Biopsychology of Emotion, Stress and Health - PDF

Here is the transcription of the provided image into a structured markdown format. ## 2 PSYCHOLOGIE ### Neural Mechanisms of Fear Conditioning * LO 1.6 Describe the role of the amygdala in fear conditioning. * LO 1.7 Describe the role of the hippocampus in contextual fear conditioning. * LO...

Here is the transcription of the provided image into a structured markdown format. ## 2 PSYCHOLOGIE ### Neural Mechanisms of Fear Conditioning * LO 1.6 Describe the role of the amygdala in fear conditioning. * LO 1.7 Describe the role of the hippocampus in contextual fear conditioning. * LO 1.8 Describe the role of two specific amygdalar nuclei in fear conditioning. ### Brain Mechanisms of Human Emotion * LO 1.9 Describe the current status of cognitive neuroscience research on emotion. * LO 1.10 Describe the role of the amygdala in human emotion. * LO 1.11 Describe the role of the medial prefrontal lobes in human emotion. * LO 1.12 Describe the research on the lateralization of emotion. * LO 1.13 Describe the current perspective on the neural mechanisms of human emotion that has emerged from brain-imaging studies. ### Stress and Health * LO 1.14 Describe the components of the stress response. * LO 1.15 Describe research on animal models of stress, including that on subordination stress. * LO 1.16 Describe how our view of psychosomatic disorders has been refined by the results of research on gastric ulcers. * LO 1.17 Define psychoneuroimmunology, and describe the four components that make up our bodies' defenses against foreign pathogens. * LO 1.18 Describe the effects of early exposure to severe stress. * LO 1.19 Describe the effects of stress on the hippocampus. This chapter is about the biopsychology of emotion, stress, and health. It begins with a historical introduction to the biopsychology of emotion and then focuses in the next two modules on the dark end of the emotional spectrum: fear. Biopsychological research on emotions has concentrated on fear not because biopsychologists 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 is one common source of stress. In the final two modules of the chapter, you will learn how some brain structures have been implicated in human emotion, and how stress increases susceptibility to illness. ### Biopsychology of Emotion: Introduction To introduce the biopsychology of emotion, this module 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. LO 1.1 Summarize the major events in the history of research on the biopsychology of emotion. This section 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 gunpowder 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. 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. 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 1.1). It was apparent that the damage to Gage's brain affected both medial prefrontal lobes, which we now know are involved in planning, decision making, and emotion. 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 that particular emotional responses, such as human facial expressions, tend to accompany the same emotional states in all members of a species. 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 1.2 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 commonsense way of thinking about the causal relation between the experience of emotion and its expression (see Figure 1.3). 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 (see Figure 1.3). 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, though there does seem to be some dampening of fear and anger. 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. SHAM RAGE. In the late 1920s, Bard 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, hiss, and expose their teeth. 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 proposed that emotional expression is controlled by several interconnected nuclei and tracts that ring the thalamus. Figure 1.4 illustrates some of the key structures in this circuit: the amygdala, mammillary body, hippocampus, fornix, cingulate cortex, 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. Indeed, many of the structures in Papez's circuit are part of what is now known as the limbic system. KLÜVER-BUCY SYNDROME. In 1939, Klüver 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 Klüver-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 Klüver-Bucy syndrome have been attributed to damage to the amygdala, a structure that has played a major role in research on emotion, as you will learn later in this chapter. The Klüver-Bucy syndrome has been observed in several species. Following is a description of the syndrome in a human patient with a brain infection. At first he was listless, but eventually he became very placid with flat affect. He reacted little to people or to other aspects of his environment. He spent much time staring at the television, even when it was not turned on. On occasion he would become extremely silly, smiling inappropriately and mimicking the actions of others, and once he began copying the movements of another person, he would persist for extended periods of time. In addition, he tended to engage in oral exploration, sucking, licking, or chewing all small objects that he could reach. The six early landmarks in the study of brain mechanisms of emotion just reviewed are listed in Table 1.1. **Table 1.1 Biopsychological Investigation of Emotion: Six Early Landmarks** | Event | Date | | :-------------------------------------- | :---------- | | Case of Phineas Gage | 1848 | | Darwin's theory of the evolution of emotion | 1872 | | James-Lange and Cannon-Bard theories | about 1900 | | Discovery of sham rage | 1929 | | Discovery of Klüver-Bucy syndrome | 1939 | | Limbic system theory of emotion | 1952 | ### Emotions and the Autonomic Nervous System LO 1.2 Summarize the research on the relationship between the autonomic nervous system and emotions. 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). The experimental evidence suggests that the specificity of ANS reactions lies somewhere between the extremes of total specificity and total generality. On one hand, ample evidence indicates that not all emotions are associated with the same pattern of ANS activity; on the other, there is no evidence that each emotion is characterized by a distinct pattern of ANS activity. POLYGRAPHY. Polygraphy (more commonly known as the "lie detector test") is a method of interrogation that employs ANS indexes of emotion to infer the truthfulness of a person'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: Volunteers 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. A review of the use of the control-question technique in real-life crime settings led to an estimated success rate of about 55 percent-just slightly better than chance (i.e., 50%). Despite being commonly referred to as lie detection, polygraphy detects ANS activity, 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 an emotional reaction from all suspects, regardless of their guilt or innocence, making it difficult to detect deception. The guilty-knowledge technique, also known as the concealed information test, 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), volunteers 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 percent of the mock criminals were correctly identified; more importantly, none of the innocent control volunteers was judged guilty. ### Emotions and Facial Expression LO 1.3 Describe some research on the facial expression of emotions. Ekman and his colleagues have been preeminent in the study of facial expression. 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. 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 early studies 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 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. They further concluded that all other facial expressions of genuine emotion are composed of mixtures of these six primaries. 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. 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 volunteers 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 volunteers were unaware of that. They 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. A recent meta-analysis of the facial feedback hypothesis confirmed the reliability of these and similar findings; however, the effects were smaller than originally believed. **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. ### 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. 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. 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. 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. FACIAL EXPRESSIONS: CURRENT PERSPECTIVES. Ekman's work on facial expressions began before video recording became commonplace. Now, video recordings provide almost unlimited access to natural facial expressions made in response to real-life situations. This technology has contributed to four important qualifications to Ekman's original theory. First, 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. Second, the existence of other primary emotions has recognized. Third, body cues, not just facial expressions, are known to play a major role in expressions of emotion. For example, 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. Fourth, there is evidence that Ekman's six primary facial expressions may not be as universal as originally believed. For example, there seem to be distinct differences, in terms of both the expression and recognition of facial expressions, between Western Caucasian and East Asian individuals. Moreover, recent studies of isolated tribes by Crivelli et al. indicate that facial expressions of emotion are not as universal as once thought. ### 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. Although one purpose of this module 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 *fear*, *happiness*, 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, the environments in which they occur, and the putative adaptive functions of such behaviors. **Journal Prompt 1.1** Because we have a word for it, many people believe that "intelligence" is a real entity. Yet, it is a complex construct that was developed by psychologists. Treating a psychological construct (e.g., intelligence) as if it actually exists is a logical error, known as an error of reification. Have you ever encountered such errors in the popular media? Give an example. ### Types of Aggressive and Defensive Behaviors LO 1.4 Describe the work that led to the distinction between aggressive and defensive behaviors in mammals. Considerable progress in the understanding of aggressive and defensive behaviors has come from the research of Blanchard and Blanchard 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: Upon encountering the intruder, the alpha male typically chases it away, repeatedly biting its back during the pursuit. The intruder eventually stops running and turns to face the alpha male. The intruder then rears up on its hind legs, still facing its attacker and using its forelimbs to ward off the attack. In response, the alpha male changes to a lateral orientation, with the side of its body perpendicular to the front of the defending intruder. Then, the alpha moves sideways toward the intruder, crowding and trying to push it off balance. If the defending intruder stands firm against this "lateral attack," the alpha often reacts by making a quick lunge around the defender's body in an attempt to bite its back. In response to such attacks, the defender pivots on its hind feet, in the same direction as the attacker is moving, continuing its frontal orientation to the attacker in an attempt to prevent the back bite. Another excellent illustration of how careful observation of behavior has led to improved understanding of aggressive and defensive behaviors is provided by Pellis and colleagues' (1988) study 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 aggressive and defensive behaviors provided by the Blanchards, Pellis and colleagues, and other biopsychologists who have followed their example, most researchers now distinguish among different categories of such behaviors. These categories of 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 for rats are described in Table 1.2 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 rate.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 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. 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 first 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 more attacks, but they are hyperdefensive when threatened. **Table 1.2 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 | Respponses that many animals to avoid attack. For example, if a human approcahes a wild rate, itw ill oftne freez until the human penetrates its safter zone, whereupon itw ill explode into flight. | | Maternal Defensive Behavior | Behaviros by whihc mothres protec theit younf. Desprie their defensvie functio, they are simlar to male social aggression i n appearance. | | Risk Assessment | Behaviors taht are performe dby animals in ordrt ot obtain psecific ifnormation taht help them defend themselves more effecitvely. For example, tras that have ebben cashed by a acvt int their burrow do npt eemgr til unetil they have spent cosniderable time at the enreance csanning tbe eurruding eenivromnemnt. | | Defensive Behavior | Rats and other rodents spray sand and dirt ahead with their forepaws to bury dangerous objects in their environemtn, ot drive off predators, dn ot consrtuct barriera i burbows. | ### Aggression and Testosterone LO 1.5 Describe the relation between testosterone levels and aggression in males. 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 male mice that do not receive testosterone replacement injections. Unfortunately, research on testosterone and aggression in other species has not been so straightforward. The extensive comparative research literature on testosterone and aggression has been reviewed several times The major conclusions: * Testosterone increases social aggression in the males of many species; aggression is largely abolished by castration in these same species. * In some species, castration has no effect on social aggression; in still others, castration reduces social aggression during the breeding season but not at other times. * The relation between aggression and testosterone levels is difficult to interpret because engaging in aggressive activity can itself increase testosterone levels-for example, just playing with a gun increased the testosterone levels of male college students. * The blood level of testosterone, which is the only measure used in many studies, is not the best measure. What matters more are the testosterone levels in the relevant areas of the brain. Although studies focusing on brain levels of testosterone are rare, it has been shown that testosterone can be synthesized in particular brain sites and not in others. It is unlikely that humans are an exception to the usual involvement of testosterone in mammalian social aggression. However, the evidence is far from clear. In human males, aggressive behavior does not increase at puberty as testosterone levels in the blood increase; aggressive behavior is not eliminated by castration; and it is not increased by testosterone injections that elevate blood levels of testosterone. A few studies have found that violent male criminals and aggressive male and female athletes tend to have higher testosterone levels than normal; however, this correlation may indicate that aggressive behaviors increase testosterone, rather than vice versa. The lack of strong evidence of the involvement of testosterone in human aggression could mean that hormonal and neural regulation of aggression in humans differs from that in many other mammalian species. Or, it could mean that the research on human aggression and testosterone is flawed. For example, human studies are typically based on blood levels of testosterone (often inferred from saliva levels because collecting saliva is safer and easier than collecting blood) rather than on brain levels. However, the blood levels of a hormone aren't necessarily indicative of how much hormone is reaching the brain. Also, the researchers who study human aggression have often failed to appreciate the difference between social aggression, which is related to testosterone in many species, and defensive attack, which is not. Most seemingly aggressive outbursts in humans are overreactions to real or perceived threat, and thus they are more appropriately viewed as defensive attack, not social aggression. ### Neural Mechanisms of Fear Conditioning Much of what we know about the neural mechanisms of fear has come from the study of fear conditioning. Fear conditioning is the establishment of fear in response to a previously neutral stimulus (the conditional stimulus) by presenting it, usually several times, before the delivery of an aversive stimulus (the unconditional stimulus). In a standard fear conditioning experiment, the subject, often a rat, hears a tone (conditional stimulus) and then receives a mild electric shock to its feet (unconditional stimulus). After several pairings of the tone and the shock, the rat responds to the tone with a variety of defensive behaviors (e.g., freezing and increased susceptibility to startle) and sympathetic nervous system responses (e.g., increased heart rate and blood pressure). LeDoux and his colleagues have mapped the neural mechanism that mediates this form of auditory fear conditioning ### Amygdala and Fear Conditioning LO 1.6 Describe the role of the amygdala in fear conditioning. LeDoux and his colleagues began their search for the neural mechanisms of auditory fear conditioning (fear conditioning that uses a sound as a conditional stimulus) by making lesions in the auditory pathways of rats. They found that bilateral lesions to the medial geniculate nucleus (the auditory replay mucleus of the thalamus)b locked fear conditionig to a tone, but bilateral lesions to the auditory cortex did not. This indicated that for auditory fear conditioning to occur, it is necessary for signals elicited by the tone to reach the medial geniculate nucleus but bot the auditory contex. It also inicated that a pathway fofm the medial geniculate nuclaus to a sturctue other than the auditiry corcex plays a key role inf ear conditioning. THis pathway proved to be teh pthrway ftom teh medial genicualte uncleus tot eth amygdalae. Lesions to the amygdala. lieke laesion sof teemdial geniculae nuclesu bocked audioryt fear conditkining treh ayingdala. and it i belived to rbe the structure in which the emotiaonal signiifcace osenssory signals is earned ana drteained. Severla pthways carrti signals from rteehygdala tobrianstem strucutser rghat cotolrthe various emtinal rponses. ore xample a pthjway tro teh pariaqeducatal gray kf te hdi rbain eletis appropriae desensive resonses wahes asnhter pthjwawt trithe lateral huthalamuyas eletis apprp[rtiae sympatehtoc responss. eht fact taht audiotoy corter lesios od hpt distrupt feer cnidtioiong to smpel tomes doe hpt mean taht tet h auditosyr cirtex us pft invlved id audotry facr cnitoimng re are wo pthuaws ftion te hdial genicilae nulceus to te hmaygdhak at ehd drievct kme whuch you hva ealry elratned abou and an indirect okme ight projecuts via te audiortry vortex bor routse are sapbl of hdiatig fear cndi tiomi g to sple sounds unly jone is testoyes condiktiong prgresses hrmally hoyevee inly the otfical rojte us kaple f hdoiati g faeraocinditomg to coilex sunds . Figure 1.9 illistrate the cirucuit of the brain taht is thought to mediate the effects of fear conditioning to am aud