Motivation Lectures - Chapter 3 (PETRI 6 ED)

CHAPTER 3: PHYSIOLOGICAL MECHANISMS OF AROUSAL I. Arousal Theory: how does the organism become activated? Motivation may be viewed on a continuum of behavioural activation. Continuum ranges from low levels of arousal (coma and sleep) to high levels of arousal (Fig. 3.1, p....

CHAPTER 3: PHYSIOLOGICAL MECHANISMS OF AROUSAL I. Arousal Theory: how does the organism become activated? Motivation may be viewed on a continuum of behavioural activation. Continuum ranges from low levels of arousal (coma and sleep) to high levels of arousal (Fig. 3.1, p. 62). a. Inverted U Function: behaviour most efficient at optimal level of arousal. Yerkes-Dodson Law: a b. Different tasks are related to arousal level and performance: higher arousal for simple, habitual tasks and lower arousal for complex, cognitive tasks. Too much arousal reduces performance. c. Emotion and motivation related to activation of nervous system. There are structures that come into play in emotion and motivation; e.g. Separating the medulla from the spinal cord and organism goes through normal sleep-wake cycle - RAS) and organism sleeps constantly (cerveau isole preparation). D. RAS: nerve cells in central core of brain stem (Fig. 3.5, p. 65). Moruzzi and Magoun (1949) stimulated RAS electrically. Changes in electrical activity of cortex were noted in EEG-brain wave recordings. Synchronous – Alpha wave activity related to a relaxed awake organism. High, slow waves. Desynchronous – Beta wave activity related to alert, attentive, aroused organism. Low, fast waves. RAS  He cut the RAS and organism slept constantly. RAS sends fibers to cortex. RAS arouses cortex. Cortex can inhibit RAS activation. II. Hebb’s Arousal Theory Sensory information serves two functions: a. to provide information, i) a cue function and ii) an arousal function. If cortex is not aroused cue function has no effect. b. sensory stimuli sent to cortex and RAS. The stimulus effect at RAS level  be processed. Motivation for Hebb is activation of the cortex via the thalamus and RAS. c. cortex sends fibers down to RAS and stimulates it when internal and external stimulation is low. d. downstream connections from cortex to RAS may explain how thoughts, images, memories can activate and motivate behaviour. While trying to sleep if RAS is activated it in turn activates the cortex and sleep becomes difficult – tossing and turning!  central nervous system (CNS) and autonomic nervous system (ANS). 1. Various types of arousal: i) behavioral as organism responds, ii) autonomic arousal by changes in bodily functioning (e.g., heart rate), and iii) cortical arousal by desynchronized, beta wave activity. 2. Chemicals: (e.g., atropine) produces EEG activity akin to sleep in cats and dogs, and yet animal responds normally. And, (e.g., physostigmine) produces EEG activity akin to being alert, yet animal behaves as if drowsy. Thus,  body systems (p. 67). 3. Correlation between hormones and emotion; e.g., adrenal hormone epinephrine may be related to anger and aggression; changes in ANS activity related to disgust, anger, fear; universal facial expressions by way of contraction of facial muscles serve as signals of emotional state (p. 67). IV. Sleep an overpowering motive showing  suggestibility. 2. Why sleep? It is adaptive, removing us from situations when we are least efficient. Circadian rhythms on a 24 hr. cycle and operate during sleep. Animals who are prey sleep less and predators sleep more. Whales and some bird species have unihemispheric slow-wave sleep where one half of the brain sleeps. 3. In humans sleep decreases with age from 14 to 16 hours in infancy; 5 yr. olds, 11 hrs.; and by age 20 years, 6  insomnia, shorter and more fragmented sleep, go to sleep earlier, and break-up 7 hr. cycle into several shorter sleep periods (naps, p. 69). V. Stages of Sleep: defined by electrical activity of the brain through 5 stages of sleep. 1. Alpha activity: relaxed wakefulness occurs before Stage 1: irregular low amplitude waves for 10-15 min. It accounts for 5% of sleep. 2. Stage 2: sleep spindles and K- Complexes: Accounts for 50% of 4. Stage 4: slow high-amplitude waves; accounts for 14% of sleep for 30-45 minutes. 5. Stage 5: a mix of theta, beta, and alpha waves. Muscle tone is low and REM takes over when dreaming occurs and accounts for 25% of sleep (p. 69-71). Sleep Stages 1 - 4 are NREM slow wave sleep and Stage 5 is correlated with dreaming. REM dreams are bizarre, emotionally a. Inhibition of motor neurons and loss of muscle tone is best indication of REM – dream sleep. REM occurs about once every 90 minutes. REM periods become longer throughout the night so by morning REM sleep can be as long as an hour. b. Cortical activity in REM is similar to Stage 1 sleep with a mixture of theta and beta waves and person is paralyzed even though cortical activity is as if the person is awake and this has been called Paradoxical sleep. Newborns  100% REM and may indicate periods of neuronal organization within the brain. A.Dreams: on average 100 minutes per night spent dreaming; brief dreams to one hour dreams. 1. Dreams not usually emotional; however, when present, emotion usually negative. Early night dreams draw on events of the day: day residues. late night dreams draw on stored memories.  adults. 3. REM sleep changes with age and becomes less stable. 1. Neurocognitive Theory of Dreams: dreams depend on maturation and maintenance of forebrain structures (p. 73). Continuity Principle: personal concerns during day enter dreams. Day residues enter dream. Repetition Principle whereby same setting, characters, social interactions 2. Threat Simulation Theory of Dreams allows one to rehearse perceived threats and avoid through rehearsal in dreams. Content: dreams mostly negative and threatening to dreamer rather than emotionally positive and rewarding dreams. Aggression attacking or being attacked is most common form of behaviour reported in social interaction dreams and when  subjects dreamed more than normal and this overshooting of dreaming continued for days. REM deprivation leads to increased aggressiveness and sexual behaviours in animals when awake. Neural structures underlying REM sleep are related to structures involved with general motivational processes. REM deprived subjects show  and if drugs abruptly withdrawn REM rebound occurs and person shows increased dreaming. Amphetamines act on the reticular activating system (RAS), help maintain arousal, wakefulness, as well as suppress REM.  Withdrawal of amphetamines leads to REM rebound accompanied by vivid nightmares.  Withdrawal from alcohol leads to REM suppression and may lead to B. Physiology of Sleep: NREM sleep reveals: blood pressure (BP), heart rate (HR), and respiration (R) decline, veins and arteries dilate (vasodilation).  Brain waves are high amplitude, slow waves. REM sleep shows: increase in BP, HR, R, and blood flow to brain. Penile erection in males C. Brain Stem Structures: Pons, medulla, RAS are involved in arousal and sleep. When RAS receives sensory information from the environment it arouses the thalamus which in turn arouses the cerebral cortex which in turn arouses RAS. when RAS is aroused it sends impulses to the lateral hypothalamus, basal ganglia, and basal forebrain. Connections from the basal forebrain activate the cerebral cortex and hippocampus. D. Neurotransmitters and Arousal: 1. Acetylcholine (ACH) cells in basal forebrain and pons activate cerebral cortex and desynchronized EEG waves occur when stimulated. ACH increases arousal. 2. Norepinephrine (NoR-Ep) cells in locus coerulus of the pons activate cerebral cortex, hippocampus, thalamus, cerebellum, pons, medulla. NoR-Ep is high in waking and drops off in sleep almost to zero in REM 3. Serotonin cells in the raphe nuclei of pons and medulla connect to cerebral cortex, hippocampus, thalamus, hypothalamus, and basal ganglia. Cells most active in waking and decreases in sleep. Serotonin influences automatic behaviours as chewing, pacing, grooming. Serotonin maintains ongoing behaviour and suppresses sensory information that might interrupt those activities.  the cerebral cortex, thalamus, hippocampus, basal ganglia and basal forebrain. Activity in these cells is high in waking and low in sleeping. Histamine producing neurons connected to the cortex lead to arousal, and histamine is related to attention to environmental stimuli. Anti-histamine drugs to treat allergies block brain histamine receptors and one becomes sleepy and less attentive. E. Brainstem and NREM Sleep: Ventrolateral Preoptic Area (VLPO) crucial to delta wave sleep. Stimulation of the VLPO neurons lead to drowsiness. Animals deprived of sleep and then allowed sleep show increase firing of neurons in VLPO. Locus Coerulus (LC) and Raphe Nuclei when active inhibit REM sleep. As neurons in these regions become inactive during NREM sleep, REM sleep can then occur (p. 76). VLPO neurons produce GABA  sites associated with arousal such as locus coerulus, raphe, tuberomammillary nucleus and orexiogenic neurons. Too little GABA = anxiety. F. Brainstem and REM Sleep: Sub- lateral-dorsal nucleus (SLDn), pre- coeruleus region (PCr) and the medial peri-brachial-nucleus (MBn) are cells that secrete neurotransmitters, some inhibit and some cells excite. Destruction of MBn leads to reduced REM sleep (p. 77).  deprived goats into cats and cats became drowsy (p. 78). Acetylcholine as a neurotransmitter is found to be related to REM sleep. Adenosine has an inhibitory effect on neurons that maintain arousal in the pons. Adenosine has two types of receptors: A1 is inhibitory and A2 has an excitatory effect. Caffeine and Theo- phylline (in tea) block receptor sites for  attention (p. 79). REM occurs readily after full day of worry, stress, or intense learning. REM deprivation decreases access to emotionally important memories. Thus, REM responsible for connection between past memories and present memories related to past experiences. Depression and initial REM onset are positively correlated (p. 79). Stage 4 (NREM) and REM decline with age.  Infants born 4 months pre-mature spend 75% of time in REM and at 3 months of age REM drops to 30%. REM as an internal source of regulation “sets-up” brain organization. 3. Programming Device: new material in waking changes existing brain organization in REM sleep. New inputs in waking reorganized during REM. 4. Consolidation of Memories: dreaming enables short-term memories to be transferred to long-term memory.  REM deprivation Ss more anxious than normals when shown anxiety provoking film a second time. Dreaming during REM may allow for anxiety provoking material to be incorporated and lead to habituation (p. 80); a reduced anxiety response. 6. Storage of Complex Associative Information: recall of such material better after isolated REM, as compared to NREM sleep in a group of narcoleptics who are known to fall asleep quickly, and in whom REM occurs  since Syndrome, resulting from brain lesions, interrupts dreaming and memory, increased REM is brain’s way to compensate for deficits (p. 80). Other research shows that hippocampus neuron firings during learning re-fire during sleep, and this facilitates memory consolidation in sleep. Declarative memories require slow-wave sleep (NREM) to integrate old and new memories (p. 80-81). Van Der Werf (2000) found that shallow sleep reduced slow-wave activity leading to deficits in learning  formation. Slow-wave sleep “optimizes the hippocampus for encoding of novel information…” And further, sleep promotes consolidation of emotional memories. VI. STRESS: Selye defined as follows: a non-specific response of the body to any demand made upon it. A stressor is a demand that moves the body away from an optimal level of  the actual demand it places on the person. Those who have some control react less strongly to stress and stress may be reduced by one’s personal values (p. 82); i.e. importance of stressor. 1. Systemic and Psychological Stress: Stress challenges integrity of body— mind functioning. Anticipation of an event is stressful (see experienced parachutists, p.82). Emotion is a sign of stress as is disruption of ongoing behaviour. 2.Endocrine System and Stress: Glands throughout the body release hormones. A major gland is the Pituitary at the base of the brain. It coordinates its activity with a brain structure, the Hypothalamus, which releases hormones: Corticotropin Releasing Hormone (CRH) that activates the Pituitary Gland (p.83). A second major gland is the Adrenal a. Anterior hypothalamus releases corticotrophin releasing hormone (CHR). This causes the pituitary to release adrenocorticotropic hormone (ACTH) which travels to the adrenal glands and causes the adrenal cortex to release cortisol. Epi, Nor-epi and cortisol mobilize the body for action and as hormones reach critical levels a feedback system connecting to the hypothalamus shuts off the production of ACTH. when stressor disappears or is b. GAS: General Adaptation Syndrome: a common set of responses to any stressor, irrespective of the source. Selye discovered that injecting rat subjects with ovarian or placental hormones caused a series of changes, including enlargement of the adrenal cortex, shrinkage of the thymus gland and lymph nodes, and ulceration of the stomach. Any noxious or foreign material caused the same effects. i) Alarm: body mobilized for action with corticoids and Epi secreted by adrenal medulla. There is increase in heart rate, blood pressure. Resistance to stressor initially falls below normal and then moves well above normal. ii) Resistance: processes accelerated at Alarm Stage return to normal; corticoid levels decrease. Resistance stage mobilizes part of body under attack. If local defenses are inadequate or fail to limit stressor the final stage of Exhaustion is  if stressor not reduced or eliminated serious injury, illness, and death may occur (p. 84-85). These three stages comprise General Adaptation Syndrome (GAS).  Syndrome represents a set of responses triggered by stressor and designed to eliminate or contain stressor.  GAS triggered by both physical stressors and psychological stressors: loud noises, crowding. Anxiety  GAS not always adaptive leading to Diseases of Adaptation: body and mind’s responses are not always able to contain or eliminate the stressor. Body may act incorrectly: inflammation that acts as a barrier to a foreign particle but may cause more harm than good. Signal Anxiety: perception of external danger mobilizes body and mind for defense. Danger may arise from within as in internal sources of anxiety created by fear of instinctual impulses breaking  actions that violate personal norms and social norms. 3. Life Change, Stress, and Illness: Meyer’s research earliest attempt to correlate life change as a stressor and subsequent illness; physical and/or psychological. Hinkle found that illness tended to cluster around certain periods in one’s life as when the social environment or interpersonal relationships make large demands (p. 86). People who were emotionally a. Social Readjustment Scale: how many events within a short period of time, and the nature of the event, correlated with illness. Retrospective studies provided information on this relationship (p. 86). Prospective studies in which individual responds to recent life changes and then questioned again later. Prospective studies are an attempt to predict future health changes.    In one study by Popkin, the larger the number of life changes, the poorer performance in a dog-sled race between Anchorage and Nome, Alaska (p. 87).  Immigration studies show that there is no greater incidence of illness for those that immigrated as compared with the rest of the population of Canada (p. 87-88). Where illness was found, immigrant women were more likely than immigrant men to become ill (p. 88). In  perceived themselves as poorly behaved, less attractive, less popular, and less successful in school. Thus, the high stress group tended toward negative self- evaluations (p. 88). 4. Buffering Effects of Life Changes and Stress: A. Examining the variables that contribute to stress and illness: personality style and exercise. The variable of personality style was Hardiness: a combination of three  Exercise acts as a buffer by keeping life experiences in perspective by decreasing the psychological and physiological strain on the individual. Hardiness reduces the stressfulness of the events themselves, and exercise reduces the deleterious effects of stress on the person.  Subjects high in hardiness and exercise fared better and these subjects showed less illness (p. 89). B. Other Buffers to Stress: social support theory proposes social  diet, sleep, exercise. Expressive Style involves humour as a way of coping. C. Explanatory Style: optimistic- pessimistic. Expressive Style as in weeping-humour interact to buffer the effects of stress. D. Knowledge as curative by reducing the mystery associated with stressful events. E. Emotional Insulation is removing one psychologically from events around them. F. Looking Beyond the momentary 5. Psychoneuroimmunology: examining the relationship between behaviour, the nervous system, and the immune system. A bi-directional relationship exists between the brain and immune system. The brain communicates with the immune system through nervous system connections to lymphoid organs that secrete hormones which alter the immune system (p. 93). The principal organ for alerting the immune system is the pituitary gland releasing ACTH to the A.Brain-Immune System: communication through the production of cytokines (i.e., interleukins – IL) that regulate the intensity and duration of the immune response. The production of cytokines can lead to changes in brain and behaviour (p. 93). Brain secretes CRH, which stimulates the pituitary gland to secrete ACTH, which stimulates the adrenal cortex to release glucocorticoids, which have an inhibitory effect on the immune system.  neutral or novel stimulus (Conditioned Stimulus – CS) with an immunomodulating drug (Unconditioned Stimulus – UCS) and after a number of pairing trials, the CS elicits immune functioning in a manner similar to the UCS (p. 93). Conditioned animals exposed to an antigen and then re-exposed to the CS had a reduced antibody response (Conditioned Response – CR). CS’s can act as immunosuppressant - conditioned suppression- or conditioned enhancement.  show a conditioned enhancement in natural killer cell activity when re-exposed to a flavour associated with an injection of adrenaline (p. 93). D.Stress can produce a decline in natural killer cell activity - an immune system response. Acute short-lived stressors can produce immune responses that are adaptive as well as maladaptive. Chronic long-term stressors produce maladaptive,  disorders. Relationships between depression and coronary heart disease and depression and cancer. Negative emotionality is associated with many age-related diseases (p. 94). Leonard (2001): stressors activate the hypothalamic-pituitary-adrenal axis and this leads to hyper-secretion of the glucocorticoids (p. 94). Hyper- secretion of glucocorticoids and inflammatory cytokines leads to a reduction of noradrenaline and serotonin neurotransmitters in the brain and this  allows neurotransmitters to return to normal functioning (p. 95). F. Placebo Effects: an inert substance that produces healing by having, in part, physiological effects. Placebo effects may be mediated by changes in opioid and non-opioid processes in the brain. Person’s expectations, desires, context, affect the placebo reaction. Price (2008) found that social  Pain reduction greater when an analgesic is given openly and the suggestion of pain relief is made (p. 95). Conversations that imply pain relief produce larger effects than neutral ones. How does this relate to psychotherapy?  Learning plays a role since placebo effect is influenced by memories of past effects and expectancies. Thus, Price (2008) has shown that there are placebo responders and non- responders. This has led to Price proposing a desire-expectation model: placebo responses relate to feeling good or less bad about the prospects of relief that are part of avoidance goal or approach goal of pleasure associated with medications and treatment (p. 95). In this model, desire is the motivation to feel differently (less pain) and expectation is the belief that the