Cognitive and behavioural neuroscience Flashcards
is thought physical?
processes = abstract Implementation = in a physical substrate, the brain
what is dualism
the mind and brain are fundamentally different
therefore they are separate things
how are the mind and brain fundamentally different
physical (brain) vs non-physical (mind)
what is the problem for dualism
how can physical events in the brain interact with the influence of the non-physical mind
eg: damage brain = change of the mind - so the mind can be influenced by the physical despite being nonphysical
who is associated with dualism
rene descartes
how did Descartes get around the problem of dualism
the mind interacted with the brain through the pineal gland
what is monoism
there is one being not a brain and mind. this is supported by the fact you cannot distinguish between the brain and mind - they are supreme being.
so they claim brain operations lead to mental events
counter evidence for monoism
subjective factors near death experiences out of body experiences ghost sightings re-incarnation (re-calling events from past lives)
gross bits of the nervous system - big division
Central (CNS) vs Peripheral (PNS)
make up of CNS
Brain and spinal chord -covered with layers of protective tissue (three layers called the meninges) the three meninges: dura mater (hard mother) arachnoid membrane (spider membrane) pia mater (pious mother)
make up of PNS
nervous system outside central
- typically called nerves
- covered in 2 meninges:
- -dura mater
- -pia mater
what does the PNS allow and how
allows the CNS to interact with its environment
has two loops (autonomic nervous system and sensory-somatic nervous system) each containing efferent and afferent section
meaning of efferent
outgoing, motor
meaning of afferent
incoming, sensory
autonomic nervous system
what does it do
voluntary?
eg
controls internal state involuntary heart rate digestion swallowing
sensory and somatic nervous system
what does it do?
voluntary?
eg
deals with external world
skeletal muscles under voluntary control
senses
3 major divisions of the brain
forebrain
mid brain
hind brain
how is the forebrain sub divided
telencephalon
diencephalon
what are the principle structure of the telencephalon
cerebral cortex
basal ganglia
limbic system
what are the principle structures of the diencephalon
thalamus
hypothalamus
how is the mid brain sub divided
mesencephalon
principle structures of the mesencephalon
tectum
tegementum
how is the hind brain subdivided
metencephalon
myelencephalon
what are the principle structures of the metencephalon
cerebellum
pons
what are the principle structures of the myelencephalon
medulla oblongata
cerebellum, volume and musicians
Hutchinson et al 2003
MRIs of male professional keyboard players vs controls
musicians had larger cerebellum (whole brain size the same, other parts shrunk)
size of cerebellum depends on how much practice you do (lifelong intensity of practice correlation)
what does the medulla oblongata do
role in the autonomic control of cardio-vascular system, swallowing etc
what does the cerebellum do
little brain - approx. 30 billion neurones
sensory information
modulates motor commands - precise movement, sensitive to alcohol
what does the pons do
bridge between cerebellum to cortex
role is sleep / arousal, facial muscles, tongue
what experiments are used to find out about the functions of the hind and mid brains
decerebrate experiments
low-decerebrate animal experiments
hind brain intact
transect above pons / cerebellum (rest of brain apart from hind cut out)
still do basic movements but fall over
move but not coordinated
high decerebrate animals experiment
mid and hind brain intact transect above tectum / tegmentum can stand without support walk, chew, swallow have the ability to do things but no purpose - eg wont run from danger or eat if hungry
from the decerebrate experiments what does the cortex do
allows us to adapt to an unpredictable world
two major parts of the forebrain: diencephalon and what they do
thalamus - control input to cerebral cortex
hypothalamus - controls autonomic nervous system
three parts of basal ganglia
putamen - merges with head of caudate nucleus
globus pallidus - inside putamen
what is the sub-cortical nuclei involved in and where is it
control of movement
lateral to thalamus
what does the caudate nucleus do
urge to do things
related to reward system
what does the putamen do
leanred autonomic movements eg driving
what is the striatum
caudate nucleus + putamen
what doe the globus pallid so
control of voluntart movement
major output nucleus of the basal ganglia
parts of the limbic system
cingulate cortex- error signals, attention, emotion
amygdala - emotion (fear)
hippocampus - formation and recall of memories, navigation
two main parts of telencephalon by diencephalon
basal ganglia
limbic system
cerebral cortex
size
hemispheres
lobes
big bit in primates - disproportionately large in humans
2 hemispheres
4 lobes
what are the four lobes in the brain
occipital
parietal
temporal
frontal
hemispheric specialisation
looks the same but asymmetrically function
left brain controls right body; left side of brain is better at certain things
even ambidextrous have preferred actions with preferred hands
not one side or other but does show more activation
language as an example of hemispheric specialisation
pierre paul broca (1860s)
-damage to left frontal lobe
patient could understand but not generate speech
Wernicke
- damage to left superior temporal lobe
-comprehension not generation
language left dominant in 90% of right hander and right dominant in 50% of left
how are the two hemispheres connected
by commissures
corpus callosum is the biggest
masa intermedia in the thalamus (missing in many people so not important?)
sometimes commissures cut (epilepsy treatment) = split brain
testing for hemispheric specialisation
split brain patients - briefly flash words or pictures in the left or right visual field flash in right can say what was seen flash in left cannot say but can point or draw
reaction time experiments for hemisphere experiments
intact brains
present stimuli to left or right visual field
record reaction time
what evidence is there for hemispheric specialisation
left specialised for language, speech, local image feature extraction
right specialized for visuo-spatial processing, global image properties, face processing
what is the primary cortices for
first for sensory input, last for output
at back of is primary motor cortex - premotor and supplementary
rest is executive functions
what are secondary cortices
adjacent to primary, short connection distance
receive input from many different sources
Phineas Gage
iron through his cheek and brain
damage to frontal cortices
marked personality changes?
good man turned nasty
role of
dorsolateral prefontal cortex
planning of action
underactive in depression
role of
anterior cingulate cortex
errors and the feeling of self
overactive in depression
role of
orbito-frontal cortex
inhibition of changes from unusual behaviors
punishment / reward in decision making
overactive in depression
role of
ventromedial prefrontal cortex
emotional meaning
overactive in depression
what are the major cortical pathways of the brain
auditory, olfactory, visual, motor, somasensory
visual pathways
two visual pathways
lots of connections between them
-dorsal
-ventral
how does the visuo-motor system work
Pulvinar - superior colliculus visual input from LGN see look locate reach V1 - see parietal cortex (eye movements, directed reaching) - locate motor allows for reaching / grabbing
where is fear processed
thalamus
limbic and cortical interplay
most things that keep us alive skip visual cortex in order to act quicker
two types of cells in the brain and what they do
glia - keep brain alive
neurones - do psych part
anatomy of a neurone
input - dendrite
integration - cell body, soma, contains nucleus
output - axon, very long
what is neural activity
electric current and ionic flow
what are the major ions in neural activity
sodium chlorine and potassium
what forces does every ion have acting on it
chemical
electrical
explain the resting membrane potential
permeability high for K and low for Na and Cl
equilibrium point at -50 to -70mV
impulse to do all or nothing - action potential explained
sodium wants to balance sodium gradient and charge
sodium channels open and close quickly - sodium rushes in
potassium channels slow - potassium is pushed out by sodium and then channels close because of the membrane potential
how does an impulse travel - propagating the signal
start in the axon hillock and move down the axon because sodium raises membrane potential locally so channels once activated cant go again, pushes signal down the axons as next lot are activated
myelin sheath
causes a jump from one load to another which is faster = speeds up the impulse travelling
what did Sherrington’s behavioural studies find
the end of the axon - pre-synaptic terminal -axons brach and make many synapses -not all onto dendrites, but most are the dendrite -post-synaptic terminal -many inputs to each neurone -most on dendrites gap between = synaptic cleft
what two types of synapse are there and what are their relative speeds
chemical - slow, ionotropic (directly opens channel), metatropic (slowest, cascade system opens channel), amenable to drugs
electrical - fast, reliable, poor processing
chemical synapse
release of molecule into cleft
activates specific receptor (can be excitatory or inhibitory)
variable effects - good at processing
what are vesicles and what do they do
contain neuro-transmitter molecules
when calcium ions enter, vesicle fuse with membrane and release neuro-transmitter into cleft
4 step action of neurotransmitters
ligand-gated ion channels
g-protein-coupled receptors
kinase-linked receptors
nuclear receptors
estrogen changes..
the way the cell responds
ending synaptic action
after neuro transmitter recognised by post synaptic receptor it must be removed / inactivated
transporter proteins take neurotransmitter back to pre-synapse
specialised enzyme for inactivation
acetylcholine - acetate + choline
peptides vs non-peptides
effect on post-synaptic membrane
long lasting
np short lasting
peptides vs non-peptides
synthesis location
endoplasmic reticulum of soma
np nerve terminal
peptides vs non-peptides
replenishing speed
slow (not recycled)
np - fast
peptides vs non-peptides example of each
pep - enkephalins
non pep - ACh, DA, 5HT, NMDA
what types of drugs reduce transmission and by what mechanisms do they work
antagonist pre-synaptic mechanisms -decrease production of transmitter block calcium ion influx stop vesicles filling with transmitter stop vesicels emptying into cleft post-synaptic mechanisms -block receptors -stop ion channel opening
what types of drugs enhance transmission and by what mechanisms do they work
agonist pre-synaptic mechanisms -increase production of transmitter -enhance calcium ion influx -decrease re-uptake process post-synaptic mechanisms -activate receptor -decrease enzymatic breakdown (ACh)
ACh and what disease, explain
acetylcholine
alzheimers - loss of neurones which use ACh as their neurotransmitter in areas of basal ganglia and basal forebrain
drugs which block or reduce breakdown of ACh in the synaptic cleft are used to slow the process
dopamine related drugs named and explained (4)
L-DOPA - agonist, relives symptoms of parkinsons (alsom some MAOIs do too)
methylphenidate (Ritalin) - agonist treatment for ADHD
amphetamine - agonist, complex action via norepinephrine
cocaine - blocks uptake
what is unipolar depression
major depressive disorder
majority of people at sometime in their life will be affected (20-30% of total population at any given time)
women twice as likely as men to report
thought to have genetic component as 60% concordance for identical twins
environment factors important
treatment of depression
1950s reperine given for high blood (MOA reduced) pressure made some patients depressed
iproniazid for TB made patients happier
animal studies showed these drugs act on mono-amine release = mono-amine hypothesis (excess then happy) - action doesn’t really fit this
tricyclic antidepressants
block re-uptake of transmitter to increase post-synaptic response
what did Asberg’s 1990 studies find
post-mortem studies of suicide victims
measured post-synaptic serotonin 5-HT and metabolite 5-HIAA
decreases in CSF serotonin is associated with suicide
3 types of drug in the treatment of depression
SSRIs
TCAs
MAOIs
7 levels of explanation and why this matters
many individuals individual brain neural systems neuronal biochemical atomic common sense - only certain things are appropriate to study at the level of the brain, processes underlying behaviour
2 methods of study using observation
damage to the nervous system produces deficits in psychological processes
damage to other body parts can influence psychological processes but does not cause deficits
role of brain in methods of study of psychological processes
brain is the site of psychological processes
but this does not mean you must study the brain
2 ways to study the anatomy of the bran explained
computer tomography - CT (X-rays to image inside the body)
magnetic resonance imaging - MRI (pulse radio waves and use magnetic field to map reaction of hydrogen - a water and fat cell map
4 ways of monitoring brain activity
electrocephlogram EEG
positron emission tomography PET
functional magnetic resonance imaginf fMRI
single unit recording
explain EEG
electrode cap, measures voltage over time
explain PET scan
shows activity and strength of, uses injection of dye and radioactive traces
explain fMRI
MRI over time, detects changes in blood flow
explain single unit recording
fine electrodes to record single cell electrical activity
name 7 methods of studying the brain from disruption
brain damage disorders stimulation micro-stimulation cortical cooling trans-cranial magnetic stimulation lesions each technique only monitors part of the brain at once so must combine techniques
spatio-temporal resolution discussed for EEG, fMRI and single unti recording
EEG - poor spatial resolution, high temporal
fMRI - medium spatial, low temporal
single unit recording - high spatial and temporal resolution
whats wrong with low and high spatial and temporal temporal resolutions
SPATIAL
poor = miss fine details, interactions between groups or individual neurones
high = what is the rest of the brain doing
TEMPORAL
poor = miss fine timing
high = can we see the relevant signal, is there strong enough data
summary to neuroscience methods of studying the brain
use convergence of evidence
- behavioural studies
- -what is the phenomenon
- -what processes are occurring
- monitoring techniques
- -where do the processes occur
- -details of the mechanism of the processes
- disruption techniques
- -what does disruption / damage do
- -where do the processes occur
what is arousal and how is it shown in the brain / studied
basic asleep vs awake
brain shows different activity patterns (EEG)
explain the stages of sleep
4 stages with different patterns of brain activity
REM - rapid eye movement - rapid brain activity, big spikes of activity = dreaming. heart beats faster, low activity = deep sleep, gets deeper and deeper - rem spikes are most distinctive
what happens during increased arousal
faster heart beat
sympathetic nervous system activity
increased heart beat, shivers down the spine, sweaty palms, adrenaline rushes. interaction between epinephrine and norepinephrin
what is the galvanic skin response
measures the electrical resistance of skin
arousal - sweaty palms
drop n resistance
used in polygraph (lie detector)
what is a drive or a motivation
a desire to do something
explain the urge to eat
signals from the liver
when the liver converts glucose to glycogen: plenty of blood glucose = not hungry. brain uses blood glucose and rest of body uses fatty acids
when glycogen is converted to glucose: gradual decrease in blood glucose, liver converts glycogen to glucose, rapid rise in blood glucose - hungry as the body wants to maintain reserves
other signals associated with the urge to eat
detection of nutrients in the digestive juices, stomach sends signals to stop eating
small intestine releases CKK (cholecystokinin)
-presence of food (distension) and nutrients, signal to stop eating, also associated with fear / stress
where does detection occur in the urge to eat
the hypothalamus dual centres on feeding - on centre -lateral hypothalamus -lesion leads to aphagia (refusal to swallow) -off centre -ventromedial hypothalamus -lesion leads to hyperphagia (excessive eating)
Does the hypothalamus lead to overeating? evidence in rats
unclear. detection is in the hypothalamus but
neuropeptide Y
- inject and even full rats start to eat, effect is outside the hypothalamus
ventromedial lesion in a rat
-ends up obese but do stop eating
other effects (little movement)
the on off hypothesis is too simplistic
does the hypothalamus relate to eating disorders?
the on off hypothesis is too simple environment factors -time -sight of food -people sitting round a kitchen table social factors important -the time when we eat sensory specific satiety -eat one food all the time and you stop eating -replace with another food and you might eat
what is Hulls drive reduction theory
hunger drives behaviour to reduce hunger
pain drives behaviour to reduce pain etc
when drives are zero = perfect contentment
according to hulls drive reduction theory where is optimal arousal
above zero we seek zero drive / arousal but we like seeking rewards / thrills monkeys (and humans) are inquisitive so we have a base drive that is above zero
cycle in hulls drive reduction theory
homeostatis - biological need - primary drive - motivation to satisfy - goal-directed behaviour - need satisfied - bac to homeostatis
james-lange theory
in an emotion producing situation
1 the body responds
2 - sensory feedback
3 - the feeling of emotion
evidence behind james-lange theory
Ekman, Leveson and Friesen 1983
taught subjects to move facial muscles on command
when taught to make angry faces, the an expression made you angry according to changes in heart rates
the Ekman studies stimulated expression changed physiology, fear and anger increased heart rate
what is wrong with the James-lange theory
physical changes too slow
artificially induced changes rarey produce emotion
different situations can produce different emotions but similar bodily response
schachter and singer’s awareness of emotion
if you are aroused theres a celar reason why then you attribute emotion to that reason
if you are aroused and theres no clear reason why then attribute emotion to anything that’s around
how schachter and singer hypothesis tested
give subjects vitamins (actually adrenaline)
-tell some the effects, others it may produce numbness
while in the waiting room someon pretend to be angry
someone pretend to be happy
result - those that knew the effects of the injection were less annoyed than those lied to
those that knew the effects were more amused than those lied to
quick summary of how folk psychology james-lange theory schacter and singer theory see awareness of emotion
folk psychology sensory systems - awareness - response james-lange theory sensory systems - response - awareness schacter and singer sensory systems - response - interpretation awareness
brain regions in emotion - what areas
frontal cortices as shown by Phineas Gage
amygdala
Schachter and Singers ATTRIBUTION
if you know the source of the feedback, you attribute your emotion to that source
a happy person wont make you happy if you know why you have a ready explanation for your happiness
but if you don’t know the source, you will attribute it to something
Dutton and aron 1974
getting someone to like you
real world setting - swinging bridge Vancouver
offer number to phone the investigator
people who cross the bridge are more likely to phone than people who cross a low bridge
misattribute the excitement to the person - people are more likely to go on a second date if they get scared on the first
learning fear and the amygdala experiments
measure skin cinductance (sweating) to learnt scary stimuli
without stimuli the scary stimuli are not scary - don’t learn them as scary
amygdala’s role in social interactions
ask how close someone can get to you and still feel comfortable
without amygdala the idea of personal space is noticeably reduced
amygdala - why wouldn’t it be involved in fear
urbach wiethe disease = build up of calcium in the amygdala
looked into patients ability to detect fear in others facial expressions
didn’t understand what fear was
asked to rate scary films - just didn’t get scared
no amygdala person doesn’t look at the eyes - amygdala controls aspects of stimuli used to detect fear
which is the primary cortex for internal senses - and study that showed this
insula cortex
Phillips et al 1997 insula activity when viewing facial expressions of disgust
how do emotions function in the brain
there are 2 areas that each process their own different emotions
feedback from the viscera (autonomic responses) passes the insula cortex
mixes with cortical sensory signals
prefrontal uses this and adjusts
historical ideas on emotions
Aristotle believed there are a number of characteristic emotions
Darwin - universal emotions
Darwins’ universality thesis
if humans are descended from common ancestor we should share the same innate behaviours and expressions of emotions
Ekman studies - tested how different cultural groups recognised expression
basic emotions largely universal, higher not. we are all very good at recognising smiles
facial muscles
how are they defined
can we control them
activation unit defined by the groups of muscles involved in creating those expressions
we can consciously control some but not all of our facial muscles
the duchenne smile
gave electric shoks to particular facial muscles and noted the impact on facial expressions
found two ways people could smile
social/ voluntary - patients with right motor cortical damage - lopsided polite smile but true normal smile
spontaneous smile - parkinson’s patients the opposite way around
how the voluntary smile forms
starts in left motor areas
right facial nucleus and motor areas
right facial nerve to right favial muslces
right morot to left facial neucleus , left nerve to muslces
how the spontaneous smile forms
basal gangli
caudate nucleus to putamen to globus pallidus to reticular formation
to brain stem
facial nuclei to facial nerve to muscles
physical difference between the two smiles
true smile - muscles around the eyes involved, voluntary not
human lie detectors
imperfect control over facial activation units allows for leakage - spontaneous actions appear at 005 seconds = micro-expressions
most cant detect micro-expressions
people who can are natural lie detectors
three types of models of emotions
evolutionary
socio-evolutionary
social constructionist
basis of evolutionary models of emotion
emotions are labels applied to basic adaptive behaviours
basis of socio-evolutionary models of emotion
evolved from basic adaptive baviours but from early homids as social grouping became dominant
social constructionist models of emotion
emotions are a social construct and should be thought of in this way
Plutchick’s model of emotion
emotions evolved from basic adaptive behaviours - labels given to different intensities as well as axes
evolutionary model
simple explanation of socio-evolutionary models of emotion
although similar to evolutionary models, emotions may have evolved from social environment pressures
after hominids diverged from the great apes
the diversity of social life would result in a huge behavioural repertoire
a higher order control system would be needed for emotions
the strong constructionist model (averill) on emotion
emotions are purely social constructs that serve a function within the social system but have no animal basis
eg anger is an inter-personal emotion hence can only be understood in terms of the social context
anger is directed towards a perceived misdeed or injustice again a social construct
so emotion is a social construct
the moderate social constructionist model of emotion (Barrett)
different components underlying emotion are combined
emotions driven by feedback (i fell this way because i am excited not the situation is exciting)
feedback is assessed in terms of core valence (good vs bad) and secondary dimensions including
-arousal
-social
-situation
what is habituation
decline in response to stimulus when familiar
narrows the range of stimuli that elicit false alarms
Pavlov dogs
pavlov studying neural control of digestion - focsed on salivation in dogs
salivation occurs when food in mouth
salivation also occurs at other times - pavlov investigated this and manged tocondition dogs to salivate at sound of a bell
UCS - UCR - CS CR plus example from pavlov dogs
unconditioned stimuli = food
unconditioned response = salivation
conditioned stimuli = bell
consitioned response = salivation
measurements taken during conditioning experimetns eg pavolv dogs
CR probability - if appropriate
or trial by trial
CR amplitude - if appropriate (amount of saliva)
CR latency - always available - time from bell to salivation
what did pavlov propose in his dog experiments
unconditioned response is innate, conditioned response depends on learning
what is extinction in conditioning
establish conditions then repeat testing without it
repeated trials when conditioned stimuli presented alone
shows opposite learning curve
can learn and unlearn
reconditioning
speed
what does this show
very fast process
extinction doesn’t get rid of the initial conditioning
once something is learnt it is very hard to erase
stimulus generalization
the closer the stimulus is to the one you learnt, the better one generalizes
discrimination vs generalisation
with generalisation- the more similar the test stimuli to the CS the more similar the CR
with discrimination - the more similar the test stimuli, the loner to learn discrimination
conc
more similar / likely the same response to two stimuli, the harder to learn that the stimuli are different
second order conditioning
tick noise with food
repeat until dog salivates at sound of tick
present dog with black square followed by tick noise for repeated noise, but not food
dog then salivates at the sight of the black square - even though black square has never been associated with food
black square becomes the conditioned stimuli for the tick noise which in turn signals food
blocking of conditional learning
filters out unwanted info
establish classical conditioning
give repeaed pairings of new CS with old CS and the US
no conditioning occurs with new CS - the condition has been blocked
widespread nature of classical conditioning
found in many if not all animals
in humans
eating patterns (CS - time, US - food, UR - hunger)
drug abuse - greater cravings in the place where they are usually taken (US - drug, UR - drug effect, CS - needle, CR - opposite drug effect)
body starts compensating the drugs effect when it thinks its coming - cravings
phobias
prejudice
adverts
Watson and emotional conditioning
laid ground work for some behaviour therapies
peter afraid of rabbits
rabbit moved towards peter whilst given sweets, some of peters friends brought to play with the rabbit at a safe distance
by the end of the sessions peter had lost his fear of rabbits
constraints on mechanisms of learning - what is wanted for meaningful learning
flexibility in associates - potential to unlearn and relearn associations
ability to build upon earlier learning experiences (2nd other)
association of correct stimulus with the response
contiguity and contingency
they are different
what do they mean
contiguity = when cs and us presented. must be either forward pairing or simultaneous not backward for conditioning to occur
contingency = how often US presented after cs
more often = greater conditioning
neurones and classical conditioning
kandels sea snails - gill protection reflex
closes off when siphon is touched = gill withdraws
light touch US paired with sharp touch to tail CS
neural circuity is small and simple - 20 sense, 6 motor so learning mechanisms can be studied - conditioning due to increased calcium ion influx
Bliss and Lomo 1973
inducing long term potentiation
rabbit hippocampus
stimulate preforant pathway and dentate gyrus
record response in dentate
single spike will have given amplitude
if theres lots of activity the next time a little activity comes there will be an increased response - something has changed in synapses
cortical plasticity
blind readers using brille - visual cortex doesn’t have a job but is used to read braille instead
if keep doing a task - lots of activity associated with it - it will begin to take over inactive neurons
what did Bi and Poo show about LTP
shows contiguity - inputs need to be active within a short time
presynaptic LTP …… in number of vesicles
post-synaptic LTP =
increase
growth of synapses
learning can mean formation of new synapses
nitric oxide
retrograde messenger - high concentrations poisonous gas
synthesis on demand - calcium ion - NO synthesis
increases neurotransmitter synthesis in presynaptic neuron, more released during action potential
Hebb 1940s
proposed hebbian learning
suggested that a synapse should be strengthened when both the input and the target were active - if two neurons are active = two representations active at same time then connection between them is strengthened
the LTP data tends to support hebbain learning
BCM rule and LTB
Bienenstock, Cooper and Munroe proposed a change to hebbian learning suggested a synapse should - increase whe pre and post highly active -decrease (LTD) if only slightly active - stay same if some in between activity -this no change value based on past acitivty LTD has been observed so support offered for BCM rule
what is LTD
long term depression, opposite of LTP, activity dependent reduction in the efficacy (ability to produce desired result) of the synapse (following a long patterned stimulus)
summary of LTP
widespread but best understood in hippocampus
role of NMDA receptors and removal of Mg ions block
calcium ions activates cascade system for post-synaptic modification
can also act pre-synaptically (NO)
two ways to see rewards
as a drive / urge
as related to learning
what are rewards
positive
stopping of aversive stimuli
operate along multiple time scales
olds and milner 1950s experiment
reward as a drive
rat and lever
electrode into brain, lever stimulates (inter-cranial self-stimulations ICSS), rat will press lever for stimulation when electrode is on dopaminergic neurons
reward as a drive
result of human brain stimulation
when stimulated in areas in and around limbic system, reported intense pleasure (equated to sexual orgasm)
others only commented warm or glowing feeling
these were the same areas that caused rats to press levers as long as fast as they could
so areas of the limbic system underlie pleasure
why might the potential to receive rewards influence so many types of behaviour
many rewards activate dopamine into nucleus accumbens - nucleus accumbens projects directly to many cortical and sub-cortical areas = reward influences much of the brain despite source
3 dopamine pathways
1 substantia-nigra to basal ganglia to motor cortex (get up and go)
2 caudate to orbito-prefrontal and premotor cortex (i want to)
3 VTA to nucleus accumbens to frontal lobes (reward)
drug abuse and reward system = where in the brain?
VTA (ventral tegmental area) and nucleus accumbens want morphine, cerebellum doesn’t
opponent-process theory of drug addiction
assume homeostatic principle (if very happy body will adjust to put you back to normal), process becomes more efficient with practice
1st time drug taken = high, opponent process starts
subsequent times drug taken = opponent process is improving with practice, you get more addicted - no drug, opponent process gives opposite of the high
tolerance = high counteracted by opponent process, leads to tolerance so needs increasingly higher dose
withdrawal = no drug so opponent process is unchecked
how overdosing is related to conditioning (Siegel 1984)
many overdoses involve normal doses - addict found in unusual setting
in normal setting, classical conditioning increases opponent process
unusual setting and opponent process is reduced = larger drug effect
rewards and classical conditioning
reward system = widespread influence on brain
ideal for signalling good thing as a starting point for learning
classical condition with reward signals
how doe we learn new responses
reward systems are integral
operant, instruemtnal or reinforcement learning
how do rats learn to press lever for self stimulation
activation of the reward system provides drive
what about the first lever press
rats don’t have an innate us to press a ever
classical condition requires a ur so isn’t classical conditioning is operant
thorndike’s puzzle box
box with locking mechanism
lever and pulley system
hungry cat in box with food outside and observer
tried many approaches at first until found the right one. then during later trials had a tendency to perform the correct action to obtain the reward
Skinner’s box
thought thorndike’s method inefficient
developed an experimental chamber
resonse to press a lever, subject is always able to make the response, measure the rate at which the response is made
4 types of reinforcer
positive reinforcement - positive event follows response
punishment - positive state removed after response (conditioning is weakened)
punishment - discomfort follows response (conditioning weakened)
negative reinforcement - discomfort removed by response
intrinsic reinforces - children drawing experiment
allow nursery children to draw
after a time good player certificate for drawings
give opportunity to draw with and without certificate
result
initially high rate of production of drawings
continue if good player given
but draw less when no good player available
conc - at start intrinsic reward sufficient, after getting good player, the intrinsic reward lost its value
operant conditioning and generalisation - pigeons pecking experiment
train pigeons to peck yellow light for food
once pigeon is pecking fast, test for different coloured lights
result - rate of pecking declines as the colour of light moves further from yellow
conc- operant conditioning, like classical condition shows generalisation
operant conditioning and discrimination - pigeon experiment
train pieon to hop onto perch green light = reward red light = no reward pigeon learns to hop when green light, pigeon does not hop on red conc - discrimination has been shown
latent learning and rats
rats place in maze
gp1 = food in food box from day 1
gp2 = no food in food box till day 11
gp1 showed no apparent learning first 11 days but once reinforced, showed very fast learning (compared to gp2) indicating hidden or latent learning
operant conditioning summary
shows generalisation, discrimination
continguity
latent learning
method of successive approximations allows complex behaviour to be learnt
5 parts of learning theory
aversive conditioning learned helplessness contingency and reinforcement schedules bringing it all together equipotentiality and its violations
aversive conditioning
punishment as an aversive stimulus
makes the response less likely
remember contiguity - punishment must follow soon after the unwanted response
learning to avoid aversive stimulus
escape vs avoidance
escape = respond to stop aversive stimulus avoidance = stop aversive stimulus starting
learned helplessness
think an aversice stimulus in inevitable
gp 1 - executive shows avoidance learning
gp2 - subordinate and control shows no learning
conc - those in gp 2 had leant that the shock was unavoidable
possibly related to in-activity in some forms of depression
what are the four types of reinforcement schedules (brief with a side note)
what does the graph of each look like
fixed ratio - pause then lots of pressing then pause again
variable ratio - fats, continuous responding
fixed interval - scalloped - slow getting faster then slow
variable interval - slowish, little variation in rate
with all types training must start with reinforcement with every response then follow one of the schedules
contingency and unlearning with FR and VR
train rats to run on wheel using FR and VR
stop giving reinforcement
extinction is fastest in FR the VR
role if surprise and extinction in contingency with four types of reinforcement schedules
only get slower extinction with VR or VI - there no way of having an expectation
with FR or FI there is surprise in learning
therefore surprise when running extinction, get rapid extinction
classical and operant conditioning 6 key points
stimulus-reponse reinforcement = more pairings the stronger the learning
show contiguity = short delay
show contingency = CS must predict US, absence must predict absence
show extinction
show generalisation
show discrimination
Rescola-wagner 1972 -what is it
mathematical formlisation of learning based on classical conditioning
it is the simplest version of learning theory
is not meant for operatn conidtiong
many situation where it does hold but some where it doesn’t
has been updated/ extended
maths of Rescola-wagner 1972
o V = associative strength
o Vt+1 = Vt + ∆V
o ∆V = change in association V on a single trial
o ∆V = αβ(λ-V)
α = salience of the CS (attention?
Β = strength / ability of the US to promote learning
λ = maximum conditioning possible
o can then plot graphs of number of trials (x) against strength of conditioned response (y)
• in action
o second order conditioning is just more conditioning
Present CS2 and CS1 (but not US)
• α = salience of CS2
• β = strength / ability of the CS to promote learning
• λ = maximum (CS2 – CS1) association possible
• V=0
o Blocking
Present CS2, CS1 and US:
• V = association of CS2+CS1 with US
• V=VCS1+VCS2=0+100%(VCS1=100%)
• ∆V = αβ(λ-V) = αβ(100%-100%) = 0
• What about operant conditioning?
o Formulation is the same, but now
P(r) = probability of response type
• Not associative strength CS-CR
P(r)t+1 = P(r)t + ∆ P(r)
∆ P(r) = αβ(λ- P(r))
• β = strength / ability of the response to promote learning
o given by the reward signal
o 1 if rewarded, 0 if not rewarded
• λ maximum value (λ = 1 if always give the response, <1 if other responses made)
equipotentiality principle
following from learning theory
can animals and humans learn any stimulus response link?
equipotentiality principle would say yes
violations of equipotentiality principle in classical conditioning
leaned taste aversion -delay between eating food and illness -can show one-trial learning -selective for taste related stimuli other aversive stimuli like shosk - associated with non-food items like tone or light belongingness of stimuli with effect
violations of equipotentiality principle in operant conditioning
stopping aversive conditioning - species specific defence reactions
peck for food is different from peck for water - the response is related to the reinforcement
types of memory
episodic - a trip
semantic - concept of toast
procedural - how to ride a bike
amnesia - 2 types, explain
retrograde amnesia - cannot recall events before the brain damage
anteretrograde amnesia - cannot later remember events that occur after the damage
who was henry molaison and what he could and couldn’t do
bilateral removal of the hippocampal areas
had lesions on both sides to treat very severe epilepsy
couldn’t recognise new people
couldn’t learn how to get to his new home
couldn’t learn his new address
= anteretrograde amnesia
HM experiment (henry molaison) - to show anteretrograde amnesia
show picture of famous faces from different decades, asked to name, compare to age matched controls
result - same as controls for faces who had reached eminence before operations, much worse for faces who had reached eminence after operation. hm did not form memories after operation in the 1950s
hm experiment to show motor learning
mirror drawing - draw a star shape, but only see it looking in a mirror
hm got better with practice
across practices in one day and across many days
but hm did not remember doing it the previous day
conc - hm has in some sense remembered how to mirror draw, has procedural, non-declarative memory
similar done with incomplete pictures task (was better at beginning of retest than himself initially but not the controls)
short maze - repeatedly traced the same path, performance improved over time and days
korsakoffs syndrome
related to alcohol abuse
vitamin B1 (thiamine) deficiency
produces anterograde amnesia
can remember old events
implicit (procedural) memories can be formed
explicit (declarative) memories cannot be formed
damage to dorsomedial thalamic nuleus, mammillary bodies
clive wearing
musician
got herpers virus into CNS and now suffers retro and anteretrograde amnesia
anteretrograde amnesiacs explain procedural implicit confounded definitions
procedural how to mirror draw declarative memory as cant remember practising implicit no explicit memory of practising confounded definitions procedural memory is generally implicit declarative memory is generally explicit
formation of memories summary
see printed summary diagram
O’Keefe and Doctrovsky 1971
hippocampal formation and animal navigation
study of rat hippocampus, recorded while rat exploring environment
cells fire in particular locations, different cells fired when in different locations
conc - activity in hippocampus can code position in space (a mental map of space) these cells are called place cells
Morris et al 1982
animal navigation
rats in milk maze with a hidden platform
unlesioned and control animals (neo-cortical lesion) quickly learn to swim directly to platform from all parts of maze
animals with hippocamplal lesion do not earn the location of the platform
hippocampal formation needed to learn spatial map of the environment
also animals with NMDA antagonist do not leanr location as well as control animals
conc NMDA activity needed, when combined con NMDA in hippocampus
Maguire, Frackowiak and Frith 1997
PET study of London taxi drivers
compared activity between shortest route and famous landmarks
different brain areas activated
the modal model of memory
different short term memories for different things
two stage to get to long term potentiation - occurs best in sleep
short term - has to be rehearsed to be maintained
sensory stores
store large amount of infor
allow selection of which elements are further processed and stored
almost infinite stores
sensory stores - iconic memory
also whose experiment was this
Sperling 1960sflas a grid of letters to remember
delay
high, low or mid tone
report top, mid or bottom row of letter, compare
the extra que of knowing where you’re focusing allows much better memory: you remember more if instructed to remember part of something (partial)
primacy and recency: serial order effects
give a le=ist of words
asked to recall
first few words lots of chance for mental rehearsal
last few words only just heard
plot proportion of participants who recall the word against the position of that word
first and last remembered best, hard to remember the middle
short term memory can hold ….
7 plus or minus 2 numbers at once, lasts for about 30 seconds
long term memory is ….
permanently there
might have to re-learn to access it but will be there
working memory hypothesis and prediction
you need short term memory to solve problems
prediction - if the short term memory is full, it should be harder to solve problems
Baddeley and Hitch 1974 tested it - when full longer to solve
working memory in action - can study using what method
delay natch to sample (DMS)
frontal lobes and working memory - have cells signalling that stimulus is presented rather than stimulus itself
working memory in monkeys and food experiment
compare this to human brains and what does it result in
show monley food in place, delay and hide food, monkey looks in same place
encoding, delay period memory and working out have lots of overlap in prefrontal cortex
humans have far more connections especially in frontal cortices than other animals
what makes humans adaptable is using memory
Moscovitch et al 1995
recall of spatial location activates posterior parietal cortex
recall of object memory activates inferior temporal lobe
Zeineh et all 2003
encoding and recall of memory
similar but not identical brain regions active for encoding and recall
working memory model summary
short term memory needed for cognitive tasks
two STM systems
the phonological loop and the visuo-spatial sketch pad
controlled by the central executive
in the brain
frontal cortices rule with stimulus different parts of the frontal cortices involved in different aspect of working memory
recall of long term memories
involve same cortical areas as for perception
hippocampal complex involved - slightly different areas for recall and learning
long term memory contents in cortex - perceptual aspect in secondary sensory cortices, motor aspects in secondary motor cortices
imagery involves same cortices as perception - mind reading may become possible
what is attention
limitation is a central theme
attention is required to limit enry to a finite capacity processing system by slecting only a subset of all available information
attention itself is a resource of limited capacity which can be divided between tasks
processing and attention capacity linked to arousal
types of attention
focused - process single attribute
divided - multi-tasking
sustained - constant monitoring
focussed attention
object based attention
focus on a particular object - searching for your keys
feature based attention
focus on a particular stimulus aspect - colour naming and the stroop effect
visual search
easy search
hard search
pop out effect - easy to find something that's got a unique feature. no attention is required. target is defined by a single feature hard search (serial) target is defined by two features: shape and colour in the slide examples. features must be combined. requires attention. examine one by one - serially
brain and visual search
if looking for features, we don’t need to use parietal areas
if looking for conjunction do use parietal - certain areas within parietal (has superior lobe and inferior sulcus)
what happes if parietal lobe damaged (connectivity damaged)
can be damaged
unilateral neglect - usually ignore the left visual field. have difficulty seeing the left side. are processing just not reporting
neglect = damage to the attentional system
what is the stroop effect
seeing words in colour - torn between sayin word and colour. isf asked to say colouyr then the word interferes. but does not work backwards - is biased, is easier to say the word
works for policemen assuming a black person is holding a weapon as more black people in prison - not necessarily racist?
interference from words on colour naming in the stroop effect
also brain areas active
words processed automatically
generate word response
interferes with colour response
response conflict
no (little) interference of colour on word naming
colour not automatically extracted and named
counter intuitive - meaning of words automatic, colour ‘word’ effortful
anterior cingulate and lateral prefrontal are active
AC - picks up conflict
Lateral Prefrontal
focused attention summary - 3 main points
constant bombarded by stimuli - limited capacity
focused or selsctive attention - processing of taks relevant information, successfully ignoring irrelevant information
brain areas
-pre-frontal cortex
-parietal lobes
-anterior cingulate
divided attention
dual tasks - doing two things at once
Dreher and Grafman
used sequence of letters upper vs lower case, vowel vs consonant
tell one, tell the other, both hard
what brain areas are involved in divided attention
prefrontal cortex (DLPFC and task switching) parietal lobes (selection for processing) anterior cingulate (resolving response)
sustained attention - how did the study into this work
rapid visual information processing - steady stream of digits, respond when 3 odd numbers follow each other and respond when 3 even numbers follow each other
control - rapid serial visual presentation, respond when digit 0 appears
brain studied
sustained attention study brain area results
lots of areas - the usual attention areas
pre-frontal
parietal
anterior cingulate
the new one compared to temporally restricted attention
thalamus / basal ganglia
ADHD what does it stand for who main 3 symptoms other common symptonms
Attention deficit / hyperactivity disorder
behavioural and neurological disorder (3-5% school children)
-inattention
-impulsivity
-hyperactivity
other common symptoms are distractability, memory, emotional reactivity, self-discipline, hyperfocusing
3 types of ADHD
inattentive AHDH-I
hyperactive / impulsive ADHD-H
combination (most common) ADHA-C
effects of ADHD
deficient self-regulation if behaviour, mood, response - diminished social effectiveness and adaptability
impaired ability to organize and plan behaviour over time - inability to direct behaviour towards future
show deficits in focused, divided and sustained attention
ADHD and the brain
overall 3-4% smaller brain size
decreased blood flow to the prefrontal cortex and pathways connecting limbic system (caudate nucleus and striatum)
PET scan shows decreased glucose metabolism throughout the brain
frontal functioning and ADHD
deficient self-regulation of behaviour, moo and response
impaired ability to organize / plan behaviour over tie
inability to direct behaviour toward future
diminished social effectiveness and adaptability
causes of ADHD
norepinephrine, epinephrine, acetylcholine, serotonin
reticular activating system
influence awareness, memory functions and concentrations
dopamine - low levels can cause attention problems and distractibility
RAS
reticular activating system
involved in arousal
sleep - locus coereleus, pons, NE
awake - raphe nucleus, pons/medulla, 5HT
ADHD and RAS
decreased NE activity in RAS
poor attention, learning difficulties, memory deficits, lack of behaviour control
treatment with amphetamines increases RAS activities
increased RAS activity - hyperactivity, hyper vigilant, resyless
treatment of ADHD
treatments of ADHD relating to NE
NE antagonist = poor (clonidine, antomoxetine)
learning and ADHD
if response is quickly rewarded then can hyper-learn something
impulsive - want to do now and get reward now. wont wait and build
treatments of ADHD
psychostimulants - Ritalin
also cylert, Dexedrine, concerta
takes an hour for effects to start
side effects including insomnia, growth retardation, weight loss, irritability, depression, elevated blood pressure
if bad side effects NE antagonists - clonidine
behavioural treatment is recommended aong with stimulant medication
how does Ritalin work
Effects DA (and NE) re-uptake: agonist – Increases “value” or “motivation” • Helps overcome learning difficulty? – Calms ADHD children and improves concentration – Rebound effect • ADHD characteristics return later in day when medication wears off (after ~ 4hours) • Irritability, hyperactivity and impulsiveness exceeding untreated symptoms – Is safe but follow the doctor’s orders • Over-subscribed because of mis-diagnosis
DA and NE attentional system
interplay between dominaergic systems and parietal systems
ADHD reflects deficits in the two attention sub-systems
