Learning and Motivation

Lect. 1: Intro to Learning

Learning?
Reflex?
Instinct?
Habituation?
Maturation?
Sensitisation?

Learning = ? Enduring (stable) change (in behaviour) brought about by experience

Learning ≠ Performance
Performance is also dependent on:
- Opportunity
- Motivation
- Sensory & Motor capabilities

Reflexes = innate, automatic behavioural change which does not require experience, hence
is NOT learning. Reflexes require an eliciting stimulus which trigger a corresponding
response e.g. knee tap  knee jerk, rooting reflex, startle reflex

Instincts = changes in behaviour, genetically determined however more complicated than

reflexes. Learning is NOT required, typical of all members of a species e.g. mating rituals

Maturation = behavioural change through ageing/development (physiology) e.g. ‘learning’

to walk. Maturation is NOT learning

Fatigue = transient state of discomfort/loss of efficiency, is not stable and therefore is not
learning

Types of Learning:
- Habituation:
o Habituation: decreased response when a stimulation is repeated e.g. rat jump
less with the presentation of successive loud noises (stimulus). Habituation is
stimulus specific
o Habituation is not the result of fatigue (rat is unable to physically perform
the response) or sensory adaptation (rat’s sense organs adapt to become
insensitive to noise). Habituation is response-specific
- Sensitization
o Sensitization: increase responding produced by repeated stimulation e.g.
exposing rats to the same amount of cocaine after pre-exposure
- Habituation and Sensitization enables different stimuli to be categorised as
important/unimportant allowing organisation and focus of behaviour
- Schizophrenia impairs ability to habituate
Lect. 2 – Pavlovian/Classical Conditioning

Unconditioned stimulus (US) e.g. food

Unconditioned response (UR) e.g. salivation

Conditioned stimulus (CS) = stimulus for response after association with US e.g. bell
Conditioned response (CR) = response evoked by CS e.g. salivation

Classical Conditioning:
o Appetitive e.g. food preferences
o Aversive e.g. conditioned fear, taste aversion

John Watson  Behaviourism: behaviour is the result of conditioning

2nd Order Conditioning: CS1 with CS2  CS2 produced CR

Factors affecting classical conditioning:

1. Volume  no. of CS-US pairing  approaches asymptote of learning
2. Intensity:
a. Salience of CS e.g. louder tone vs weaker noise  slower rate of learning
b. Salience of US e.g. low shock vs strong shock  lower level of learning
3. Contiguity  time between CS and US
4. Contingency: higher contingency  better learning

Contingency:
1. Probability that the US follows CS
2. Probability that the US occurs anyway
Contribute to overall contingency  learning about causal, structural and predictive
relation between event and stimuli

Positive contingency: the CS signals an increase in the probability that the US will occur
(compared to before the CS)  excitatory response

Negative contingency: the CS signals a decrease in the probability that the US will occur
(compared to before the CS)  inhibitory response

Zero contingency: CS predicts neither an increase nor a decrease in the probability of the
US.
Excitatory conditioning: the subject learns to perform a certain response

Inhibitory conditioning: the subject learns to withhold a certain response

Extinction = repeated CS without CR after acquisition, lowers CR  ‘unlearning’

Lect. 3 – Instrumental Learning

Darwin initiated the idea that animals are intelligent and possess mental capabilities and
insight.

Edward Lee Thorndike questioned whether animals show insight  Thorndike’s Puzzle Box
observed progressive improvement over trials through trial and error

Thorndike’s Law of Effect: immediate consequences of one’s past behaviour influences

future behaviour

Situation  Behaviour 3  Satisfaction  Favour Behaviour 3 in future

Thorndike objectively measured dependent variables and performed single/discrete trials

B.F Skinner highlighted limitation with discrete trial  animal producing behaviour results in
termination of trial, one response and one reinforcer ratio per trial

Skinner Box  solved limitation of discrete trial  automation, measures effects of

reinforcement on behaviour continuously  ‘Free Operant Procedure’

Skinner constructed tripartite contingency:

Antecedent - Discriminative Stimulus Sd  stimulus controlling behaviour (is behaviour
appropriate in situation)
Behaviour - response
Consequence – outcome of behaviour  Reinforcing Stimulus Sr
Sd  R  Sr

Instrumental vs Classical Conditioning:

Pavlov: Subject has no control over events, but responds (innate)
Skinner: Subject has to respond to control the consequence i.e. behaviour is instrumental in
determining consequence

Shaping enables introduction of new behaviours e.g. cats ringing bells achieved through
principle of successive approximation i.e. reinforce behaviours that are closer to the target
and gradually make conditions of reinforcement more precise/stringent.

Primary reinforcers are intrinsically valued e.g. food

Secondary reinforcer: acquire reinforcing property through experience e.g. clicker training
Social reinforcement e.g. attention, praise  attention as reward

What makes a good reinforcer?

- Valuable
- High Contiguity i.e. faster reinforcer is given after response
- Strong Contingency  if and only if response is made
Types of Instrumental Learning:
(i) Reinforcement increasing response
a. Positive reinforcement increases responding
b. Negative reinforcement (escape/avoid) increases responding  behaviour
that results in the termination of an unpleasant outcome. Avoidance learning
creates hard to change behaviour due to absence of negative event as the
response is successful if nothing occurs.
(ii) Punishment decreasing response
a. Positive punishment decreases responding
b. Negative punishment (omission) decreases responding
Consequence Appetitive (Good) Aversive (Bad)
R produces consequence Positive Reinforcement: Positive punishment:
Responding increases Responding decreases
R terminates consequence Negative punishment Negative reinforcement
(omission): Responding (escape/avoid): Responding
decreases increases

Negative Reinforcement is NOT punishment!

Way of reinforcement more important than amount of reinforcement!

 Fixed Variable
Ratio (# Responses) Reinforced every N Reinforced on average every
responses N response
Interval (Time) Reinforced every N sec/min Reinforced on average N
sec/min

Partial Reinforcement Extinction Effect:

Partial reinforcement produces more persistent learning than continuous reinforcement
because the less reliably a response is reinforced the more persistent it is during extinction

Application: Once a behaviour has been acquired through a continuous reinforcement

schedule changed to a partial reinforcement schedule to increase persistence of behaviour.

Unlike Classical Conditioning, Instrumental learning involves circumstances where behaviour

determines events that follow

Question Test:
1) What is Thorndike’s law of effect?
2) What is the difference between discrete trial and free operant procedures?
3) What is instrumental conditioning?
4) What are the different types of instrumental conditioning and what do they involve?
5) Difference between instrumental and classical conditioning?
6) What is shaping?
7) What makes a good reinforcer?
8) What are the different schedules of reinforcement and what do they involve?
9) What is the partial reinforcement extinction effect?

Lect. 4 – Stimulus control

Instrumental conditioning: Discriminative stimulus (Sd)  Response followed by Reinforcer
(Sr) or Punisher (Sav)

Generalisation: other stimuli similar to CS  weaker conditioned responses

Generalisation: conditioned performance with a stimulus similar to original CS

Discrimination: Learning to differentiate between cues e.g. two CS

Initial generalisation  Discrimination

Stronger CRs i.e. more generalisation from meaning

Thorndike  likelihood of response:

1) Response
Instrumental behaviour only controlled by situational cues if the cues determine
reinforcement

Herrnstein  discrimination learning occurs with realistic stimuli (pecking only when human
present)

Successive Discrimination vs Simultaneous Discrimination (decision between responses both

S- and S+ present)

No. of exemplars/examples increases discriminative ability

Punishment is very specific and short-lived does not generalise

L5 – Social Learning
Behaviourist (Skinner/Watson) direct experience  behaviour
Social Learning: response influenced by observation of others (models)
Lab-raised monkeys vs Wild monkey fear of snake

Social facilitation (do not reflect social learning, may contribute):

- Goal enhancement  facilitate trial & error
- Stimulus enhancement  observe/approach others
- Increased motivation to act  in groups
- Contagious behaviour  mimicking a behaviour

Two-action test

Social (instrumental) learning:

- Mimicry  action without goal
- Emulation  goal without understanding of specific response required
- Imitation  copied action with goal

Bobo doll  modelled aggression

Modelling is reinforcement dependent (consequence of action)

Social cognition theory

1. Attention to model
2. Memorise model’s actions
3. Capacity to reproduce model’s actions
4. Motivation (reinforcement? Positive or negative)
Motivation

L6 – Instincts and Drives

Motivation is temporary NOT learning
Hebb’s analogy:
- Motivation = power  behaviour
- Learnt = direction  behaviour

Fixed action patterns: same behaviour by all species members to same stimulus i.e. set seq
of behaviours e.g. Stickleback mating behaviour (sign stimulus = red underbelly)

1. Biological change
2. Initiated by sign stimuli
3. Innate releasing mechanism  action specific energy
4. Fixed action pattern

Instinctual human learning:

- Non-verbal communication

Problems with Instinct only theories:

- Circularity problem  circular reasoning
- Proliferation 
- Behavioural flexibility & learning  influences behaviour

Drive Theories:
- Movement away from homeostasis  Tension (D)  energises behaviour 
behaviour that reduces D are reinforced
- Problems:
o Drive theory  linear relationship: arousal & performance
o Drive theory not necessary for reinforcement
o Drive stimulation can be reinforcing
o Ignores quality of reinforcement

Harlow & Maternal Deprivation:

Wire surrogate satisfied biological need, monkey preferred cloth surrogate

Sensory deprivation  arousal has a hedonic value

Sex drive  non-homeostatic drive 

I&D
Lect. 7 – Long-term Motivation

Humanist reaction to behaviourism & psychodynamic movement

Humanism  Optimism  Freedom
Carl Rogers: innate motivation to become “fully-functioning” (fulfil potential)
Rogers  self-concept (perception of self)  need for positive regard (others) & positive
self-regard
Fully functioning person has a consistency between positive regard and self-regard 
positive self-concept
Unconditional positive regard  growth
Conditional positive regard  anxiety

Maslow: hierarchy of needs  self-actualisation (highest)

Physiological  Safety  Love  Esteem  Self-actualisation
Criticisms:
1. Weak empirical support
2. Hierarchy
3. Circularity of self-actualisation
4. Based on Western ideals

Henry Murray  Projective test: study needs and goals  describe an ambiguous image,
interpretation thought to reveal goals etc
Thematic appreciation test

Need for Achievement:

- People high in nAch attempt harder tasks
- Achievement = successful completion of difficult job

Expectancy-Value Theory:
- Expected utility of action = value of goal x probability of obtaining goal
- If Ps of success high  utility of success (Us) is low
o Us=1-Ps
- EU (expected utility) = Us x Ps
- EU = (1-Ps) x Ps

Neuroscience

Lect. 1 – Nervous System

Behaviour Neuroscience: study of biological bases of psychological process (emotion,
behaviour, thought)

1. Central Nervous System  Brain & Spinal cord

 a. Protected by bone, meninges, blood brain barrier. Central nervous cells
cannot be regenerated
b. Meninges: flexible membrane/sheet between brain/spinal cord and bone,
composed of three membranes
i. Dura mater
ii. Arachnoid membrane  blood vessels
iii. Pia mater
c. Blood brain barrier: high energy needs met by blood supply, vessels in CNS
restrict entry of many chemicals into CNS
d. Spinal cord: cable of neural fibres that branch off  and is an interface
between brain and enP nervous system  connected to sensory, motor and
autonomic nerves
2. Peripheral Nervous System  everything else e.g. sensory, motor nerves etc…
a. Sensory Nerves input to CNS from sensory organs
b. Motor Nerves output from CNS to muscles
i. Autonomic Nervous System
1. Controls non-voluntary bodily function the 4Fs, fight, flight,
feeding, fucking
a. 2 Branches: Sympathetic  prepares for action
b. Parasympathetic  rest/recuperation
ii. Enteric Nervous System (ENS)
1. Located in gut controls digestive activity interacts with brain
through Sympathetic & Parasympathetic NS also functions
independently.

Lect. 2
Two hemispheres (Left and Right, mirror images)
Ventricles: Cavities in brain filled with cerebrospinal fluid  sewerage system of brain
1. Brainstem – at base of brain
a. Controls life-supporting functions e.g. breathing
2. Cerebellum (top right of brain stem)  most neurons
a. Control of precision movements
3. Thalamus & hypothalamus (top of brain stem)
a. Sensory relay to cortex
b. Hypothalamus  hormonal regulation and motivational control
4. Limbic system (wraps around thalamus)
a. Involved in emotion and memory
5. Basal ganglia (wraps around thalamus)
a. Involved in action & thought
6. Neocortex (convoluted/wrinkled sheet on top of brain)
a. Folding increases SA fit in small area, different functions in different area
b. Four lobes:
i. Frontal lobe  movement and executive functions; decision making,
planning
ii. Parietal lobe  understanding space and motion
iii. Temporal lobe  memory + language
 iv. Occipital lobe  vision
7. Corpus Callosum

Lect. 3 – Anatomy & Physiology of Neuron

 Send binary (“On/Off”) signals i.e. 2 states

 Membrane semipermeable enables control of concentration of positive and negative
ions inside/outside.
 In normal “resting” state, inside of neuron has greater negative charged
concentration of ions, neuron is polarised in this state.
 Action potential (all or none): neuron can open channels enables ions enter/exit
cause neuron to depolarise, greater concentration of positively charged ions inside
neuron
 “off” when polarised, “on” when depolarised
 Action potential is localised to a small area of membrane and propagates down the
axon
 Hyperpolarisation after AP prevents AP doubling back on itself
 Myelin prevents depolarisation, polarisation occurs at gaps between myelin sheath
o Myelin speeds up propagation of action potential (AP jumps from gap to gap)
 Neurons are digital
 Sophistication of Brain Function:
o High speed of neuron transmission
o No. of neurons
o Complexity of neuron connections
 Anaesthetics block opening of neuronal ion channels
 Alcohol impairs generation of Aps
 Neuron communicate across synapses via chemical transmissions “s” which are
released into synapse from axon terminals to dendrites of another neuron
 Neurotransmitter binds to receptor at dendrites of 2nd neuron and causes changes in
neuron
 Excitatory NTs promote action potential in 2nd neuron
 Inhibitory NTs block action potential
Lect. 3 -

Mapping the functional organisation of the brain:

 Transcranial Magnetic Stimulation (TMS)  brief magnetic pulse induce electrical

current that depolarise neurons and provoke action potentials.
 Single cell recording

Functional imaging of the brain:

Measuring which brain areas become active when:

 Electroencephalography (EEG)  electrode plates against skull record electrical
fields of neurons  high temporal resolution (shows when activity changes) but
poor spatial resolution (where activity occurs)
 Positron Emission Tomography (PET)  measures brain activity thru blood flow
changes (active areas require blood flow), given radioactively-labelled oxygen gives
good spatial resolution (not good temporal resolution)
 Magnetic Resonance Imaging (MRI)  MRI: bombard head with high frequency
waves, while inside a magnetic field  identify/visualise brain structures
 Functional Magnetic Resonance Imaging (fMRI)  fMRI: measures changes in O2 in
blood  good spatial resolution, BOLD (O2 depleted) response lags therefore
temporal resolution low
 Magnetoencephalography (MEG)  measures magnetic fields emitted from brain,
3D reconstruction of brain electrical activity  temporal +spatial resolution and non-
invasive + expensive

Brain activity + physiological function ≠ causal link

Regulation of Feeding: Hunger and Satiety triggered by contents of stomach/substances

circulating in blood
Brain is responsible for hunger/satiety and behaviour
Lateral Hypothalamus (LH) regulates:
 Release of insulin  reduces appetite
 Regulates attention
 Influence taste
Ventromedial Hypothalamus (VMH):
 Lead to overeating due to increase in gut motility
 Excessive release of insulin
Paraventricular Nucleus of Hypothalamus:
Lect. 4 – Sleep

Sleep is very important for brain function  attention, speed, mood, memory
Lack of sleep  increase appetite + weight gain + activity of sympathetic nervous system
(stress reaction)

Pons (Acetylcholine), Locus Coeruleus (Non-adrenaline neurons), Raphe Nuclei (serotonin):

structures in brainstem are responsible for arousal. Disconnection  continuous sleep

What contributes to sleep:

1. Suprachiasmatic nucleus releases melatonin from pineal gland signals nighttime
2. Adenosine builds up in brain increases sleepiness inhibits alertness centres in Pons
and stimulates sleep in pre-optic area with GABA. Caffeine blocks adenosine
receptors

Sleep Cycles:
1. Sleep characterised by slow rhythmic patterns of electrical activity in brain
controlled by thalamus which orchestrates synchronised neuronal activity
through its reciprocal connection to cortex. (SLOW-WAVE SLEEP)
2. REM Sleep or rapid eye movement sleep  waves become desynchronised
(associated with dreaming)
a. Pons that contain acetylcholine stimulate thalamus neurons which
stimulate visual cortex
b. During REM sleep we are paralysed, ACh neurons stimulate neurons in
medulla which inhibit motor neurons in spinal cord

Neural Mechanism of Reward:

- Motivate action/learning
- Olds & Milner  electrical self-stimulation of medial forebrain bundle (mfb)  rat
returned to same place it received electrical brain stimulation, further
experimentation showed that rats will learn specific behaviours in order to receive
electrical stimulation. Explanation: Dopamine axons in mfb provide rewarding effect
Lect. 6 – Lateralisation of function & Memory
Hemispheric Lateralisation:
- Right hemisphere sensory input from left, controls left
- Left hemisphere sensory input from right, controls right
Hemispheric Dominance e.g. hand preference and language
Left hemisphere controls speech/comprehension, evident with strokes in left, brain imaging,
dichotic listening task (word understood faster through right ear)
Individuals with damage to Broca’s Area (lower posterior left frontal lobe) have difficulty
speaking but can understand speech
Wernicke’s Area (posterior left temporal lobe): damage  loss of comprehension, fluent but
meaningless speech  cannot read
Split Brain  removal of lateralisation of function can be due to removal of corpus callosum
Split Brain patients can walk, talk, suffer no emotional or intellectual impairments, struggle
to relate action of left and right hands e.g. choosing clothes
- Roger Sperry  identify object in right hand, not object in left hand
- Functions in right hemisphere contributes to identifying non-verbal meaning i.e. tone
e.g. sarcasm, interpreting emotion
- Functions in left hemisphere

Henry Molaison  normal procedural learning

Hippocampus = major memory structure in brain

Hippocampal amnesia:
- Brenda Milner  damage to anterograde amnesia  anterograde amnesia
(remember old stuff, cannot learn new things) i.e. deficit in creating new long-term
memories

Wernicke-Korsakoff’s Syndrome  Amnesia due to disease:

- Severe vitamin B1 (thiamine) deficiency in alcoholics  Wernicke’s Encephalopathy,
untreated  profound anterograde and some retrograde amnesia due to
irreversible damage to mammillary bodies and thalamus

Alzheimer’s Disease:
- Progressive neuro-degenerative memory disease  loss of newly learned
information followed by loss of distant memories/skills/knowledge

Abnormal Psychology
Lect. 1 – What is abnormal psychology?
Abnormal psychology: study/explanation of abnormal behaviour, emotion and cognition
Empirical methods used as three different levels:
1. Description
o Classification/Diagnosis
2. Causation
o Biological/Social/Psychological
3. Treatment
o Effectiveness
3D’s of defining abnormality
1. DEVIANT: (unusual, unexpected, rare) e.g. fetishism
2. DISTRESSING: self + others e.g. depression + anxiety
3. DYSFUNCTIONAL: (maladaptive, interfering with life goals) e.g. ADHD

No D alone is necessary/sufficient to determine if a behaviour/feeling/thinking is abnormal

Psychological abnormality is not as definable as physical illness

Psychological abnormality exists on a continuum with normality
Definition of psychological abnormality reflect cultural values and social norms

Theories/approaches to ‘mental illness’ (Abnormality)

- Supernatural model: Cause = demons, evil spirits. Treatment = exorcism etc.
- Biological model: Cause = internal physical problems. Treatment = bleeding, rest
- Psychological model: Cause = beliefs, values, goals. Treatment = psychotherapy
- Sociocultural model: Cause = poverty, prejudice, cultural norm. Treatment = social
work

- Integrative model  Bio-Psycho-Social Model

Psychiatrist: Medical doctor with specialist training responsible for treating/prevention of

complex mental health problems
Medical Degree  Internship  Residency  Vocational Training (Average 11 Years)
Can prescribe medication

Clinical Psychologist: 8 years  experts in psychological assessment, treatment formulation

and prevention of behavioural, mental and emotional health issues
Therapy = bio-psycho-social approach
Cannot prescribe medication
Registered/General Psychologist: generalist training, not specialised e.g. depression,
anxiety for less serious/complex mental disorders

Social Workers: Work in direct services, clinical field, environment and cultural factors help
patients develop practical plans to improve well-being

Counsellor: Assist understanding + life changes, non-judgemental listening, work in

particular field e.g. school/family/marriage. Qualification varies greatly

Lect. 2 –
Biological/Medical Model is the most dominant in psychiatry:
- Mental illnesses can be diagnosed similar to physical illnesses
- Mental disorders can be explained as a biological disease process e.g. Schizophrenia
brain abnormalities
Caused by biological deficiencies medication targeting biology e.g. depression 
neurochemical imbalance

Criticisms of Biological Model:

- Extreme reductionism of sociocultural and psychological model
- Over-extrapolation from animal research
- Assuming causation from treatment efficacy e.g. Antidepressants i.e. depression not
being addressed
- Difficulty using to conceptualise and diagnose physiological/mental illness

Psychoanalytic Model:
- Unconscious mind is the primary source of our behaviour
- ID: completely unconscious, instinctual self  driven by pleasure principle for
gratification.
- Ego: Conscious/Rational self-obeys reality principle, balances conflicting demands of
ID and Super-Ego
- Super-Ego: Morality developed through socialisation
- Id + Super-Ego = constant conflict which ego must negotiate
- Unresolved conflicts (ego unable to resolve conflict between id and superego) 
anxiety, shame, guilt and embarrassment, develop defence mechanisms:
o Distorting id impulses into acceptable forms
o Repressing id impulses into unconscious
- Maladjustment: excessive defence mechanisms  suffering  mental illness
o Displacement  Depression
- Symptoms are NOT central to diagnosis it is the process/thought
- Treatment: Gain insight into unconscious to develop awareness of unresolved
conflict and defence mechanisms used.
- Significance:
o Revolutionised concept of mental illness, no clear division between
normal/abnormal conditions/processes  DSM
- Criticism:
o Lack of empirical evidence
 o Incapable of empirical evaluation  unfalsifiable
o Lengthy + Expensive

Humanistic Model:
- 60s & 70s in response to negativity of psychoanalytic model
o Self-actualised (Maslow)
o Fully functioning human (Rogers)
- Maladjustment: Self-actualisation threatened/prevented
o Unsafe environment
o Experience/Emotions are blocked
- Treatment: Empathy (and unconditional positive regard) to assist/promote self-
actualisation
- Criticisms:
o Difficult researching
o When is self-actualisation achieved?

Behavioural Model:
- Reaction to un-falsifiability of psychoanalysis  behavioural model  observable
- Classical Conditioning
- Operant Conditioning
- Normal and abnormal behaviour/adjustment/maladjustment due to learning history
- Treatment: Variety e.g. exposure therapy
- Criticism:
o Overemphasis on behaviour exclusion of cognition

Cognitive-Behaviour Model:
- Most dominant model in abnormal psychology
- Thoughts influence feelings influence behaviour
- Maladjustment: Latent core negative beliefs
o Guide world understanding
o Interpretation of experience aligns with beliefs
o Cognitive distortions/biases
o Automatic negative thoughts

Lect. 3 –

Specific Phobias: obsessive, consistent fear to presence/anticipation of item/situation 

anxiety un-proportional  avoidance behaviour
Panic Attack: abrupt, intense fear, symptom of anxiety disorders:
 Situationally bound (cued)  presence/anticipation of stimulus
 Unexpected (uncued)  panic disorder

Panic Disorder  Unexpected spontaneous panic attacks, without identifiable trigger:

 Cognitive theory: High sensitivity/misinterpretation to bodily experiences
Agoraphobia: DSM 5 – Marked fear/anxiety about 2 (or more) of:
o Public transport
o Open spaces
o Enclosed spaces
o Crowd
o Outside alone
 excessive avoidance

Social Anxiety Disorder: Intense fear and avoidance of social/performance situations 

embarrassment
- Desire to convey favourable impression, insecurity surrounding their own ability

Generalised Anxiety Disorder (GAD): excessive, uncontrollable worry about many outcomes
i.e. What if?
Cognitive processes/factors:
- High trait anxiety
- Intolerance of uncertainty
- Inability to tolerate distress
- Reduced PS confidence/success

Obsessive Compulsive Disorder (OCD)

- Obsessions: intrusive, irrational thoughts  anxiety/distress
- Compulsions: ritualised behaviours  relieve anxiety/distress caused by obsessions

Lect. 4 –
Recap: Models
- Psychoanalytic:
o Cause: Repression of unresolved conflict
o Treatment: Insight
- Humanistic
o Cause: Thwarted self-actualisation
o Treatment: Empathy
- Behavioural
o Cause: Learned associations
o Treatment: Learn new associations
Cognitive-Behavioural Model:
- Reaction to lack of cognition in behaviour model  Mid 20th century:
- What we THINK influences how we FEEL and BEHAVE
o Maladjustment: latent NEGATIVE CORE BELIEF
o Cognitive Behavioural Therapy (CBT)  exposure therapy
 Cognitive restructuring
Classification & Diagnosis of Mental Disorders:
 - Diagnosis on causation is goal of classification
- Diagnosis improves communication, understanding and reduce social stigma
- DSM = Diagnostic and Statistical Manual of Mental Disorders
- ICD = International Classification of Diseases and Health Related Problems
- DSM & ICD describe symptom clusters which form criteria to guide clinician in
diagnosis
- DSM: American Psychiatric Association
- ICD: World Health Organisation (WHO) holistic not solely focused on mental
disorders
- ICD and DSM are comparable but NOT identical
- Homosexuality removed from DSM
- DSM used in Australia describes psychopathology/mental disorders,
symptoms/criteria  differential diagnosis. Only a GUIDELINE

Evolution of DSM:
- DSM-1 (1952), DSM2 (1968) heavily influenced by psychoanalytic theory:
o Problematic reliability: Agreement on diagnosis across clinicians. What if
some symptoms are missing/varies in strength?
o Problematic validity: Unproven theories e.g. What is depression? Is the
psychoanalytic approach to depression valid? Depression as a defence from
unacceptable unconscious ambivalent feelings. Unfalsifiable
- DSM-3 reflects medical/biological model, does not make theoretical assumptions on
causation. Knowledge of causation is not required rather description of symptoms.
Improved reliability
- DSM-5: 5 or more symptoms needed

Experience of anxiety is same in normal and abnormal anxiety:

- Physical
- Cognitive
- Behavioural

1. Physical System:
a. Fight/Flight response
2. Cognitive System:
a. Perception of threat
b. Attentional shift
c. Hypervigilance
3. Behavioural System:
a. Escape/Avoidance
b. Aggression
c. Freezing
Normal Anxiety:
- Evolutionary value  survival
- Eliciting condition  physical vs. social threat
- Specific ‘prepared’ stimuli e.g. insects, animals
- Novel stimuli (unknown)
 - Threat appraisal  expectancy of harm, product of perceived probability of outcome
and perceived cost of outcome based on past experiences and observations

Abnormal Anxiety:
- Trait anxiety  tendency to perceive threat in ambiguous situation
- Extent of anxiety response
- Specific fears  ABNORMAL
- Not qualitatively different from abnormal anxiety same systems activated
- Difference is occurrence is EXCESSIVE or INAPPROPRIATE e.g. absence of objective
threat, OVERESTIMATION of threat; COST or PROBABILITY of harmful outcome
- Physical fears  probability overestimation
- Social fears  cost overestimation

Lect. 5 – Treatments

Cognitive Behavioural Therapy (CBT)  aims to reduce threat appraisal i.e. likelihood of
perceived harm
Three mains components of Cognitive Behavioural Therapy:
1) Psycho-education: identifying an individual’s specific triggers, responses, impact on
life  explanation of anxiety  role of avoidance  teach relaxation techniques to
address fight & flight response
2) Cognitive techniques: Cognitive restructuring/thought challenging, thought diaries:
attempt to recognise automatic thoughts, Socratic questioning
3) Behavioural techniques: Exposure therapy directly challenging avoidance
mechanisms, vitro exposure: imagination, vivo exposure: real scenario, anxiety
causing stimulus present, virtual reality

Systematic Desensitisation vs Flooding:

Flooding: exposure of patient to greatest fears straight away
Desensitisation:
Exposure to feared stimuli/situation  reduce judgment of probability of harm
Exposure to feared outcomes  reduce judgment of cost of harm

Pharmacotherapy/medication:
- Treat symptoms not cause, short-term only
a. Barbiturates  Quick acting, addictive, interacts with alcohol, high relapse
b. Benzodiazepines  Valium, quick acting, less addictive, interacts with
alcohol, high relapse
c. Antidepressants – SSRIs  slower acting
Major Depressive Episode  5 or more symptoms in 2-week period
Affective symptoms: depressed mood
Cognitive symptoms: indecisiveness, lack of concentration
Somatic symptoms: fatigue, sleep change

Major Depressive Disorder  single or recurrent depressive episode, common

Medication for Major Depression:

 Selective Serotonergic Reuptake Inhibitors (SSRIs)
 Electroconvulsive Therapy (ECT)  brief electrical current to brain
Psychological treatment: CBT

Lect. 6 – Anorexia Nervosa, Bulimia Nervosa

Anorexia Nervosa
- Intense fear of gaining weight
- Body image distortion
- Self-starvation and low body weight BMI < 18.5
Two types: Restricting/Purging types
Occurrence greater in females
Onset between 12-25, 5-7-year duration slow recovery
40% AN  Bulimia Nervosa
High suicide risk
Psychological features: low self-esteem, irritability, withdrawn, depression
Behavioural features: excessive exercise, secretive behaviour, sensitive to references about
weight, frequent checking of appearance
Physical features: low body temp, brittle hairs and nails, osteoporosis, yellow skin,
malnutrition.

Bulimia Nervosa (BN)

characterised by:
- Binge eating compensated by behaviours that prevent weight gain
- Distorted body image
- Differentiable from Anorexia Nervosa as sufferers of
Bulimia have normal weight or overweight
- Binge eating in discrete period of time, large
amount of food, lack of control, followed by
shame, anger
- Recurrent inappropriate compensatory
behaviours to prevent weight gain e.g.
induced vomiting, laxative misuse
- Inappropriate compensatory behaviours
follow period of binge eating
- 90% female, onset adolescence, chronic
- Muscle dysmorphia
- Genetic factors suggesting inheritance
- Serotonin involved in appetite regulation
- Anorexia and Bulimia both related to issues with self-worth
Eating Disorders: Proposed psycho-social causes
- Family factors: parental criticism, low empathy/support, modelling
- Peer factors: social approval
- Sociocultural factors: emphasis on thinness

Cognitive Psychology
Lect. 1
- Behaviourism: Measure Stimulus-Response, however did not accept that there are
many behaviours that cannot be explained via stimulus-response
- Tolman  rats will learn without reward
- Tolman’s radical and revolutionary proposal in 1948 was that rats form an internal
map of their environment
- Mental Chronometry is timing how long thoughts take e.g. simple reaction time:
press button to any light
- Choice reaction time = press one button to red light another for green light
- Choice RT – Simple RT = Estimate of stimulus evaluation time
- Humans perform serial exhaustive searches: search through items one at a time,
once we find desired item and keep going through search.
Pseudo-certainty effect shows importance of framing when asking questions

Lect. 2 – Attention
Focused attention: Properly focused on specific assigned task
Diffused attention: General attention, not focused
Inattentional blindness:
What is processed without attention?
Why is attention limited?
- Limited attentional resources
Where is the locus of selection?
- Point at which filter is applied, what is processed and what isn’t?
- Where in the processing chain the filter is?
a. Early locus of selection: not much processed on stimuli, only physical
properties
b. Late locus of selection:
- Evidence for locus of selection, stereo headphones must shadow input
- Proportion of Wood & Cohen participants reported hearing own name  35%
- Lavie  location of attention field  Depends on cognitive load
- When cognitive load is high selection occurs early
- When cognitive load is low selection occurs late
- Unique features are detected easily, but unique combinations of features are harder
to find, what does this suggest about the role of attention?  to bind features
together
- Treisman: Feature Integration Theory proposes that we process features
independently in pre-attentive manner, then attention binds features together into
objects

Control of attention:
- Exogenous/involuntary/stimulus driven
- Endogenous/voluntary/controlled

Change blindness: We encode very little about the world

Lect. 3 – Short term memory and working memory:

Types of memory:
- Iconic and echoic / sensory memory
a. Decays faster than you can empty it
b. Iconic memory: visual sensory memory
c. Echoic memory: sensory memory for sounds  lasts longer
- Short-term memory / working memory
- Long-term memory
Short-term memory (STM) Long-term memory (LTM)
Capacity Limited, 7+/ 2 Unlimited
Rate of forgetting Decays within 20 seconds Forgetting due to
interference than decay
Type of coding Phonological (speaking) Semantic

Serial position effects in short term recall:

- Primacy  info transferred to LTM
- Recency  info dumped from short-term buffer
Peterson and Peterson (1959) measured memory of three consonants with no rehearsal 
only 10% of consonants remembered on average
Without rehearsal
Without rehearsal short term memory is gone after 10-20 seconds
A strategy for memorisation is to turn a number/sequence of letters into a fewer number of
units  CHUNKING

Phonological coding  Short term memory  easily confused by things sounding same
Semantic coding (what things mean)  Long term memory

Clive Wearing  No ability to encode long-term memories, no long-term memories,

memory span 30 seconds
Working memory consists of:
- Central Executive & Episodic buffer:
a. Number of things remembered and ability to focus on something and
rehearse
- “Salve” systems:
a. Phonological loop  component of working memory model that deals with
auditory information  phonological store (which holds words we hear) and
the articulatory process (which allows us to repeat words in a loop).
b. Visuo-spatial scratch pad  stores image
Lect. 4 – Structure of Long-Term Memory:

- Declarative memory system:

a. Episodic memory system  memory of life events (explicit memory)
b. Semantic memory system  memory of what things mean (explicit memory),
knowing vs remembering:
i. Collins & Loftus (1972)  spreading activation  activate one node
everything connected activated. Example canary activated then bird
then animal will activate: typicality + category size effects

In connectionist or paralleled distribution processing (PDP) models of attention, how are

memories meant to be stored? Particular patterns of activation

We use schema to interpret the world  Schema = generalised mental representations or

concepts describing a class of objects, people or events: Example: birthday parties’ schema
 expectations of certain events, cake, balloons
E.g. office schema  expect chairs, books, desks
Schema improve memory encoding but can also DISTORT

Stereotype is a subset of schema  stereotype is a person schema  used for ease of

understanding

Script transference

Schema: Lectures are boring, Houses with three or more bedrooms have at least two toilets
Scripts: When you arrive at a lecture, find a seat, be quiet, take notes, before intimate
contact ask for consent [Scripts are a kind of schema]

Lect. 5 – Implicit memory and false memory

- Implicit memory = classical conditioning and priming i.e. an unconscious association
between stimuli
a. Priming = display or mention of one concept leads to ‘spreading activation’ to
other related concepts. Example: Money  Withdraw  Robbery

- Declarative memory (explicit)

a. Semantic memory
b. Episodic memory
- Procedural memory (implicit) e.g. kissing, riding a bike, mirror drawing
a. Memory for how to do things
b. Learnt thru gradual, incremental experience

Levels of processing and memory:

- More deeply processed stimuli are better remembered
- Structural  Phonemic (sounding)  Semantic (meaning)
 - By examining/considering meaning of something memory is expected to be better
- Abstract: concept, construct, adjective
- Concrete: thing, person/place, noun
- Implicit memory test  unaware memory is being tested
- Explicit memory test  aware memory is being tested
- Implicit memory performance varies from explicit memory performance, does not
follow that more deeply processed level of processing are more deeply remembered.
- Shallow level processing e.g. how many letters does this word have? Improve implicit
memory performance
- Differences in explicit and implicit memory can be explained by differences in the
way encoding is done. Memory is dependent on match between encoding and
retrieval:
TRANSFER APPROPRIATE PROCESSING:
Implicit Memory: Perceptual  Encoding: activation, Retrieval: familiarity
Explicit Memory: Conceptual  Encoding: elaboration, Retrieval: recollection
In implicit memory testing, words related to actual words on list are often confused

Declarative memories include your understanding of facts, words, concepts, idea

Procedural memories are associated with skills and performance of actions

Implicit memory is assessed by performance on various tasks

Explicit memory is when you know your memory is being assessed

Pseudoforgetting is most likely due to: Lack of attention at encoding

Forgetting something you never really remembered

False memory:
- Misleading information post-event e.g. Loftus (1974)  Eyewitnesses  leading
questions/ emotive language
- From social pressure
- Source confusion
Flashbulb memories: highly detailed, vivid snapshot of the moment and circumstances in
which a piece of surprising news was heard e.g. 9/11  HOWEVER, current research just
shows they are just normal memories and decay as normal.

Confabulation = filling in of gaps with something coherent

Lect. 6 – Encoding and retrieving strategies, studying and memory
Infantile amnesia  may be a result of children not having a developed schema
Reminiscence bump  large number of memories from 15-25
 Schema greatly affects memory
- Free recall task: report items from an early episode
- Recognition task: select previously studied items
- Recognition is easier than recall as provides a retrieval cue

Magnocellular cells are responsible for resolving motion and coarse outlines
Saving vs remembering
 Remembering is superior
Retrieval is best when encoding and retrieval MATCH

- Interference affects study:

- Retroactive – new material affects old material
- Proactive – old material affects new material

Semantic structuring  effective chunking  allows relation of info

 Method of loci: each piece of information is mentally attached to location

Summarisation:
- Better than copying, low utility
Highlighting and underlining:
- Low utility, ineffective
Rereading:
- Good for recall, low utility
Practice testing:
- High utility
Distributed practice:
- Spacing effects  high utility  materials reprocessed

Lect. 1 – Human Mental Abilities:

Mental abilities: capacity to perform higher mental processes e.g. reasoning, understanding,
problem solving
- Intelligence is a construct
- Infer intelligence from observing behaviour
- Construct = theoretical (hypothetical) entity
- Intelligence is sometimes described as a latent variable (underlying disposition)
- Measure intelligence from observable behaviour
- To test intelligence must operationalise the construct, test must reflect the construct

Implicit Theories of Intelligence:

- Informal definitions of intelligence, beliefs held
 Entity theorist  mental ability fixed
 Incremental theorist  Abilities are changeable
Implicit beliefs of intelligence can affect our own lives, belief that intelligence is malleable
(incremental theory)  upward trajectory in grades. Entity theory of fixed intelligence 
flat trajectory

Steinberg (1981) 3 factors:

 1. Verbal intelligence
2. Problem solving
3. Practical significance

Explicit Theories of Intelligence:

- Use data collected from people performing tasks that require intelligent cognition
- Test whole domain (intelligence) or specific subsets (verbal performance)
- Theories supported by mostly indirect evidence:
a. Must be internally consistent
b. Correlate with other behavioural messages

Lect. 2 – History of Intelligence Testing

- Alfred Binet  series of reasoning tasks related to everyday problems of life  basic
reasoning processes  BINET’s SCALE
a. Attempted to separate natural ability from education
b. Age level assigned to each reasoning task
c. Mental age – age assigned to most difficult task completed e.g. 5 year old
solving 7 year old task  mental age of 7
d. Binet’s scale was designed to attempt to identify students in need of remedial
education  education is NOT fixed
- Binet’s stipulations:
a. Scores were a practical device  are NOT innate, support theories of
intelligence, or measure “intelligence”
b. Scale is ROUGH
c. Scale should NOT be used to MARK children as innately incapable focus on
improvement
- H.H Goddard introduces Binet’s test to USA
a. Goddard sought to prevent immigration/propagation of “morons”,
misconstrued Binet’s scale regarding measures as a single, innate entity
- Lewis Terman revised Binet’s test and was publicized as “intelligence” testing
a. Measuring intelligence: From mental age to IQ
i. IQ = intelligence quotient
ii. Differences in age were a problem in assessing intelligence through
their mental age
iii. Ratio IQ allowed for comparison of intellectual performance across
differences in age
1. Ratio IQ = mental age / chronological age x 100%
2. Ratio IQ assumes mental age and increases proportionally with
chronological age  difficult application for adults
- -

Deviation scores are useful as the percentiles vary for different groups  same score
can have different percentiles ranks and then different psychological interpretations
depending on subject at hand. Where do some individuals sit in comparison to the
score some other people obtained?
- Standardising (norming a test): Raw scores  Z-scores  Deviation IQ scores
 - Decided by convention  mean of 100, and SD of IQ measure is 15

IQ = 100 + Z*15  Z is how many SDs away from mean, 15 is size of SD

Therefore, IQ scores mean same thing regardless of comparison group

Lect. 3 - Intelligence tests and the factor analysis of intelligence

- Stanford-binet tested cognitive ability in four areas
a. Verbal reasoning
b. Quantitative reasoning
c. Abstract/visual reasoning
d. Short-term memory
- A basal and ceiling level is established for each task
a. Basal level = four items passed in a row
b. Ceiling level = three or more out of four consecutive items are failed
- Verbal reasoning  picture + oral vocabulary  age/performance determines entry
levels of other tests
- Abstract/visual reasoning  pattern analysis and copying
 - Short-term memory  object memory: series of objects presented one at a time,
must recall correct order

Group-testing: Raven’s Progressive Matrices  pyrotypical test of fluid intelligence (Gf) 

broad ability concerned with basic processes that depend only minimally on learning and
acculturation

Single factor (g) vs multiple mental abilities:

- Factor analysis of intelligence: Spearman  trying to find underlying factors that
explain pattern of correlations  all mental abilities correlate with each other to
some extent, something common underlying all tests  Spearman’s g
- There is also a separate factor underlying performance

Spearman’s Single factor ‘general factor’ (g)  Vocabulary, Verb comprehension, General
knowledge

Lect. 4 –
Most mental abilities are positively correlated this is called positive manifold

You need a well-standardised test of intelligence that can be administered to a large group
at once. Which would you choose? Raven’s progressive matrices
Stanford Binet is not suited to group testing but is well standardised

Intelligence Theory Development:

- Single Factor ‘g’  Charles Spearman  General intelligence:
a. Evidence was the existence of positive manifold: correlation between all the
tests of mental abilities
b. ‘g’  good predictor of life performance

- Primary Mental Abilities  Thurstone  7 separate areas of mental ability revealed

on tests
a. Verbal comprehension
b. Inductive reasoning
c. Numerical fluency
d. Word fluency
e. Spatial ability
f. Memory
g. Perceptual speed

- Hierarchical models of intelligence:

a. General intelligence (g) at top feeding into more specialised abilities

- Gf-Gc Theory  Raymond Cattell:

a. Gf  General Fluid Intelligence  ability to grasp relations between things,
not influenced by culture
 i. Induction
ii. Reasoning
iii. Tracking
b. Gc  General Crystallised Intelligence  acquired knowledge and skills
i. Verbal comprehension.
ii. General information
iii. Spelling ability

- General Fluid Intelligence Gf, rises during childhood to early adulthood then starts to
decline
- General Crystallised Intelligence Gc, rises and plateaus

Goal of Psychological Assessment:

- Good psychological assessment depends on:
a. How well we can measure the ability/trait of interest
 i. Is test accurate? Reliable
ii. Is it measuring what we think its measuring? Validity
iii. is answer used in an appropriate way? Validity
- :
a. If a test measures a consistent trait in a person then it should consistently
produce the same answer
b. If a test is reliable it should be able to distinguish between people who differ
on a particular construct
Observed Score (X) = True score (T) + Error component (E)
We attempt to estimate the true score by taking multiple measurements  long term mean
= true score
A reliable test minimises the variance due to random error:
How to test reliability:
- Test-retest reliability:
a. Same group of people are measured twice on same test
b. Issues:
i. Carry-over effects  remember original responses
ii. Change in true score amount i.e. from reactivity to test
- Equivalent forms  measure same phenomenon with two different forms of test 
correlation between form 1 and form 2 or split-half correlation
- Internal consistency – Cronbach’s alpha (a)
a. If every split-half correlation was computed, their average is Cronbach’s a

Systematic (non-random) error variance:

- E.g. set of scales giving readings 1kg too light
- E.g. assessor gives extra unwarranted mark
- Systematic error will not decrease estimated reliability
- Systematic error reduces the validity  we are not measuring what we think we are
measuring

- Validity:
a. Is test measuring what we think its measuring
b. Is test used appropriately, for its intended use e.g. test developed for adults,
not applicable for children
- Content Validity: How well your test assesses behaviour that is representative of the
domain which is being measured
a. Boundary: what is considered part of domain and what is not
b. Structure: test content reflects structure of the domain
- Construct Validity: how well defined is the construct being measured?
a. Convergent Validity: is construct related to other constructs  expect higher
correlation
 b. Discriminant validity: is construct independent of other unrelated,
psychological constructs  expect low correlation

Systematic error will not affect its reliability

If scores on a test of fluid intelligence do not correlate with scores on a

depression questionnaire, this indicates good discriminant validity

Lect. 5 –
Francis Galton  Hereditary Genius  prominent people have prominent relatives 
intelligence is genetically determined

Nature vs Nurture problem: Is intelligence genetically or environmentally determined?

3 studies:
- Family resemblance studies:
If a trait affected by genetic factors, then individuals with similar genetics
should present similar trait  issue that genetic relatedness is closely related
to environmental similarity
- Adoption studies:
Genetically similar people raised in different environments
Genetically different people raised in same environments
 - Twin studies

- Clear difference in genetics, very similar environment displays effect of genetic

material on intelligence. Monozygotic vs Dizygotic twins

Siblings:
- Share some genetic similarity
- Shared environment  socio-economic status, family climate, geography, nutrition
- Non-shared environment  pregnancy, sibling order, parental preference, illnesses

Through comparison of monozygotic twin’s intelligence correlation  differences must be

due to non-shared environmental features

Through comparison of dizygotic twin’s intelligence correlation  if lower correlation

between dizygotic twins than monozygotic twins than this suggests genetic determination of
intelligence

Heritability (H)  the proportion of the total variation in a given characteristic in a given
population that can be attributed to genetic differences
- Genotype: underlying genetic factors (Gv)
- Phenotype: expression of underlying genetics (Gv) and can be influenced by
environment
Heritability is simply the proportion of the phenotypic variance (Pv) that is due to the
genetic influences (Gv) and always valued between 0 and 1:
- H = Gv/Pv
- 1-H  attributed to environmental & residual effects
- H is best estimated by correlation between MZ twins reared apart, Gv is constant, Ev
is maximally different as they are apart
Heritability of a particular trait is not absolute  statistic for a given population at a given
time, depending on:
- Genetic variability in population: reduce variability  environment more significant
- Degree of variation in its environment  reduce environmental variability 
increase genetic influence

Issues with heritability estimates:

- Genetic and environmental contribution are NOT independent
- HIGH SES  MZ correlations are higher than DZ correlations enhances genetic
potential
- LOW SES  MZ correlations are similar to DZ correlations suppresses genetic
potential
- Age of comparison, H changes depending on age, with growth  realisation of
genetic potential
- Selective placement of adoption  children tend to be adopted into high SES
environments reducing variability in this population

H changes  if trait has high heritability, it is not greatly affected by existing environmental
differences  does not reveal consequences of NEW environmental manipulations

H is a population statistic  not for individual cases

H is based on assumption we can distinguish between observed data (phenotype) and

genetic (G) and environment (E) effect

Lect. 6 – Group differences in IQ + Flynn Effect (change in IQ over time)

- Females tend to have better verbal abilities (Females > Males)
- Males tend to have better visual/spatial abilities (Males > Females)
- IQ between males and females is the same, differences in verbal abilities and visual
abilities even out.
- Racial differences in IQ exist. But why?
a. Genetics?
b. Environment? Or both
- “Bell Curve”  Herrnstein & Murray suggested racial differences on IQ tests were
inherent following from heritability of intelligence  focus on supporting high
intelligence racial groups
- Flynn + Gould  argued against this non-scholarly proposal of the “bell curve”
- Basis of Bell Curve:
a. Intelligence can be measured by a single number, not necessarily true
b. People must be able to be ranked according to that intelligence number and
predict social outcomes, people have different underlying strengths in
intelligence
c. IQ has to be highly heritable, mixed evidence
d. IQ has to be effectively unchangeable, Flynn effect and stereotype threat
 - Bias = Do IQ tests systematically underestimate the IQ of certain groups?
- Fairness = is a social issue
- The content of an IQ test may be more familiar to some cultures compared to others
- Beliefs and attitudes can affect performance on IQ tests, Steinberg examined
attitudes towards schooling and performance  e.g. Asian-Americans believed in
importance of high achievement and expected to maintain effort.
- The Flynn Effect: IQ increasing over time, why?  Flynn suggested IQ tests measure
abstract problem-solving ability through modernisation people are becoming more
accustomed to abstract concepts

Perception
Lect. 1 –
Sensation = how your senses transform physical properties of the environment into
electrical signals relayed to brain
Perception = process of organising, selecting and interpreting electrical signals
- Six Senses:
a. Vision
b. Hearing
c. Somatosensorial: awareness of body
d. Taste
e. Smell (olfaction)
f. Vestibular: inner ear senses gravity and movement
- Problem of ‘qualia’  How does brain know what a pattern of electricity signals
about the world?
- Fallibility of senses (illusions)  Our knowledge is mediated by our senses;
therefore, how do we know what’s real.

Perception is an ACTIVE process of organising info into useful representations of the world
Illusions indicate we don’t know exactly how the world is structured, and reveal
assumptions to infer about physical world

Lect. 2 – The Ear

The Vestibular System:
- Assists control of gaze and posture
- Contains sensory structures with receptor cells that detect gravitational forces,
including angular and linear head accelerations in space
- Consists of:
a. Three semicircular canals (ANGULAR ACCELERATORS): all at different angles
and contain of fluid, and small hair cells line inside of the semicircular canals.
b. Two otoliths (LINEAR ACCELERATORS)
- Acceleration is a change in direction or speed
- Bending a vestibular hair-cell receptor in its preferred direction excites the neuron
- Bending same neuron in opposite direction inhibits neurons
 - We need info about head movement to make precise and rapid compensatory eye
movements to stabilise images on retina  Vestibulocochlear reflex (VOR)
Sound and Hearing:
- Sound is a wave; a set of compressions and rarefactions through a medium 
longitudinal waves
- Sound waves can be measured by frequency in Hz  Hertz, 1Hz = 1 cycle per sec
- Hertz is number of cycles per second
- Amplitude = loudness  height of sin wave  loudness measured in decibels, 0dB is
defined as sound level for human hearing; I0
a. Decibels measured on a log scale, so value of x dB means its 10 x/10 greater
than threshold for hearing  traffic 70dB, 107 times greater than threshold
for hearing
- Frequency = pitch  Hertz, Hz
- Purity = timbre or ‘colour’ quality of sound
- Instruments all generate same component frequencies when played at given pitch
and differ in relative amplitudes of these component frequencies they produce
- Amplitude of upper harmonics (overtones) contribute to timbre
- Pitch of an instrument is conveyed by the fundamental (lowest) frequency, and
timbre by relative amplitudes of overtones
- What determines what a clarinet or guitar sounds like is the pattern of overtones
Harmonic Singing:
- Normal humans can generate one note of pitch when singing, consisting of a
fundamental frequency, and range of upper harmonics (overtones)
- Some people can suppress/increase amplitude of one or more upper harmonics
making one or more harmonic frequencies stand out against fundamental frequency
giving perception of multiple notes.

Lect. 3 –
1. Pinna and eardrum  directional microphone
 2. Middle ear  impedance matching, overload protection
3. Inner ear  frequency analysis
Middle Ear:
The middle ear transmits eardrums vibrations to oval window:
- Ossicles  3 smallest bones  transmit vibrations to oval window
- Perilymphatic fluid filling cochlea denser than air, offers resistance
a. Greater mechanical energy is required to transmit sound wave through
denser fluid of cochlea
- At air-fluid boundary, most of incoming sound is reflected, ossicles transfer energy
generated by air pressure applied to large SA of tympanic membrane to smaller oval
window
- Impedance matching = middle ear transfers the incoming vibration from the
comparatively large, low impedance tympanic membrane to the much smaller, high
impedance oval window
- For transduction to occur, air pressure in middle ear needs to be same as
atmospheric pressure outside eardrum, eustachian tube equalises pressure

Inner Ear:
- Semicircular canals
- Cochlea: Vibrations at oval window cause basilar membrane to wiggle. These wiggles
cause voltage change in hairs in Organ of Corti. The electrical signals are carried to
Oval window and round window move simultaneously in opposite directions

- How does Basilar Membrane signal difference frequencies?

a. Rutherford  whole membrane moves like a diaphragm HOWEVER problem
is the basilar membrane varies in thickness and stiffness
b. Georg von Bekesy  constructed crude model of cochlea  found for each
different frequency each part of the membrane would vibrate the most.
i. Frequency sensitivity changes along the basilar membrane: Base (high
freq)  Apex (low freq)

- Vibrations of oval window induce pressure changes in cochlear fluid that create a
wave on basilar membrane, the wave peaks in different places depending on
frequency
 - For low frequencies, auditory nerve spikes are phase-locked to stimulus i.e. neuron
always fires in line with sound wave peaks, and phase locking declines with increased
frequency
- Two cues to frequency in sound:
a. Place of excitation in cochlea
b. Frequency of firing

Sound Localisation:
- Azimuth  left, right, back and forward
- Elevation  up and down
- Binaural and monaural information on sound localisation
- Binaural Localisation Cues:
a. Interaural intensity differences (IID) created by sound shadow  Intensity
hits right ear and left ear is different
 Intensity differences are negligible for low frequencies therefore only one
subwoofer needed

b. Interaural time differences (ITD)created by difference in path length

A sound wave coming from side will hit nearer ear first, create time lag between two ears
Cone of confusion: ambiguity, know side of sound wave but not if at back or front of cone.
IID and ITD will be same for sources of two yellow dots, no information on elevation of
sound
Elevation is determined using properties of pinna, sound is “coloured”/filtered differently
depending on elevation (ONLY CUE FOR ELEVATION, monaural), frequencies are different
for different ears due to different shape of pinna.

Lect. 4 – Body Senses

Two major subsystems:
- Somatosensory system = touch and proprioception (where body positioned, and
forces acting upon them)
- Interoception = sense of physiological condition of body
- Touch is very important for coordination
- Tactile afterimages e.g. removing a hat
- Tactile adaptation  importance of movement in perceiving spatial patterns e.g.
stabilised non-moving objects on skin less salient
- Active tactile system improves perception

Somatic Sensory System composed of:

- Detection of mechanical stimuli (light touch, vibration)  monitor internal/external
forces acting on body
- Detection of pain and temperature

Mechanosensory processing:
- Detect external stimuli: cutaneous/subcutaneous mechanoreceptors at body
surface
- Proprioceptors: receptors in muscles, joints, tendons report on status of
pressure/contraction/forces
- All receptors work same way  stimuli applied to skin deforms nerve endings,
affects ionic permeability of receptor cell membrane  depolarising current 
action potentials (sensory transduction)
Mechanoreceptors  respond to mechanical deformations in skin
Nociceptors  pain receptors
Thermoreceptors  heat receptors

Perceptual quality of stimulus (what and where) depends on the receptors that respond
Quantity or strength of stimulus depends on number of action potentials generated

Two types of touch fibres:

- Rapidly adapting  info about change/dynamic quality of stimuli, stop firing quickly
- Slowly adapting  info about shape, text, edges, persisting features, continue firing

Local anaesthesia: absence of sensation is attributed to world, not body  response of

fibres provides info about external world, not self

Nociceptors: two types Aσ myelinated and C fibres: unmyelinated

Two waves of pain:
- Diffuse
- Acute and sharp
Pain Hyperalgesia i.e. enhanced sensitivity to stimuli over time
Change from reference skin temperature: physiological zero

Proprioceptors  receptors for self:

- Muscle spindles provide info on muscle length
- Golgi tendon organ provide info on muscle tension
- Joint receptors provide info on positions and tensions on joints

2-point thresholds  info on size of receptive fields

Input (sensory cortex)  Output (motor cortex)

Lect. 5 – Taste, Smell, Flavour

- Dimensionality problem lots of different chemicals, we can’t have receptors to
detect them all, dimensionality  reduced to five taste categories
- Tongue anatomy and physiology:
a. Papillae  bumps on tongue, four types, three with taste receptors
i. Filiform  no taste function assist in mastication
ii. Fungiform
iii. Foliate
iv. (Circum)vallate
- Huge variation in papillae
- 5 primary taste sensations:
a. Sweet  energy rich nutrients
b. Salty  electrolyte
c. Sour  acidity
d. Bitter  poison
e. Umami (savoury)  amino acids e.g. MSG
- Taste: chemical molecules make direct contact with chemoreceptors on tongue
 - The 5 categories of taste aren’t intrinsic properties of the chemicals, it’s about their
biological utility
- Labelled-lined model: different receptors in taste bud: some signalling: sweet, sour,
salty, bitter, umami  the receptors for taste sensation e.g. sweet/salty/sour
terminate on the same axon, axon sends message to brain indicating its level of taste
e.g. its sourness, saltiness, sweetness  signal mixture of taste sensations
- Cross fibre models:
Supertasters  genetically prone to have more fungiform taste receptors identified using
bitter chemical PROP
Spice different neural pathway  pain receptor

Smell (Olfaction)
- Chemicals enter nose dissolve in mucosa provides info about chemicals suspended in
air
- Shape pattern theory of olfaction  not well supported
- No good understanding on qualia of smell
- Odour identification
- Olfactory adaptation e.g. adapts to own smell
- Pheromones organ in nose detecting sexual signals
Lect. 6 – Vision
3 stages:
- Form image
- Transduce light energy to electrical impulses
- Transmits info to brain for interpretation
- Light is an electromagnetic wave (400-700nm  Visible spectrum detected by
humans)
- Sound radiates in all different directions simultaneously, however light doesn’t.
- Light also acts as a bullet that moves in a straight line but can be described as
particles as well; photons
- Diffuse reflection
- Specular reflection
Types of eyes:
- Compound
- Convex mirrors
- Pinhole
- Single chambered e.g. human
All image formation works by the same principle: one region of the world mapping onto one
receptor
Forming Image:
Pinhole camera: light travels in straight lines, and viewing scene at a fixed distance, but
doesn’t matter since can’t unfocus, if trace ray through pinhole only connects to one
position in world, therefore only the light rays scattered from that one position make it to
that position in the image.
Problem with pinhole camera: very limited light, only work in extremely bright illumination
conditions
Hole too big generates blur, brings in more light, new light needs to bended so that lands in
only one position
Compound eyes:
- Don’t form images
- Series tube called
Single chambered eye:
- Use refraction using convex lens: diverging light reflected from all different
directions from an object to converge to single point to form an image

- Different wavelengths are bent different amounts and therefore have focal planes
- Blue end of the spectrum is very low resolution
- Accommodation: focussing of light through refraction on retina performed by
cornea (majority), lens (changes shape to adjust our focus at different distances)
- Far accommodation = lens becomes flatter, near objects become behind retina
resulting in image blurring
- Near accommodation = lens becomes rounder to focus on light from a nearby object

Sampling the images (transduction)

- Duplicity theory of vision  use two different photosensitive receptors
- Scotopic vision: low-light  rod dominated
- Photopic vision: high light levels  cone dominated

Four types of photoreceptors:

 - One rod
- Three cones

Light adaptation mechanisms:

1. Pupil dilation/contraction
2. Isomerisation of photopigments  can’t absorb photons at altered shape

Lect. 7 –
Retinal distribution of rods and cones:
Rods: Cones = 20: 1
Rods night vision scotopic vision
Cones daylight vision
Cones focused in fovea  cells that give sharpest image
Blindspot = no receptors
Blood vessels are in front of receptors, eyes become desensitised to these and thus we do
not see it.
Three cones (S,M,L; short, medium, long) responsible for blue, green, red
Need at least two types of photoreceptors to experience colour:
- Trichromatic theory  different colour experiences due to activation of just 3
receptor types
- Opponent processes theory  colour perception depends on six psychological
primaries arranged into pairs  evidence: do not perceive reddish greens, bluish
yellows: red + green  grey (property of psychology)
White light strikes object, some light absorbed (not seen) what is reflected is what we see
e.g. red apple  absorbs S, M light and reflects L light  long wavelength reflected  L
cones highest response

e.g. yellow banana  L, M (more M) reflected  M cones (most) and L cones (significant
but less) , S (small)

Firing proportions of S, M, L cones signals different colours of objects

Colour-vision deficiencies:
- Red-green
- Blue-yellow
- Complete
Most common anomalous trichromats  3 cone types but sensitivity to wavelengths are
overlapped

Depth perception:
- Linked to perceived size: objects of a fixed physical size will project different sizes on
retina, and objects of different sizes can project same retinal size if they’re at
different depths
- Monocular cues: linear perspective  set of parallel lines in space converge to single
vanishing point
Most powerful depth cues from parallax: when you look at things from different
positions things shift by different amounts depending how far away, they are from you:
Two types:
- Binocular parallax (stereopsis): due to different vision from right and left eye
- Motion parallax: self-motion causes distant object to appear to move more slowly
than closer objects e.g. in a car things close to you flying by you