Arousal Theory

Assumes behaviour changes as we become more aroused
Motivation is on continuum of behavioural action ranging from: low levels of arousal = coma or sleep vs. high levels of arousal = stress
Some changes in arousal i.e. sleepiness to wakefulness = increased efficiency of performance vs. wakefulness to extreme arousal = interference w/efficient responding
Interval U function: curve indicating increasing arousal improves performance to certain point of optimal arousal (where behaviour is most efficient); after that, continued increase in arousal interferes with responding o Yerkes-Dodson Law: name for this arousal-performance relationship
Relationship between arousal and performance only applies to some situations

i.e. for matching or concept formation o Also, what is optimal for one task, may not be optimal for another task

There are structures in nervous system that trigger its activation, causing emotion and motivation: o Encephale isole: cut through brain stem of animal between medulla and spinal cord, depriving animal of its higher cortical brain tissues  animal continues w/normal sleep-wake cycle
- Cerveau isole: cut higher up brain stem where colliculi  abolishes wakesleep cycle
- Result: brain structure(s) near pons, between 2 cuts, controls changes in arousal level involved in moving from sleeping to waking

The Reticular Activating System

Group of neuron (nerve cells) in brain’s central core, running from medulla level through thalamus
Electrical simulation of RAS led to change of electrical activity of cortex (recorded by EEG) that were same as changes seen when external stimuli (i.e. loud noise) occurred
What is shown by EEG:
- Alpha waves: quiet sound = resting = regular electrical activity pattern of cortical cells = cell activity occurs at same time = synchronous
- Beta waves: loud sound = alert = cortex cells act independently of each other = desynchronized
Stimulation of RAS led to beta wave activity, like environmental stimuli do, thus it seems that RAS is also responsible for activation of organism; support for this: o RAS receives sensory input from external sensory systems and muscles and internal organs, thus it can trigger arousal
- When all brain structures around RAS are cut in experimental animals, they still had normal sleep-wake cycles, but cutting RAS w/everything else intact results in permanent sleep (like cerveau isole)
- RAS sends fibers to whole cortex, thus it is part of brain circuitry that arouses organism from sleep to wakefulness, and determines where on arousal continuum we find ourselves and what to pay attention to
- This all led theorists to argue that emotion and motivation = arousal of cortex

Hebb’s Theory

2 purposes of sensory info: (1) cue function of stimulus: provides info and (2) arousal function: arouses person; if cortex is not aroused, cue function of stimulus had no effect i.e. we do not react to sounds when we are asleep b/c cortex is not aroused by RAS
Sensory stimuli = activation of cortex by RAS = motivation
Cortex sends fibers down to RAS, so cortex can activate RAS and keep arousal high even when external or internal stimulation is low
Downstream connections from cortex to RAS provide explanation for how thoughts and external stimuli = arousal = motivation:

o i.e. lie in bed and think about exams = RAS activation = aroused cortex = hard to sleep

Psychophysiological Measures

Arousal theory assumption: can measure arousal by monitoring activity of brain changes in automatic nervous system and correlating them w/behaviour changes o However, these correlations are small, causing diff theories

Lacey

More than one type of arousal; behaviour arousal is indicated by: (1) responding organism, (2) autonomic arousal (shown by bodily functions) or (3) cortical arousal shown by desynchronized, fast brain waves o These 3 arousals occur together but do not have to and are independent

i.e. certain chemicals produce EEG activity like sleep in animals, but behave as if awake vs. other chemicals make EEG activity like alert animal, but animal behaves as if it is drowsy

Sometimes there is little relationship between central nervous system activity and autonomic changes, thus, arousal is multidimensional: diff situations = diff somatic response i.e. heart rate
Periphery of body is also important in his arousal model i.e. stretching of carotid sinus (in carotid artery) changes EEG activity from alert, high-frequency activity to low-frequency activity generally associated w/sleep o Thus, feedback from bodily systems can directly influence arousal system and suggest that bodily systems may also play role in length of arousal episodes
Thus, physiological mechanisms in midbrain are involved w/arousal of organism, sleep-wake cycle and alert attention to environment

Problems with Arousal Theory

Weak relationship between measures of behavioural, cortical and autonomic arousal
Assumes diff patterns of bodily responses, but clear diffs are not shown (Lacey’s theory) o Studies have shown that adrenal hormone norepinephrine are related to anger and epinephrine for anxiety

o Another study has shown that changes in autonomic activities are discernible for emotions of disgust, anger, fear and sadness; suggests that autonomic changes can be activated by contraction of facial muscles into universal signs of these emotion; facial muscular patterns may provide diff bodily response patterns that arousal theory indicates

Assumes that understanding of arousal needs only understanding of underlying physiological mechanisms o May need knowledge of environmental factors and history of organism

Sleep

Sleep: behaviour we are in for 1/3 of life where our brains are active at times
Much of sleep process is known, but not much is known for reasons of sleep
Effects of sleep deprivation are specific to type of task needed for sleep-deprived individual:
- 2 days without sleep = problems w/continuing long, hard tasks needing high levels of attention and cognitive processing (but no indication on accuracy of performance declining)
- Sleep deprivation increases suggestibility in humans
- Complete sleep deprivation in rats = death, possibly b/c of changes in immune system

General Properties of Sleep

Variability in amount of sleep people need: most people  7-8 hrs. vs. some less – We sleep b/c we are least efficient at certain times:
- Circadian rhythms: cyclic changes of 24 hrs. that our body goes through; operate in lowest part of their cycle during sleep
Evolutionary perspective: sleep is adaptive b/c it prevents us from responding at unnecessary or dangerous times
Sleep is controlled by 2 separate processes: (1) homeostatic process: longer we are awake = increased chance we will sleep and (2) circadian process: determines when we wake up

Animals

Spend diff amounts of time in sleep, but there is universal need for sleep
Adaptiveness of sleep: amount of time sleeping depends on danger of attack:
- Animals likely to be attacked (prey) when sleeping, sleep little and VV
Unihemispheric slow-wave sleep (USWS): ½ of brain sleeps at a time i.e. whales o May have evolved in whales b/c of sleeping while breathing in water and in birds b/c of antipredator function as one eye stays open during USWS

Humans

Time spent sleeping decreases w/age o However, sleep in elderly is variable: some sleep more then when they did when they were younger and some sleep less
Sleep of older adults vs. young adults: (1) more night awakenings, (2) more insomnia, (3) more daytime naps, (4) shorter and more broken up nighttime sleep, (5) go to sleep earlier, (6) decreased time in S3 and S4 sleep (more severe in women)
Sleep is gradual transition from waking through S1 and 2; if awakened right before S2, people say they are awake
Stages of sleep are defined by changes in EEG pattern

Stages of Sleep (know REM and NREM esp.)

Relaxed wakefulness: alpha wave activity before S1 – 5 stages:

Stage 1: replaces relaxed wakefulness w/fast, irregular waves of low amplitude (10-15 min)
Stage 2: sleep spindles and K-complexes
Stage 3: delta waves: large slow waves of high amplitude; occur 20-50% of S3 o When they occur 50%+, person is in S4
Stage 4: delta waves are dominant

30-45 min after falling asleep
During S4, EEG patterns change to S3, to S2, then to S5
Decreases w/age; sometimes disappears by age 50

Stage 5/REM sleep: rapid eye movement; when most dreaming happens; more emotional and like-life, unlike in NREM

Mix of theta, beta and alpha waves
Frequency of eye movement in REM is related to activity reported in REM dreams i.e. more emotional dreams
Best indicator of REM sleep: loss of skeletal muscle tone caused by inhibition of motor neurons in brain = temp. paralysis
Paradoxical sleep b/c: during REM sleep, EEG activity is similar to EEG of S1 sleep and awake person: mix of theta and beta activity
Kittens, puppies and rat pups have 100% REM sleep
REM sleep organizes connections in brain
Since animals show REM sleep similar to humans, it is thought that animals may have dreams

 REM and NREM Sleep

NREM sleep: no eye movements; delta waves; S1 and S4 o Believed to have restorative function: chance for body to rebuild resources
- Where snoring happens
- Person awakened during this time does not report dreaming, but reports random, nonemotional thoughts, similar to waking thoughts; some dreaming does happen here though
Reduced sleep in S3 and S4 for healthy, older people; suggests REM shifts to earlier part of night
Sleep time is not equally divided among stages; from least to most time spent: S1, S3, S4, S5, S2
Not all stages occur evenly through the night: S4 occurs early and REM occurs later (S4 and REM have been studied most)

Dreams

Everyone dreams (shown by REM activity), on average 100min/night
Important dreams and dreams that occur right before we wake up are likely to be remembered
Usually not very emotional, but when they are, they are usually negative
Dreams early in night are usually about previous day vs. later dreams are usually based on stored memories
Change w/age: younger people recall dreams more often and show more aggressiveness, friendliness and emotion in their dreams o Reason why is unclear, but REM sleep does change w/age: time spent on it is reduced and less stable w/age
Neurocognitive theory of dreams by Domhoff: dreaming is developmental, cognitive achievement that depends on maturation and maintenance of forebrain structures o Incorporates “continuity principle”: personal concerns during day appear in person’s dreams
- “Repetition principle”: same characters, settings, social interactions, etc.

show up in person’s dreams

Suggested continuity between waking thoughts and dreams implies we are dealing w/same basic issues during waking and dreaming and that these issues include conceptions of ourselves and others

Threat Simulation Theory by Revonsuo: dreaming functions to simulate threatening events o Allows person to rehearse behaviours that would occur if there was perceived threats and how to avoid them
- Evolutionary b/c: helped ancestors survive and reproduce o Consist w/point above: (1) dreams are often emotionally negative and threatening (vs. positive), (2) aggression is most common form of behaviour in dreams, (3) usually attacked by male or animal in dream

(makes sense in hunter-gatherer societies) o Children dream a lot about wild animals and being victim of animal attack

Virtual rehearsal mechanism by Franklin and Zyphur: extension of Revonsuo’s theory; dreaming serves other cognitive processes in addition to simulations of threatening situations (more general)

Sleep Deprivation

Effects of sleep deprivation vary w/task: short task w/sufficient motivation = minor effects of sleep deprivation vs. long task needing high motivation = deficits in sustaining attention
Sleep deprivation can have therapeutic effects for depressed individuals i.e. one night w/out sleep has antidepressant effect on depressed patients

Dream Deprivation

Experiment of dream deprivation: to deprive sleepers of REM sleep, you need to awake them more often during REM o REM pressure: builds up as a result during REM sleep
REM rebound: when dream-deprived subjects are allowed to sleep, they dream more than normal (as if rebounding from low level during dream-deprivation) for few days after dream deprivation
Effects of REM deprivation in animals that are not understood: (1) shift in eating pattern (relative to dark-light cycle), (2) increase in aggressiveness and sexual behaviours and (3) rebound effects are reduced by intracranial self-simulation
Might be link between neural structures underlying REM sleep processes and other neural structures subserving motivational processes
REM-deprived subjects were anxious and irritable; thus, REM sleep may be needed for psychological well-being; however, these findings are not consistent with other studies
Drugs (i.e. barbiturates) suppress REM sleep (REM-deprivation); if drugs are suddenly withdrawn = REM rebound occurs = increased dreams w/nightmares
- Thus, some cures for sleeplessness, i.e. barbiturates, may be worse than sleep loss
- Even alcohol (if a lot is consumed) leads to REM suppression delirium tremens (DTs): REM rebound causes vivid hallucinations that occur when alcohol is withdrawn

Physiology of Sleep

Vasodilation: blood pressure, heart rate and respiration declines, causing veins and arteries to dilate; happens during NREM sleep
During REM sleep: blood pressure, blood flow to brain, heart rate and respiration increase; penile erection in M and vaginal secretion in F
REM sleep electrical activity of cortex: changes from slow, high-amplitude delta waves  fast, low-amplitude waves similar to during waking
Structures within brainstem and even forebrain may be related to changes in cortical activity, which have control over sleep processes

Brain Stem Mechanisms That Promote Arousal

Many structures within area of pons contribute to production of wake and sleep, not just brainstems structures in area of pons (as previously found)
When reticular system is activated, it arouses cerebral cortex along 2 separate paths:

Reticular formation  thalamus  cerebral cortex
Reticular formation  lateral hypothalamus  basal ganglia  basal forebrain o Connections from basal forebrain activate cerebral cortex and hippocampus

Thus, info available to reticular formation can have wide range of influences on structures important to hypothalamus
Changes in arousal result from complex interplay of these subsystems

Neurotransmitters That Promote Arousal

Acetylcholine

Cells producing acetylcholine in basal forebrain and pons activate cerebral cortex and lead to synchronized EEG when simulated
Blocking acetylcholine reduces arousal levels vs. increased acetylcholine increases general arousal of cortex

Norepinephrine

– Cells producing norepinephrine in locus coerulus of pons activate areas in brain – Important for vigilance

Its production is high during waking, decreases during sleep and almost 0 during REM sleep

Serotonin

Cell producing serotonin in raphe nuclei of pons and medulla connect to many brain regions
Active during waking and decrease during sleep
May be involved w/maintaining ongoing activities (i.e. chewing) and suppressing sensory info hat interrupt those activities

Histamine

Produced by cells of tuberomammilary nucleus: in hypothalamus; connect to may brain regions, including cerebral cortex, thalamus, hypothalamus, basal ganglia and basal forebrain o Connections to cerebral cortex increase arousal directly vs. connections to basal forebrain indirectly increase arousal via TN
Active during waking and decrease during sleep
Related to attention to environmental stimuli

Orexin

Made by neurons in lateral hypothalamus that respond when rats are alert

Brainstem Regions that Promote NREM Sleep

Ventrolateral preoptic area (VLPO): imp for delta wave sleep
If it is destroyed in rats, they do not sleep and stimulation of these neurons causes drowsiness and sleep in cats
When animals are deprived of sleep, then allowed to sleep freely, VLPO neurons increase
Activation of locus coerulus and ralphe nuclei inhibit REM sleep and as their activity decreases during NREM sleep, REM sleep becomes possible

Neurotransmitters that Promote Sleep

VLPO neurons make GABA (gammaaminobutyric acid): inhibitory neurotransmitter
VLPO promotes sleep through GABA connections that inhibit activity of many sites including locus cerulus, raphe, TN and orexiogenic neurons in lateral hypothalamus that have arousal properties
These areas increase arousal levels, thus, their inhibition by VLPA neurons should promote sleep

Brainstem Regions that Promote REM Sleep

Cells responsible for REM sleep are in upper part of pons

Cells active during REM sleep: sublateralalodorsl nucleus (SLD), precoerulus region (PC) and medial peribrachial nucleus o Secrete inhibitory and excitatory neurotransmitters o If cells in peribrachial area are destroyed, REM sleep is reduced

Brainstem Neural Flip-Flops

How arousal mechanisms move from waking to sleep and VV: cells in brainstem word like electrical flip-flop switch: when one system is active (i.e. waking) it inhibits other system (i.e. sleep) and VV o May be located in brain stem area of pons
Another, independent flip-flop mechanism controls transitions from NREM to REM states

A Sleep Chemical

Body produces one or more chemicals that promote sleep as a result of being awake o Evidence: when normal dogs were injected w/cerebrospinal fluid of dogs that were sleep deprived, normal dogs slept a lot
- Conclusion: sleep promoting chemical develops during long periods of wakefulness
Adenosine: may be the chemical that produces sleep as a result of being awake o Made by brain metabolism during waking
- Has inhibitory effect on neurons in pons that make EEG arousal, leading to lower arousal and sleep
- Has 2 receptors: A1 = inhibitory and A2 = excitatory

Possible Functions of Sleep 1. Restorative function:

S3 and S4 are restorative sleep processes
REM sleep: restorative to attention and emotion
REM sleep helps us cope w/stress b/c more REM sleep occurs after stressful days, allowing us to be more efficient when we awake from a lot of REM sleep
NREM sleep also has restorative function
REM sleep: restorative to attention and emotion; evidence for importance to emotion:
- REM sleep = access to emotionally imp memories; thus, REM sleep may help make connections between present emotionally imp experiences and emotional memories related to present experiences o Positive correlation between depression and initial REM onset

Problem w/this theory: S4 and REM sleep decline w/age, yet some people do not show S4 at 50

Organization of brain:

REM sleep is particularly involved in this
Based on fact that 1) young mammals show more REM than adult mammals and

2) REM in humans can be detected before birth o Thus, REM can be internal source of stimulation that “sets up” young brain correctly

o Thus, REM in adults would be vestigial (not useful, but still there) system

Programming device:

– Material learned during waking is incorporated into brain organization and changes brain organization during REM sleep (like self-programming pc)

Consolidation of memories:

Enables material to be transferred from short-term memory to long termmemory
Storage process is based on emotional aspects of info, which is why dreams are emotional
Emotion felt during learning process serves as tag that determines where info goes and label that determines w/what other memories info is stored

Helps learn responses and retain tasks:

REM deprivation would interfere with this
REM deprivation causes more anxiety in anxiety-provoking events o Conclusion: dreaming may allow us to incorporate situations creating anxiety and thus familiarize w/them

Storage of complex associative info

Alcohol interrupts memory and dreaming process, thus, increased REM is attempt by brain to compensate
Damage to LC = more memory disruption; thus, LC plays role in memory process
Model of declarative memory (i.e. memory of events and facts) consolidation during sleep: during slow-wave sleep, newly-encoded info in hippocampus is repeatedly activated = better memory consolidation

Stress

Stressed = high levels of arousal = body forced to adapt; we are stressed even when good things happen to us i.e. marriage

Definition of Stress

Nonspecific response of body to demands made on it
There is optimal level of bodily functioning and stressors; stimuli or situations that create stress in person cause movement away from optimal level o Stress response is an adaptive, homeostatic mechanism b/c it tries to return body to normal state

Systemic and Psychological Stress

Stress does not have to be physical, can be due to psychological reasons i.e.

losing job

Endocrine System Activity and Stress

Endocrine system: set of glands located throughout body that secrete substances directly into bloodstream
Substances secreted are hormones: chemical signals that regulate activity of distant organs
Pituitary: ‘master gland’ in endocrine syste,
Hypothalamus: brain structure active in many motivated activities – Adrenal gland: located on top of each kidney; 2 parts:
1. Adrenal cortex: outer covering; secretes 17-hydroxycorticoid hormones
2. Cortisol: corticoid that does major secretion – Detection of stressor = activation of hypothalamus; then:

Posterior portion of hypothalamus activates sympathetic nervous system = stimulates adrenal medulla = secretes 1) epinephrine and 2) norepinephrine  mobilizes body for action
Anterior portion of hypothalamus secretes corticotropin releasing hormone (CRH) = causes pituitary gland to secrete adrenocorticotropic hormone (ACTH) into bloodstream  relaxed state

The General Adaption Syndrome

Nonspecific , generalized response of body to any demand, physical or pscyhological
General adaptation syndrome (GAS): body’s reaction to stressor:

Alarm reaction: forces of body are mobilized so life can be maintained while local adaptive responses (i.e. inflammation at point of infection) progress
Stage of resistance: stage after local adaptive responses have been established; processes accelerating during alarm reaction drop back almost to normal levels

(i.e. corticoid levels decrease to a bit above normal)

Stage of exhaustion: occurs if local defenses are inadequate or fail to limit effects of stressor reaction to stressor becomes general again; corticoid levels rise similarly to their rise during the alarm reaction o Demonstrates relationship between life stress and illness o Stress is escapable, but there are coping strategies  “buffers of stress”

Disease of Adaptation

Life Change, Stress and Illness

Life-change research says: events of our lives (i.e. adjustments) influence our susceptibility to physical and mental illness o Some people are less likely to become ill than others
Emotional insulation: step back from emotional events and keep them in perspective
Social Readjustment Rating Scale (SRRS): scale of (43) major life changes clinically related to illness
Retrospective studies: individuals are asked to indicate when illnesses and life changes occurred; researchers look for relationships between illness and life changes that may have come before the illness
Prospective studies: individuals supply info about recent life changes and are questioned later about changes in health

Problems of Life-Change Research

SRRS predicts general changes in health resulting from changes across large groups of people, but predicts little about chances of illness for certain individual

Buffering the Effects of Life Change and Stress

Hardiness: combo of 3 personality traits: commitment, control and challenge o Believe they can control what happens to them and that change is natural o Able to put changing life events in perspective
Exercise also serves as buffer of stress b/c it decreases the physiological and psychological strain on individual by life-changing events

Criticisms of the Hardiness Concept

Measures of hardiness are confounded w/neuroticism: can be measuring lack of neuroticism vs. hardiness

Other Buffers of Stress

Social Support Theory: social relationships buffer effects of stress through the encouragement an individual or individuals offer to person experiencing stress
Explanatory style: the way we explain events; pessimistic style = poor health vs. optimistic style = more healthy
Expressive style: use of humor as a way of coping w/stress
Knowledge: can be curative b/c knowing more about our stress and reactions to stress make it less frightening and help us to deal w/it
Emotionally insulate: be objective and accept situations that cannot be changed
Looking beyond the momentary: look beyond current frustrations
Alternative plans: one of the most adaptive responses to stressors; helps you be prepared
Mediation: promotes relaxation by counteracting overactivity of sympathetic nervous system at level of hypothalamus

Health Psychology

Behaviour influences health in 3 ways:

Biological Changes

e. angry (behaviour) causes increase in blood pressure (biological change)
Psychoneuroimmunology: looks at relationship between behaviour, nervous system and immune system

Behavioural Risk

Behaviours can influence chances of illness
e. smoking (behaviour) causes cancer (illness)

Illness Behaviours

Behaviours influence illness
Can go to doctor, but other behaviours (i.e. early detection and interpretation of symptoms) will also play part in determining overall health

Psychoneuroimmunology

It is now clear that there is bi-directional communication between brain + immune system and that immune system influences endocrine system and behaviour
Antigen: activates immune system; produces hormonal and chemical changes recognized by the brain
Cytokinesis/ interleukins (IL): hormone-like proteins; regulates intensity and duration of immune response and cell-to-cell communication

Conditioning of Immune Responses

Conditioned suppression: immunosuppressant; occurs when animal is exposed to CS just before being injected w/immunosuppressive drug (UCS)
Conditioned enhancement: if antigens are used as UCS, CS can produce enhanced immune response

Psychosocial Factors and the Immune System

Acute, short-lived stressors produce adaptive and maladaptive immune responses
Chronic, long-lived stressors produce maladaptive immune responses = immunosuppression

Emotion and Immune Functioning

Immune system has role in neuroendocrine and behavioural features of depressive and anxiety disorders

Placebo Effects

Placebo: inert substance that people report making them feel better
Some people show much larger placebo effect than others; there are placebo responders and non-responders
Desire-expectation model: accounts for many observed placebo effects; placebo responses relate to feeling good about prospects of relief (avoidance goal) or pleasure (approach goal) that are associated w/treatments or medications o These feelings can be separately influenced by desire and expectation or combo of both factors

o Desire is motivation to feel differently (less pain) and expectation is belief that treatment (placebo) will allow one to reach that goal

Sexual Arousal

Stages of the Human Sexual Response Cycle

Vasocongestion: [] of blood in certain parts of body: in males it makes penile enlargement and erection vs. in females, it makes clitoral enlargement
Myptonia: increase in muscle tone in body; happens in M and F until orgasm

Excitement: induced by physical stimuli (i.e. touch) or psychological stimuli (erotic pictures); penis becomes erect due to Vasocongestion and vagina lubricates and lengthens
Plateau: changes of excitement phase continue
Orgasm: sexual climax; sexual tension: M: one orgasm + time ejaculation takes place vs. F: many orgasms or 0 orgasms
Resolution: refractory period in M where sexual behaviour does not occur vs. F do not have definable refractory period- capable of continued sexual activity

Other Bodily Changes during Sexual Behaviour

Female Bodily Changes
- Carpopedal spasm: involuntary contractions of hand and feet
- Sex flush: increase of blood flow to skin
Male Bodily Changes
- Sexual desire: one must be sexually aroused before arousal can occur
- Hypoactive sexual desire: some people lose sexual appetite and become uninterested in sexual behaviour