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Chapter 12 Emotional Behaviors. What is Emotion? An emotional state has three aspects: 1.Cognition 2.Readiness for action 3.Feeling.

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Presentation on theme: "Chapter 12 Emotional Behaviors. What is Emotion? An emotional state has three aspects: 1.Cognition 2.Readiness for action 3.Feeling."— Presentation transcript:

1 Chapter 12 Emotional Behaviors

2 What is Emotion? An emotional state has three aspects: 1.Cognition 2.Readiness for action 3.Feeling

3 What is Emotion? The “readiness for action” component of emotions is a product of the autonomic nervous system. The James-Lange theory of emotion suggests that the autonomic arousal and skeletal action occurs first in an emotion. The emotion that is felt is the label that we give the arousal of the organs and muscles.

4 Fig. 12-1, p. 355

5 What is Emotion? According to the James-Lange theory: 1.People with a weak autonomic or skeletal response should feel less emotion. 2.Increasing one’s response should enhance an emotion.

6 What is Emotion? Research indicates the following: Paralyzed people report feeling emotion to the same degree as prior to their injury People with “pure autonomic failure” report feeling emotion less intensely. –Pure autonomic failure - output from the autonomic nervous system almost entirely fails. Thus research is contradictory and suggests other factors are involved in the perception of emotion.

7 What is Emotion? Creating certain body actions may also slightly influence emotion. –smiling slightly increases happiness. –Inducing a frown leads to the rating of stimuli as slightly less pleasant. Indicates that perception of the body's actions do contribute to emotional feeling Does not imply that feedback from the body is sufficient to distinguish emotions. –Also requires the cognitive aspect.

8 Fig. 12-3, p. 357

9 What is Emotion? Emotional experiences arouse many areas of the brain. The limbic system includes the forebrain areas surrounding the thalamus and has traditionally been regarded as critical for emotion. PET and fMRI studies also suggest many other areas of the cerebral cortex, especially the frontal and temporal lobes, are activated during an emotional experience.

10 Fig. 12-3, p. 357

11 What is Emotion? Emotions tend not to be localized in specific parts of the cortex. A single emotion increases activity in various parts of the brain. Inactivation of the medial frontal cortex appears to impair the ability to recognize angry expression.

12 What is Emotion? Localization in the brain seems to exist for the emotion of disgust. The insular cortex is strongly activated during exposure to stimuli perceived as “disgusting”. –Also the primary taste cortex. –Also reacts to frightening stimuli as well.

13 What is Emotion? The two hemispheres of the brain play different roles in emotion. Activation of the frontal and temporal areas of the left hemisphere is associated with “approach” and the Behavioral Activation System. –Marked by low to moderate arousal. –Characterizes either happiness or anger.

14 What is Emotion? The Behavioral Inhibition System (BIS) is associated with increased activity of the frontal and temporal lobe of the right hemisphere. –Increases attention and arousal. –Inhibits action. –Stimulates emotions such as fear and disgust.

15 What is Emotion? Differences in frontal cortex activity relates to personality. People with greater activity in the left hemisphere tend to be happier, more out- going and friendlier. People with greater right hemisphere activity tend to be socially withdrawn, less satisfied with life, and prone to unpleasant emotions.

16 What is Emotion? The right hemisphere seems to be more responsive to emotional stimuli than the left. Damage to the right temporal cortex causes problems in the ability to identify emotions of others.

17 What is Emotion? One major function of emotion is to help us make decisions. The consequences of our decisions have emotional components. Emotions are an important component to moral decisions. Failure to anticipate the unpleasantness of an event can lead to bad decision making.

18 Attack and Escape Behaviors Pain, threat or other unpleasant stimuli usually trigger an attack behavior. Attack behaviors are associated with increased activity in the corticomedial area of the amygdala. After experiencing a provocation, people are more likely to attack for a period of time afterwards. An initial attack behavior increases the probability of a second attack behavior.

19 Fig. 12-5, p. 361

20 Attack and Escape Behaviors Twins studies suggest genetic contribution to the likelihood of violent behavior. During childhood and adolescence, Dizygotic twins resemble each other in delinquent behaviors just as much as monozygotic twins. Monozygotic twins resembled each other much more in delinquent behaviors occurring in adulthood.

21 Attack and Escape Behaviors Smoking habits of the mother have been identified as an important correlational prenatal factor as influencing violent behavior. The effect is particularly strong if the mother smoked and also had complications during pregnancy.

22 Fig. 12-6, p. 362

23 Attack and Escape Behaviors Environmental factors can combine with genetic factors to influence behavior. Adopted children have the highest probability of violent behavior if the biological parent has a criminal record and there is discord in the adopted family household. A biological predisposition alone, or a troubled adoptive family by itself, produces only moderate effects.

24 Attack and Escape Behaviors On average, males engage in more aggressive and violent behaviors than do females. Male aggressive behavior is influenced by the hormone testosterone. Research shows that men with the highest rates of violent behavior also have slightly higher testosterone levels.

25 Fig. 12-7, p. 363

26 Attack and Escape Behaviors Testosterone alters the way people respond to stimuli. Increased testosterone levels show: –Increases in heart rate. –The tendency to attend longer and more vigorously to situations related to conflict and aggression.

27 Attack and Escape Behaviors Electrical stimulation of certain areas of the brain can evoke aggressive behaviors. The exact area of the stimulation affects the type of response: –Ranging from attack to facial movements or growls in animals.

28 Attack and Escape Behaviors Intermittent explosive disorder is a condition marked by occasional outbursts of violent behavior with little or no provocation. –Sometimes linked to temporal lobe epilepsy. Symptom include hallucinations, lip smacking, repetitive acts and occasional emotional outbursts.

29 Attack and Escape Behaviors Studies also suggest a connection between aggressive behavior and low serotonin release. Turnover is the amount of release and resynthesis of a neurotransmitter by presynaptic neurons. Valzelli’s (1973) study with mice found that isolating male mice for 4 weeks increased aggressive behavior and decreased serotonin turnover.

30 Attack and Escape Behaviors 5-hydroxyindoleacetic acid (5-HIAA) is a serotonin metabolite found in the blood, cerebrospinal fluid, and urine that allows researchers to infer turnover rate. High levels of 5-HIAA imply much serotonin release and turnover. Research with monkeys has demonstrated that low levels of 5-HIAA increases the probability of attack on larger monkeys and few survived past age 6.

31 Attack and Escape Behaviors Monkeys with high levels of 5-HIAA were more likely to survive. Evolution seems to select for an intermediate amount of anxiety and aggression. Evolution might also select for high aggressive behaviors. –may die young, but are more likely to achieve a dominant position within the troop.

32 Attack and Escape Behaviors In human studies, low serotonin turnover has been linked to: –People with a history of violent behavior and violent crime. –People who attempt suicide by violent means. –Recurrent violent behaviors and subsequent suicide attempts. A simple blood tests does not enable the reliable identification of such people.

33 Fig. 12-9, p. 365

34 Attack and Escape Behaviors Genes control the production of tryptophan hydroxylase. Tryptophan hydroxylase is the enzyme that converts tryptophan into serotonin. People with less active form of this enzyme are more likely than others to report frequent anger and aggression.

35 Attack and Escape Behaviors Genes also control the production of the enzyme monoamine oxidase. Monoamine oxidase breaks down serotonin into inactive chemicals. Thus, low production of this enzyme in conjunction with mistreatment in childhood increases the probability of violence and antisocial behavior.

36 Attack and Escape Behaviors The role of serotonin is very complicated and should not be thought of as the “anti- aggression” transmitter. During aggression, the brain, in fact, releases serotonin.

37 Attack and Escape Behaviors “Fear” is associated with a strong tendency to escape from an immediate threat. “Anxiety” is a general sense that something dangerous might occur. –Not necessarily associated with the desire to flee.

38 Attack and Escape Behaviors The startle reflex is the extremely fast response to unexpected loud noises. –found in young infants and thus unlearned. Auditory information stimulates an area of the pons that commands the tensing of the neck and other muscles. –Information reaches the pons within 3 to 8 milliseconds after a loud noise. The startle response occurs within two-tenths of a second.

39 Attack and Escape Behaviors Stimuli previously associated with the startle response enhances the startle response. –Cells in the amygdala, especially the basal lateral and central nuclei, are responsible. Cells in the amygdala receive information from pain, vision, and hearing circuits. Axons extend to areas in the midbrain that relay information to the nucleus in the pons. –The relay enhances the startle reflex.

40 Fig. 12-10, p. 367

41 Attack and Escape Behaviors Output from the amygdala to the hypothalamus controls autonomic fear responses. Axons extending from the amygdala to the prefrontal cortex regulate approach and avoidance responses.

42 Attack and Escape Behaviors Damage to the amygdala interferes with: – the learning of fear responses –retention of fear responses previously learned –interpreting or understanding stimuli with emotional consequences

43 Attack and Escape Behaviors In the early 1900s, studies of monkeys with Kluver-Bucy syndrome illustrated the effects of amygdala damage. Monkeys with this syndrome are calm and placid and display less than normal fear of snakes and larger, more dominant monkeys. Also alters social behaviors in that they have decreased ability to interpret threat gestures. Amygdala damage can also lead to an increase in the approach motive.

44 Attack and Escape Behaviors fMRI studies of humans suggest the amygdala responds strongly to emotional stimuli and facial expressions. –Not necessarily associated with just fear. Activity is strongest when the meaning is unclear and requires some processing. With some exceptions, looking at happy faces activates the amygdala only weakly. Amygdala also responds to stimuli not consciously perceived.

45 Attack and Escape Behaviors In humans, damage to the amygdala does not result in the loss of emotion. Damage to the amygdala impairs the processing of emotional information when the signals are subtle or complicated. Amygdala damage affects the ability to judge “trustworthiness” in people. People with amygdala damage focus on emotional stimuli the same as irrelevant stimuli or details.

46 Attack and Escape Behaviors Amygdala damage also affects the ability to recognize emotions specifically in photographs or pictures. –Effect is particularly strong for fear or disgust. Amygdala damage does not affect the ability to recognize fear in real life. –Attention to certain aspects of the face (eyes versus mouth) may account for the difference.

47 Fig. 12-14, p. 370

48 Attack and Escape Behaviors Genetic variations in amygdala arousal may thus underlie some of the variations of anxiety in the population and related disorders. Arousal of the amygdala relates to the tendency to experience some negative emotions. Excessive fear and anxiety disorders are associated with hyperactivity in the amygdala

49 Attack and Escape Behaviors Drugs intended to control anxiety alter activity at amygdala synapses. The main excitatory neuromodulator in the amygdala is CCK, and the main inhibitory transmitter is GABA. –Injections of CCK-stimulating drugs into the amygdala enhance the startle response. –Drugs that increase GABA activity trigger panic.

50 Attack and Escape Behaviors Barbituates were a drug widely used to control anxiety in the past, but have high overdose potential. Benzodiazepines are the most commonly used anti-anxiety drugs. Benzodiazepines bind to the GABA A receptor complex, and facilitate the effects of GABA. Benzodiazepines exert their effects in the amygdala, hypothalamus, midbrain, and other areas.

51 Fig. 12-16, p. 372

52 Attack and Escape Behaviors Diazepam-binding inhibitor (DBI) is a naturally occurring protein which attaches to the same sites as benzodiazepines and blocks their effects. Endozepines are neuromodulators that include DBI and other related proteins that work to increase levels of fear and anxiety.

53 Attack and Escape Behaviors Ethyl alcohol has behavioral effects similar to benzodiazepines. Alcohol, benzodiazepines, and barbituates all exhibit cross-tolerance. Cross-tolerance is tolerance that develops to one drug when a similar drug is taken. Alcohol enhances GABA effects. An experimental drug Ro-15-4513 blocks the effect of alcohol on the GABA A receptors complex.

54 Stress and Health Behavioral medicine emphasizes the effects of diet, smoking, exercise, stressful experiences, and other behaviors on health. Emotions and other experiences influence illness and pattern of recovery.

55 Stress and Health Hans Selye (1979) defined stress as the non-specific response of the body to any demand made upon it. Threats on the body activate a general response to stress called the general adaptation syndrome.

56 Stress and Health The General Adaptation Syndrome: Alarm stage - characterized by increased sympathetic nervous system activity. Resistance stage - sympathetic response declines, the adrenal cortex releases cortisol and other hormones that enable the body to maintain prolonged alertness. Exhaustion stage - occurs after prolonged stress and is characterized by inactivity and decreased immune system.

57 Stress and Health Sapolsky (1998) argues that the nature of today’s crises are more prolonged. –Accounts for widespread stress-related illnesses and psychiatric problems in industrial societies. Long-term, inescapable issues activate the general adaptation syndrome which is harmful to our health over time.

58 Stress and Health Stress activates two systems in the body: 1.The autonomic nervous system - “fight or flight” response that prepares the body for brief emergency responses 2.The HPA axis - the hypothalamus, pituitary gland, and adrenal cortex.

59 Stress and Health The HPA axis becomes the dominant response to prolonged stressors. Activation of the hypothalamus induces the pituitary gland to secrete adrenocorticotropic hormone (ACTH). ACTH stimulates the adrenal cortex to secrete cortisol. Cortisol enhances metabolic activity and elevates blood levels of sugars and other nutrients to mobilize energies.

60 Fig. 12-18, p. 377

61 Stress and Health Prolonged increased cortisol levels impair the immune system. The immune system consists of cells that protect the body against viruses and bacteria. –Leukocytes – white blood cells. –B-cells – leukocytes that mature in the bone marrow and secrete antibodies. –Antibodies – Y-shaped proteins that attach to particular kinds of antigens. –Antigens – surface proteins that are antibody-generator molecules.

62 Stress and Health –T cells – attack intruders directly and help other T cells or B cells to multiply. –Natural killer cells – leukocytes that attack tumor cells and cells that are infected with viruses.

63 Fig. 12-19, p. 378

64 Stress and Health During an infection, leukocytes and other cells produce small proteins called cytokines. –Combat infection and communicate with the brain to inform of illness. Cytokines in the brain produce symptoms of illness. –Fever, sleepiness, lack of energy etc. –Sleep and inactivity are the bodies way of conserving energy to fight illness.

65 Stress and Health Psychoneuroimmunology is the study of the relationship between the nervous system and the immune system. Deals with the way in which experiences, especially stressful ones, alter the immune system. Also deals with how the immune system influences the central nervous system.

66 Stress and Health In response to a stressful experience, the nervous system activates the immune system. Immune system increases production of natural killer cells, leukocytes and cytokines. The cytokines can trigger symptom of illness as a reaction to the stress itself.

67 Stress and Health Prolonged stress response is damaging to the body. Prolonged increase of cortisol detracts from the synthesis of proteins of the immune system. Prolonged stress of longer than a month significantly increases the likelihood of illness.

68 Stress and Health Prolonged stress can also be harmful to the hippocampus and can affect memory. Cortical enhances metabolic activity in the body. When metabolic activity is high in the hippocampus, the neurons are more sensitive to damage by toxins or over-stimulation. Stress also impairs the adaptability and the production of new hippocampal neurons.

69 Stress and Health Posttraumatic stress disorder (PTSD) occurs in some people after terrifying experiences and includes the following symptoms: –Frequent distressing recollections. –Nightmares. –Avoidance of reminders of the event. –Exaggerated arousal in response to noises and other stimuli.

70 Stress and Health Studies have revealed most PTSD victims have a smaller than average hippocampus. PTSD victims show lower than normal cortisol levels after the trauma. People with low cortisol levels may be ill- equipped to combat stress and more prone to the damaging effects of stress.

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