Consequently, many studies of polygraphy have employed the mock-crime procedure: Volunteer subjects participate in a mock crime and are then subjected to a polygraph test by an examiner who is unaware of their “guilt” or “innocence.” The usual interrogation method is the control-question technique, in which the physiological response to the target question (e.g., “Did you steal that purse?”) is compared with the physiological responses to control questions whose answers are known (e.g., “Have you ever been in jail before?”). The assumption is that lying will be associated with greater sympathetic activation. The average success rate in various mock-crime studies using the control-question technique is about 80%.

Despite being commonly referred to as lie detection, polygraphy detects emotions, not lies. Consequently, it is less likely to successfully identify lies in real life than in experiments. In real-life situations, questions such as “Did you steal that purse?” are likely to elicit a reaction from all suspects, regardless of their guilt or innocence, making it difficult to detect deception. The guilty-knowledge technique circumvents this problem. In order to use this technique, the polygrapher must have a piece of information concerning the crime that would be known only to the guilty person. Rather than attempting to catch the suspect in a lie, the polygrapher simply assesses the suspect’s reaction to a list of actual and contrived details of the crime. Innocent suspects, because they have no knowledge of the crime, react to all such details in the same way; the guilty react differentially.

In the classic study of the guilty-knowledge technique (Lykken, 1959), subjects waited until the occupant of an office went to the washroom. Then, they entered her office, stole her purse from her desk, removed the money, and left the purse in a locker. The critical part of the interrogation went something like this: “Where do you think we found the purse? In the washroom? . . . In a locker? . . . Hanging on a coat rack? . . .” Even though electrodermal activity was the only measure of ANS activity used in this study, 88% of the mock criminals were correctly identified; more importantly, none of the innocent subjects was judged guilty—see MacLaren (2001) for a review.

Emotions and Facial Expression

Ekman and his colleagues have been preeminent in the study of facial expression (see Ekman, 2003). They began in the 1960s by analyzing hundreds of films and photographs of people experiencing various real emotions. From these, they compiled an atlas of the facial expressions that are normally associated with different emotions (Ekman & Friesen, 1975). For example, to produce the facial expression for surprise, models were instructed to pull their brows upward so as to wrinkle their forehead, to open their eyes wide so as to reveal white above the iris, to slacken the muscles around their mouth, and to drop their jaw. Try it.

Universality of Facial Expression

Several studies have found that people of different cultures make similar facial expressions in similar situations and that they can correctly identify the emotional significance of facial expressions displayed by people from cultures other than their own. The most convincing of these studies was a study of the members of an isolated New Guinea tribe who had had little or no contact with the outside world (Ekman & Friesen, 1971). However, some studies have identified some subtle cultural differences in facial expressions (see Russell, Bachorowski, & Fernandez-Dols, 2003). Remarkably, human facial expressions are similar in many respects to those of our primate relatives (see Parr, Waller, & Fugate, 2005; Parr, Waller, & Vick, 2007).

Primary Facial Expressions

Ekman and Friesen concluded that the facial expressions of the following six emotions are primary: surprise, anger, sadness, disgust, fear, and happiness (however, see Tracy & Robins, 2004). They further concluded that all other facial expressions of genuine emotion are composed of predictable mixtures of these six primaries. Figure 17.5 illustrates these six primary facial expressions and the combination of two of them to form a nonprimary expression.

Facial Feedback Hypothesis

Is there any truth to the old idea that putting on a happy face can make you feel better? Research suggests that there is (see Adelmann & Zajonc, 1989). The hypothesis that our facial expressions influence our emotional experience is called the facial feedback hypothesis. In a test of the facial feedback hypothesis, Rutledge and Hupka (1985) instructed subjects to assume one of two patterns of facial contractions while they viewed a series of slides; the patterns corresponded to happy or angry faces, although the subjects were unaware of that. The subjects reported that the slides made them feel more happy and less angry when they were making happy faces, and less happy and more angry when they were making angry faces (see Figure 17.6).

Voluntary Control of Facial Expression

Because we can exert voluntary control over our facial muscles, it is possible to inhibit true facial expressions and to substitute false ones. There are many reasons for choosing to put on a false facial expression. Some of them are positive (e.g., putting on a false smile to reassure a worried friend), and some are negative (e.g., putting on a false smile to disguise a lie). In either case, it is difficult to fool an expert.

There are two ways of distinguishing true expressions from false ones (Ekman, 1985). First, microexpressions (brief facial expressions) of the real emotion often break through the false one (Porter & ten Brinke, 2008). Such microexpressions last only about 0.05 second, but with practice they can be detected without the aid of slow-motion photography. Second, there are often subtle differences between genuine facial expressions and false ones that can be detected by skilled observers.

FIGURE 17.5 Ekman’s six primary facial expressions of emotion, and one combination facial expression. (Generously supplied by Kyung Jae Lee and Stephen DiPaola of the iVizLab, Simon Fraser University. The expressions were created in video game character style using FaceFx 3D software, which allows DiPaola and Lee to create and control facial expressions of emotion in stills and animated sequences; see

The most widely studied difference between a genuine and a false facial expression was first described by the French anatomist Duchenne in 1862. Duchenne said that the smile of enjoyment could be distinguished from deliberately produced smiles by consideration of the two facial muscles that are contracted during genuine smiles: orbicularis oculi, which encircles the eye and pulls the skin from the cheeks and forehead toward the eyeball, and zygomaticus major, which pulls the lip corners up (see Figure 17.7). According to Duchenne, the zygomaticus major can be controlled voluntarily, whereas the orbicularis oculi is normally contracted only by genuine pleasure. Thus, inertia of the orbicularis oculi in smiling unmasks a false friend—a fact you would do well to remember. Ekman named the genuine smile the Duchenne smile (see Ekman & Davidson, 1993).

FIGURE 17.6 The effects of facial expression on the experience of emotion. Participants reported feeling more happy and less angry when they viewed slides while making a happy face, and less happy and more angry when they viewed slides while making an angry face. (Based on Rutledge & Hupka, 1985.)

Facial Expressions: Current Perspectives

Ekman’s work on facial expression began before video recording became commonplace. Now, video recordings provide almost unlimited access to natural facial expressions made in response to real-life situations. As a result, it is now clear that Ekman’s six primary facial expressions of emotion rarely occur in pure form—they are ideals with many subtle variations. Also, the existence of other primary emotions has been recognized. For example, Ekman (1992) agrees that there is evidence for adding contempt and embarrassment to his original six.

FIGURE 17.7 A fake smile. The orbicularis oculi and the zygomaticus major are two muscles that contract during genuine (Duchenne) smiles. Because the lateral portion of the orbicularis oculi is difficult for most people to contract voluntarily, fake smiles usually lack this component. This young man is faking a smile for the camera. Look at his eyes.

Check It Out

Experiencing Facial Feedback

Why don’t you try the facial feedback hypothesis? Pull your eyebrows down and together; raise your upper eyelids and tighten your lower eyelids, and narrow your lips and press them together. Now, hold this expression for a few seconds. If it makes you feel slightly angry and uncomfortable, you have just experienced the effect of facial feedback.

Have you noticed that only one of the eight primary emotions, happiness, has a positive emotional valence? (Emotional valence refers to the general positive or negative character of an emotion.) This imbalance has led some to hypothesize that all positive emotions may share the same facial expression. The research on pride by Tracy and Robins (2004, 2007a, 2007b) argues against this view. The expression of pride is readily identified by individuals of various cultures, cannot be created from a mixture of other primary expressions, and involves postural as well as facial components (Tracy & Robins, 2007a). Pride is expressed through a small smile, with the head tilted back slightly and the hands on the hips, raised above the head, or clenched in fists with the arms crossed on the chest—see Figure 17.8.

FIGURE 17.8 An expression of pride. (Reproduced with permission of Jessica Tracy, Department of Psychology, University of British Columbia.)

17.2 Fear, Defense, and Aggression

Most biopsychological research on emotion has focused on fear and defensive behaviors. Fear is the emotional reaction to threat; it is the motivating force for defensive behaviors. Defensive behaviors are behaviors whose primary function is to protect the organism from threat or harm. In contrast, aggressive behaviors are behaviors whose primary function is to threaten or harm.

 Simulate Coping Strategies and Their Effect; Defense Mechanisms

Although one purpose of this section is to discuss fear, defense, and aggression, it has another important purpose: to explain a common problem faced by biopsychologists and the way in which those who conduct research in this particular area have managed to circumvent it. Barrett (2006) pointed out that progress in the study of the neural basis of emotion has been limited because neuroscientists have often been guided by unsubstantiated cultural assumptions about emotion: Because we have words such as fearhappiness, and anger in our language, scientists have often assumed that these emotions exist as entities in the brain, and they have searched for them—often with little success. The following lines of research on fear, defense, and aggression illustrate how biopsychologists can overcome the problem of vague, subjective, everyday concepts by basing their search for neural mechanisms on the thorough descriptions of relevant behaviors and the environments in which they occur, and on the putative adaptive functions of such behaviors (see Barrett & Wager, 2006; Panksepp, 2007).

Types of Aggressive and Defensive Behaviors

Considerable progress in the understanding of aggressive and defensive behaviors has come from the research of Blanchard and Blanchard (see 1989, 1990) on the colony-intruder model of aggression and defense in rats. Blanchard and Blanchard have derived rich descriptions of rat intraspecific aggressive and defensive behaviors by studying the interactions between the alpha male—the dominant male—of an established mixed-sex colony and a small male intruder:

Evolutionary Perspective

The alpha male usually bites the intruder [on the back], and the intruder runs away. The alpha chases after it, and after one or two additional [back] bites, the intruder stops running and turns to face its attacker. It rears up on its hind legs, using its forelimbs to push off the alpha. . . . However, rather than standing nose to nose with the “boxing” intruder, the attacking rat abruptly moves to a lateral orientation, with the long axis of its body perpendicular to the front of the defending rat. . . . It moves sideways toward the intruder, crowding and sometimes pushing it off balance. If the defending rat stands solid against this “lateral attack” movement, the alpha may make a quick lunge forward and around the defender’s body to bite at its back. In response to such a lunge, the defender usually pivots on its hind feet, in the same direction as the attacker is moving, continuing its frontal orientation to the attacker. If the defending rat moves quickly enough, no bite will be made. (From “Affect and Aggression: An Animal Model Applied to Human Behavior,” by D. C. Blanchard and R. J. Blanchard, in Advances in the Study of Aggression, Vol. 1, 1984, edited by D. C. Blanchard and R. J. Blanchard. San Diego: Academic Press. Copyright 1984 by Academic Press. Reprinted by permission.)

Another excellent illustration of how careful observation of behavior has led to improved understanding of aggressive and defensive behaviors is provided by the study of Pellis and colleagues (1988) of cats. They began by videotaping interactions between cats and mice. They found that different cats reacted to mice in different ways: Some were efficient mouse killers, some reacted defensively, and some seemed to play with the mice. Careful analysis of the “play” sequences led to two important conclusions. The first conclusion was that, in contrast to the common belief, cats do not play with their prey; the cats that appeared to be playing with the mice were simply vacillating between attack and defense. The second conclusion was that one can best understand each cat’s interactions with mice by locating the interactions on a linear scale, with total aggressiveness at one end, total defensiveness at the other, and various proportions of the two in between.

Pellis and colleagues tested their conclusions by reducing the defensiveness of the cats with an antianxiety drug. As predicted, the drug moved each cat along the scale toward more efficient killing. Cats that avoided mice before the injection “played with” them after the injection, those that “played with” them before the injection killed them after the injection, and those that killed them before the injection killed them more quickly after the injection.

Based on the numerous detailed descriptions of rat aggressive and defensive behaviors provided by the Blanchards and other biopsychologists who have followed their example, most researchers now distinguish among different categories of such behaviors. These categories of rat aggressive and defensive behaviors are based on three criteria: (1) their topography (form), (2) the situations that elicit them, and (3) their apparent function. Several of these categories are described in Table 17.2 (see also Blanchard et al., 2001; Dielenberg & McGregor, 2001; Kavaliers & Choleris, 2001).

The analysis of aggressive and defensive behaviors has led to the development of the target-site concept—the idea that the aggressive and defensive behaviors of an animal are often designed to attack specific sites on the body of another animal while protecting specific sites on its own. For example, the behavior of a socially aggressive rat (e.g., lateral attack) appears to be designed to deliver bites to the defending rat’s back and to protect its own face, the likely target of a defensive attack. Conversely, most of the maneuvers of the defending rat (e.g., boxing and pivoting) appear to be designed to protect the target site on its back.

TABLE 17.2 Categories of Aggressive and Defensive Behaviors in Rats

Aggressive Behaviors

Predatory Aggression

The stalking and killing of members of other species for the purpose of eating them. Rats kill prey, such as mice and frogs, by delivering bites to the back of the neck.


Social Aggression

Unprovoked aggressive behavior that is directed at a conspecific (member of the same species) for the purpose of establishing, altering, or maintaining a social hierarchy. In mammals, social aggression occurs primarily among males. In rats, it is characterized by piloerection, lateral attack, and bites directed at the defender’s back.

Defensive Behaviors

Intraspecific Defense

Defense against social aggression. In rats, it is characterized by freezing and flight and by various behaviors, such as boxing, that are specifically designed to protect the back from bites.


Defensive Attacks

Attacks that are launched by animals when they are cornered by threatening members of their own or other species. In rats, they include lunging, shrieking, and biting attacks that are usually directed at the face of the attacker.


Freezing and Flight

Responses that many animals use to avoid attack. For example, if a human approaches a wild rat, it will often freeze until the human penetrates its safety zone, whereupon it will explode into flight.


Maternal Defensive Behaviors

The behaviors by which mothers protect their young. Despite their defensive function, they are similar to male social aggression in appearance.


Risk Assessment

Behaviors that are performed by animals in order to obtain specific information that helps them defend themselves more effectively. For example, rats that have been chased by a cat into their burrow do not emerge until they have spent considerable time at the entrance scanning the surrounding environment.


Defensive Burying

Rats and other rodents spray sand and dirt ahead with their forepaws to bury dangerous objects in their environment, to drive off predators, and to construct barriers in burrows.

The discovery that aggressive and defensive behaviors occur in a variety of stereotypical species-common forms was the necessary first step in the identification of their neural bases. Because the different categories of aggressive and defensive behaviors are mediated by different neural circuits, little progress was made in identifying these circuits before the categories were delineated. For example, the lateral septum was once believed to inhibit all aggression, because lateral septal lesions rendered laboratory rats notoriously difficult to handle—the behavior of the lesioned rats was commonly referred to as septal aggression or septal rage. However, we now know that lateral septal lesions do not increase aggression: Rats with lateral septal lesions do not initiate attacks at an experimenter unless they are threatened.

Aggression and Testosterone

The fact that social aggression in many species occurs more commonly among males than among females is usually explained with reference to the organizational and activational effects of testosterone. The brief period of testosterone release that occurs around birth in genetic males is thought to organize their nervous systems along masculine lines and hence to create the potential for male patterns of social aggression to be activated by the high testosterone levels that are present after puberty. These organizational and activational effects have been demonstrated in some mammalian species. For example, neonatal castration of male mice eliminates the ability of testosterone injections to induce social aggression in adulthood, and adult castration eliminates social aggression in males that do not receive testosterone replacement injections. Unfortunately, research on testosterone and aggression in other species has not been so straightforward (see Wingfield, 2005).

Evolutionary Perspective

Soma and his colleagues have reviewed the extensive comparative research literature on testosterone and aggression (Demas et al., 2005; Soma, 2006). Here are their major conclusions:

Evolutionary Perspective

• Testosterone increases social aggression in the males of many species; aggression is largely abolished by castration in these same species.


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