Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PS1002 > Cognitive and behavioural neuroscience > Flashcards

Cognitive and behavioural neuroscience Flashcards

1
Q

is thought physical?

A 
processes = abstract
Implementation = in a physical substrate, the brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is dualism

A

the mind and brain are fundamentally different

therefore they are separate things

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how are the mind and brain fundamentally different

A

physical (brain) vs non-physical (mind)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the problem for dualism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

who is associated with dualism

A

rene descartes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how did Descartes get around the problem of dualism

A

the mind interacted with the brain through the pineal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is monoism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

counter evidence for monoism

A 
subjective factors
near death experiences
out of body experiences
ghost sightings
re-incarnation (re-calling events from past lives)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

gross bits of the nervous system - big division

A

Central (CNS) vs Peripheral (PNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

make up of CNS

A 
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

make up of PNS

A

nervous system outside central

  • typically called nerves
  • covered in 2 meninges:
  • -dura mater
  • -pia mater
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does the PNS allow and how

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

meaning of efferent

A

outgoing, motor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

meaning of afferent

A

incoming, sensory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

autonomic nervous system
what does it do
voluntary?
eg

A 
controls internal state
involuntary
heart rate
digestion
swallowing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

sensory and somatic nervous system
what does it do?
voluntary?
eg

A

deals with external world
skeletal muscles under voluntary control
senses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

3 major divisions of the brain

A

forebrain
mid brain
hind brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how is the forebrain sub divided

A

telencephalon

diencephalon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the principle structure of the telencephalon

A

cerebral cortex
basal ganglia
limbic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the principle structures of the diencephalon

A

thalamus

hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how is the mid brain sub divided

A

mesencephalon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

principle structures of the mesencephalon

A

tectum

tegementum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how is the hind brain subdivided

A

metencephalon

myelencephalon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the principle structures of the metencephalon

A

cerebellum

pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the principle structures of the myelencephalon

A

medulla oblongata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

cerebellum, volume and musicians

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does the medulla oblongata do

A

role in the autonomic control of cardio-vascular system, swallowing etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what does the cerebellum do

A

little brain - approx. 30 billion neurones
sensory information
modulates motor commands - precise movement, sensitive to alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what does the pons do

A

bridge between cerebellum to cortex

role is sleep / arousal, facial muscles, tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what experiments are used to find out about the functions of the hind and mid brains

A

decerebrate experiments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

low-decerebrate animal experiments

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

high decerebrate animals experiment

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

from the decerebrate experiments what does the cortex do

A

allows us to adapt to an unpredictable world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

two major parts of the forebrain: diencephalon and what they do

A

thalamus - control input to cerebral cortex

hypothalamus - controls autonomic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

three parts of basal ganglia

A

putamen - merges with head of caudate nucleus

globus pallidus - inside putamen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the sub-cortical nuclei involved in and where is it

A

control of movement

lateral to thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what does the caudate nucleus do

A

urge to do things

related to reward system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what does the putamen do

A

leanred autonomic movements eg driving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is the striatum

A

caudate nucleus + putamen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what doe the globus pallid so

A

control of voluntart movement

major output nucleus of the basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

parts of the limbic system

A

cingulate cortex- error signals, attention, emotion
amygdala - emotion (fear)
hippocampus - formation and recall of memories, navigation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

two main parts of telencephalon by diencephalon

A

basal ganglia

limbic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

cerebral cortex
size
hemispheres
lobes

A

big bit in primates - disproportionately large in humans
2 hemispheres
4 lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are the four lobes in the brain

A

occipital
parietal
temporal
frontal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

hemispheric specialisation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

language as an example of hemispheric specialisation

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how are the two hemispheres connected

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

testing for hemispheric specialisation

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

reaction time experiments for hemisphere experiments

A

intact brains
present stimuli to left or right visual field
record reaction time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what evidence is there for hemispheric specialisation

A

left specialised for language, speech, local image feature extraction
right specialized for visuo-spatial processing, global image properties, face processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the primary cortices for

A

first for sensory input, last for output
at back of is primary motor cortex - premotor and supplementary
rest is executive functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are secondary cortices

A

adjacent to primary, short connection distance

receive input from many different sources

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Phineas Gage

A

iron through his cheek and brain
damage to frontal cortices
marked personality changes?
good man turned nasty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

role of

dorsolateral prefontal cortex

A

planning of action

underactive in depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

role of

anterior cingulate cortex

A

errors and the feeling of self

overactive in depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

role of

orbito-frontal cortex

A

inhibition of changes from unusual behaviors
punishment / reward in decision making
overactive in depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

role of

ventromedial prefrontal cortex

A

emotional meaning

overactive in depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what are the major cortical pathways of the brain

A

auditory, olfactory, visual, motor, somasensory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

visual pathways

A

two visual pathways
lots of connections between them
-dorsal
-ventral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

how does the visuo-motor system work

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

where is fear processed

A

thalamus
limbic and cortical interplay
most things that keep us alive skip visual cortex in order to act quicker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

two types of cells in the brain and what they do

A

glia - keep brain alive

neurones - do psych part

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

anatomy of a neurone

A

input - dendrite
integration - cell body, soma, contains nucleus
output - axon, very long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is neural activity

A

electric current and ionic flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what are the major ions in neural activity

A

sodium chlorine and potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what forces does every ion have acting on it

A

chemical

electrical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

explain the resting membrane potential

A

permeability high for K and low for Na and Cl

equilibrium point at -50 to -70mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

impulse to do all or nothing - action potential explained

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

how does an impulse travel - propagating the signal

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

myelin sheath

A

causes a jump from one load to another which is faster = speeds up the impulse travelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what did Sherrington’s behavioural studies find

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what two types of synapse are there and what are their relative speeds

A

chemical - slow, ionotropic (directly opens channel), metatropic (slowest, cascade system opens channel), amenable to drugs
electrical - fast, reliable, poor processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

chemical synapse

A

release of molecule into cleft
activates specific receptor (can be excitatory or inhibitory)
variable effects - good at processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what are vesicles and what do they do

A

contain neuro-transmitter molecules

when calcium ions enter, vesicle fuse with membrane and release neuro-transmitter into cleft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

4 step action of neurotransmitters

A

ligand-gated ion channels
g-protein-coupled receptors
kinase-linked receptors
nuclear receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

estrogen changes..

A

the way the cell responds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

ending synaptic action

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

peptides vs non-peptides

effect on post-synaptic membrane

A

long lasting

np short lasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

peptides vs non-peptides

synthesis location

A

endoplasmic reticulum of soma

np nerve terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

peptides vs non-peptides

replenishing speed

A

slow (not recycled)

np - fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

peptides vs non-peptides example of each

A

pep - enkephalins

non pep - ACh, DA, 5HT, NMDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what types of drugs reduce transmission and by what mechanisms do they work

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what types of drugs enhance transmission and by what mechanisms do they work

A 
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

ACh and what disease, explain

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

dopamine related drugs named and explained (4)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what is unipolar depression

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

treatment of depression

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

tricyclic antidepressants

A

block re-uptake of transmitter to increase post-synaptic response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what did Asberg’s 1990 studies find

A

post-mortem studies of suicide victims
measured post-synaptic serotonin 5-HT and metabolite 5-HIAA
decreases in CSF serotonin is associated with suicide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

3 types of drug in the treatment of depression

A

SSRIs
TCAs
MAOIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

7 levels of explanation and why this matters

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

2 methods of study using observation

A

damage to the nervous system produces deficits in psychological processes
damage to other body parts can influence psychological processes but does not cause deficits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

role of brain in methods of study of psychological processes

A

brain is the site of psychological processes

but this does not mean you must study the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

2 ways to study the anatomy of the bran explained

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

4 ways of monitoring brain activity

A

electrocephlogram EEG
positron emission tomography PET
functional magnetic resonance imaginf fMRI
single unit recording

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

explain EEG

A

electrode cap, measures voltage over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

explain PET scan

A

shows activity and strength of, uses injection of dye and radioactive traces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

explain fMRI

A

MRI over time, detects changes in blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

explain single unit recording

A

fine electrodes to record single cell electrical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

name 7 methods of studying the brain from disruption

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

spatio-temporal resolution discussed for EEG, fMRI and single unti recording

A

EEG - poor spatial resolution, high temporal
fMRI - medium spatial, low temporal
single unit recording - high spatial and temporal resolution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

whats wrong with low and high spatial and temporal temporal resolutions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

summary to neuroscience methods of studying the brain

A

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
104
Q

what is arousal and how is it shown in the brain / studied

A

basic asleep vs awake

brain shows different activity patterns (EEG)

105
Q

explain the stages of sleep

A

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

106
Q

what happens during increased arousal

A

faster heart beat
sympathetic nervous system activity
increased heart beat, shivers down the spine, sweaty palms, adrenaline rushes. interaction between epinephrine and norepinephrin

107
Q

what is the galvanic skin response

A

measures the electrical resistance of skin
arousal - sweaty palms
drop n resistance
used in polygraph (lie detector)

108
Q

what is a drive or a motivation

A

a desire to do something

109
Q

explain the urge to eat

A

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

110
Q

other signals associated with the urge to eat

A

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

111
Q

where does detection occur in the urge to eat

A 
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)
112
Q

Does the hypothalamus lead to overeating? evidence in rats

A

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

113
Q

does the hypothalamus relate to eating disorders?

A 
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
114
Q

what is Hulls drive reduction theory

A

hunger drives behaviour to reduce hunger
pain drives behaviour to reduce pain etc
when drives are zero = perfect contentment

115
Q

according to hulls drive reduction theory where is optimal arousal

A 
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
116
Q

cycle in hulls drive reduction theory

A

homeostatis - biological need - primary drive - motivation to satisfy - goal-directed behaviour - need satisfied - bac to homeostatis

117
Q

james-lange theory

A

in an emotion producing situation
1 the body responds
2 - sensory feedback
3 - the feeling of emotion

118
Q

evidence behind james-lange theory

A

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

119
Q

what is wrong with the James-lange theory

A

physical changes too slow
artificially induced changes rarey produce emotion
different situations can produce different emotions but similar bodily response

120
Q

schachter and singer’s awareness of emotion

A

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

121
Q

how schachter and singer hypothesis tested

A

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

122
Q 
quick summary of how 
folk psychology
james-lange theory
schacter and singer theory
see awareness of emotion
A 
folk psychology
sensory systems - awareness - response
james-lange theory
sensory systems - response - awareness
schacter and singer
sensory systems - response - interpretation awareness
123
Q

brain regions in emotion - what areas

A

frontal cortices as shown by Phineas Gage

amygdala

124
Q

Schachter and Singers ATTRIBUTION

A

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

125
Q

Dutton and aron 1974

A

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

126
Q

learning fear and the amygdala experiments

A

measure skin cinductance (sweating) to learnt scary stimuli

without stimuli the scary stimuli are not scary - don’t learn them as scary

127
Q

amygdala’s role in social interactions

A

ask how close someone can get to you and still feel comfortable
without amygdala the idea of personal space is noticeably reduced

128
Q

amygdala - why wouldn’t it be involved in fear

A

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

129
Q

which is the primary cortex for internal senses - and study that showed this

A

insula cortex

Phillips et al 1997 insula activity when viewing facial expressions of disgust

130
Q

how do emotions function in the brain

A

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

131
Q

historical ideas on emotions

A

Aristotle believed there are a number of characteristic emotions
Darwin - universal emotions

132
Q

Darwins’ universality thesis

A

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

133
Q

facial muscles
how are they defined
can we control them

A

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

134
Q

the duchenne smile

A

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

135
Q

how the voluntary smile forms

A

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

136
Q

how the spontaneous smile forms

A

basal gangli
caudate nucleus to putamen to globus pallidus to reticular formation
to brain stem
facial nuclei to facial nerve to muscles

137
Q

physical difference between the two smiles

A

true smile - muscles around the eyes involved, voluntary not

138
Q

human lie detectors

A

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

139
Q

three types of models of emotions

A

evolutionary
socio-evolutionary
social constructionist

140
Q

basis of evolutionary models of emotion

A

emotions are labels applied to basic adaptive behaviours

141
Q

basis of socio-evolutionary models of emotion

A

evolved from basic adaptive baviours but from early homids as social grouping became dominant

142
Q

social constructionist models of emotion

A

emotions are a social construct and should be thought of in this way

143
Q

Plutchick’s model of emotion

A

emotions evolved from basic adaptive behaviours - labels given to different intensities as well as axes
evolutionary model

144
Q

simple explanation of socio-evolutionary models of emotion

A

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

145
Q

the strong constructionist model (averill) on emotion

A

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

146
Q

the moderate social constructionist model of emotion (Barrett)

A

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

147
Q

what is habituation

A

decline in response to stimulus when familiar

narrows the range of stimuli that elicit false alarms

148
Q

Pavlov dogs

A

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

149
Q 
UCS - 
UCR - 
CS
CR
plus example from pavlov dogs
A

unconditioned stimuli = food
unconditioned response = salivation
conditioned stimuli = bell
consitioned response = salivation

150
Q

measurements taken during conditioning experimetns eg pavolv dogs

A

CR probability - if appropriate
or trial by trial
CR amplitude - if appropriate (amount of saliva)
CR latency - always available - time from bell to salivation

151
Q

what did pavlov propose in his dog experiments

A

unconditioned response is innate, conditioned response depends on learning

152
Q

what is extinction in conditioning

A

establish conditions then repeat testing without it
repeated trials when conditioned stimuli presented alone
shows opposite learning curve
can learn and unlearn

153
Q

reconditioning
speed
what does this show

A

very fast process
extinction doesn’t get rid of the initial conditioning
once something is learnt it is very hard to erase

154
Q

stimulus generalization

A

the closer the stimulus is to the one you learnt, the better one generalizes

155
Q

discrimination vs generalisation

A

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

156
Q

second order conditioning

A

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

157
Q

blocking of conditional learning

A

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

158
Q

widespread nature of classical conditioning

A

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

159
Q

Watson and emotional conditioning

A

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

160
Q

constraints on mechanisms of learning - what is wanted for meaningful learning

A

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

161
Q

contiguity and contingency
they are different
what do they mean

A

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

162
Q

neurones and classical conditioning

A

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

163
Q

Bliss and Lomo 1973

A

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

164
Q

cortical plasticity

A

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

165
Q

what did Bi and Poo show about LTP

A

shows contiguity - inputs need to be active within a short time

166
Q

presynaptic LTP …… in number of vesicles

post-synaptic LTP =

A

increase
growth of synapses
learning can mean formation of new synapses

167
Q

nitric oxide

A

retrograde messenger - high concentrations poisonous gas
synthesis on demand - calcium ion - NO synthesis
increases neurotransmitter synthesis in presynaptic neuron, more released during action potential

168
Q

Hebb 1940s

A

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

169
Q

BCM rule and LTB

A 
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
170
Q

what is LTD

A

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)

171
Q

summary of LTP

A

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)

172
Q

two ways to see rewards

A

as a drive / urge

as related to learning

173
Q

what are rewards

A

positive
stopping of aversive stimuli
operate along multiple time scales

174
Q

olds and milner 1950s experiment

A

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

175
Q

reward as a drive

A

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

176
Q

why might the potential to receive rewards influence so many types of behaviour

A

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

177
Q

3 dopamine pathways

A

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)

178
Q

drug abuse and reward system = where in the brain?

A

VTA (ventral tegmental area) and nucleus accumbens want morphine, cerebellum doesn’t

179
Q

opponent-process theory of drug addiction

A

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

180
Q

how overdosing is related to conditioning (Siegel 1984)

A

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

181
Q

rewards and classical conditioning

A

reward system = widespread influence on brain
ideal for signalling good thing as a starting point for learning
classical condition with reward signals

182
Q

how doe we learn new responses

A

reward systems are integral

operant, instruemtnal or reinforcement learning

183
Q

how do rats learn to press lever for self stimulation

A

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

184
Q

thorndike’s puzzle box

A

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

185
Q

Skinner’s box

A

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

186
Q

4 types of reinforcer

A

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

187
Q

intrinsic reinforces - children drawing experiment

A

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

188
Q

operant conditioning and generalisation - pigeons pecking experiment

A

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

189
Q

operant conditioning and discrimination - pigeon experiment

A 
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
190
Q

latent learning and rats

A

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

191
Q

operant conditioning summary

A

shows generalisation, discrimination
continguity
latent learning
method of successive approximations allows complex behaviour to be learnt

192
Q

5 parts of learning theory

A 
aversive conditioning
learned helplessness
contingency and reinforcement schedules
bringing it all together
equipotentiality and its violations
193
Q

aversive conditioning

A

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

194
Q

escape vs avoidance

A 
escape = respond to stop aversive stimulus
avoidance = stop aversive stimulus starting
195
Q

learned helplessness

A

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

196
Q

what are the four types of reinforcement schedules (brief with a side note)
what does the graph of each look like

A

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

197
Q

contingency and unlearning with FR and VR

A

train rats to run on wheel using FR and VR
stop giving reinforcement
extinction is fastest in FR the VR

198
Q

role if surprise and extinction in contingency with four types of reinforcement schedules

A

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

199
Q

classical and operant conditioning 6 key points

A

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

200
Q

Rescola-wagner 1972 -what is it

A

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

201
Q

maths of Rescola-wagner 1972

A

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)

202
Q

equipotentiality principle

A

following from learning theory
can animals and humans learn any stimulus response link?
equipotentiality principle would say yes

203
Q

violations of equipotentiality principle in classical conditioning

A 
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
204
Q

violations of equipotentiality principle in operant conditioning

A

stopping aversive conditioning - species specific defence reactions
peck for food is different from peck for water - the response is related to the reinforcement

205
Q

types of memory

A

episodic - a trip
semantic - concept of toast
procedural - how to ride a bike

206
Q

amnesia - 2 types, explain

A

retrograde amnesia - cannot recall events before the brain damage
anteretrograde amnesia - cannot later remember events that occur after the damage

207
Q

who was henry molaison and what he could and couldn’t do

A

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

208
Q

HM experiment (henry molaison) - to show anteretrograde amnesia

A

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

209
Q

hm experiment to show motor learning

A

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

210
Q

korsakoffs syndrome

A

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

211
Q

clive wearing

A

musician

got herpers virus into CNS and now suffers retro and anteretrograde amnesia

212
Q 
anteretrograde amnesiacs 
explain 
procedural
implicit
confounded definitions
A 
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
213
Q

formation of memories summary

A

see printed summary diagram

214
Q

O’Keefe and Doctrovsky 1971

A

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

215
Q

Morris et al 1982

A

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

216
Q

Maguire, Frackowiak and Frith 1997

A

PET study of London taxi drivers
compared activity between shortest route and famous landmarks
different brain areas activated

217
Q

the modal model of memory

A

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

218
Q

sensory stores

A

store large amount of infor
allow selection of which elements are further processed and stored
almost infinite stores

219
Q

sensory stores - iconic memory

also whose experiment was this

A

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)

220
Q

primacy and recency: serial order effects

A

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

221
Q

short term memory can hold ….

A

7 plus or minus 2 numbers at once, lasts for about 30 seconds

222
Q

long term memory is ….

A

permanently there

might have to re-learn to access it but will be there

223
Q

working memory hypothesis and prediction

A

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

224
Q

working memory in action - can study using what method

A

delay natch to sample (DMS)

frontal lobes and working memory - have cells signalling that stimulus is presented rather than stimulus itself

225
Q

working memory in monkeys and food experiment

compare this to human brains and what does it result in

A

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

226
Q

Moscovitch et al 1995

A

recall of spatial location activates posterior parietal cortex
recall of object memory activates inferior temporal lobe

227
Q

Zeineh et all 2003

A

encoding and recall of memory

similar but not identical brain regions active for encoding and recall

228
Q

working memory model summary

A

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

229
Q

recall of long term memories

A

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

230
Q

what is attention

A

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

231
Q

types of attention

A

focused - process single attribute
divided - multi-tasking
sustained - constant monitoring

232
Q

focussed attention

A

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

233
Q

visual search
easy search
hard search

A 
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
234
Q

brain and visual search

A

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)

235
Q

what happes if parietal lobe damaged (connectivity damaged)

A

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

236
Q

what is the stroop effect

A

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?

237
Q

interference from words on colour naming in the stroop effect
also brain areas active

A

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

238
Q

focused attention summary - 3 main points

A

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

239
Q

divided attention

A

dual tasks - doing two things at once

240
Q

Dreher and Grafman

A

used sequence of letters upper vs lower case, vowel vs consonant
tell one, tell the other, both hard

241
Q

what brain areas are involved in divided attention

A 
prefrontal cortex (DLPFC and task switching)
parietal lobes (selection for processing)
anterior cingulate (resolving response)
242
Q

sustained attention - how did the study into this work

A

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

243
Q

sustained attention study brain area results

A

lots of areas - the usual attention areas
pre-frontal
parietal
anterior cingulate
the new one compared to temporally restricted attention
thalamus / basal ganglia

244
Q 
ADHD
what does it stand for
who 
main 3 symptoms
other common symptonms
A

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

245
Q

3 types of ADHD

A

inattentive AHDH-I
hyperactive / impulsive ADHD-H
combination (most common) ADHA-C

246
Q

effects of ADHD

A

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

247
Q

ADHD and the brain

A

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

248
Q

frontal functioning and ADHD

A

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

249
Q

causes of ADHD

A

norepinephrine, epinephrine, acetylcholine, serotonin
reticular activating system
influence awareness, memory functions and concentrations
dopamine - low levels can cause attention problems and distractibility

250
Q

RAS

A

reticular activating system
involved in arousal
sleep - locus coereleus, pons, NE
awake - raphe nucleus, pons/medulla, 5HT

251
Q

ADHD and RAS

A

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

252
Q

treatments of ADHD relating to NE

A

NE antagonist = poor (clonidine, antomoxetine)

253
Q

learning and ADHD

A

if response is quickly rewarded then can hyper-learn something
impulsive - want to do now and get reward now. wont wait and build

254
Q

treatments of ADHD

A

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

255
Q

how does Ritalin work

A

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

256
Q

DA and NE attentional system

A

interplay between dominaergic systems and parietal systems

ADHD reflects deficits in the two attention sub-systems

PS1002 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions