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PYSCOLOGY > PYSC 111 > Flashcards

PYSC 111 Flashcards

1
Q

what part of the eye focusses the image?

A

cornea and lens

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2
Q

what are cataracts?

A

the clouding of the lens to the point that the person is unable to see

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3
Q

What does the Critical Period mean?

How long is it in humans?

A

the time in which the beings critical systems develop (6-9 months in humans)

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4
Q

Name the 3 cell layers that stimulus is carried through, in order.

A

(Sensation) -> ganglion -> bipolar -> photo receptors

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5
Q

Name the 4 lobes of the brain

A

parietal, frontal, occipital, temporal

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6
Q

Frontal lobe role:

A

Executive lobe of the brain

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7
Q

Parietal lobe role:

A

spacial

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8
Q

Temporal lobe role:

A

multiple roles - visual, memory

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9
Q

Occipital lobe role:

A

vision

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10
Q

Name the 3 steps that visual info goes through to get to the brain

A

eyes (ganglion cells) -> lateral geniculate nucleus (subcortex) -> V1 (cortex)

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11
Q

explain why it is said that the right side of your brain sees through your left eye and vise versa.

A

half of the neural messages come out of the ganglion fibres at the back of the eye and go t the opposite side and the other half come out and got to the same side of the brain.

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12
Q

What did the Miskin & Ungerleider 1982 study show?

A

that there are different parts of the brain that are responsible for different types of perception/vision. When one is damaged the subject can no longer percieve that type of vision, however they may be able to learn to percieve the set of things in a different way eg. differentiating objects based on their shape instead of their pattern.

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13
Q

What are the 2 visual pathways in the brain and what do they do?

A

Ventral stream - pattern perception (what)

dorsal stream - spatial location (where)

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14
Q

How do you test when each cell in the visual system does?

A

by doing a test in which the cells are shown a certain stimulus and the rate at whcih they are firing electrical impulses is measured. They have a base rate and if they increase or decrease that rate then they care about that stimulus type.

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15
Q

what do rods and cone ‘care’ about?

A

diffused light (changes in illumination) ONLY

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16
Q

what do retinal ganglion cells ‘care’ about?

A

spots of light

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17
Q

what do lateral geniculate nucleus cells ‘care’ about?

A

spots of light

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18
Q

what do V1 cells ‘care’ about?

A

lines of different orientations

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19
Q

What do the cells beyond V1 do and what area are they in?

what is their nickname?

A

area: TE/IT
they identify features (eg. facial features)
‘grandmother cells’

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20
Q

Give 2 examples in how grandmother cells can help an animal:

A

merino sheep can only recognise merini sheep faces

frogs can recognise flies etc

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21
Q

explain how grandmother cells are developed:

A

there are a base number/type of cells that we are all born with, however, we develop more cells that recongise finer details of things we are more exposed to.

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22
Q

what is retinotopic mapping?

A

point to point mapping of the external world into the retina.

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23
Q

where does retinetopic mapping occur?

A

only before V1, after V1 the cells are advanced enough to recognise the stimulus no matter where it lies on the visual feild.

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24
Q

what does it mean when a cell ‘likes’ something?

A

that its architecture is such that the stimulus type will maximumly stimulate the cell.

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25
Q

what is centre surround architecture?

A

if light falls onto the middle of the cell it responds, if the light falls beyond the centre of the cell then it inhibits the cells response.

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26
Q

what is the purpose of centre surround architecture?

A

to enhance contrast (makes the image sharper or crisper)

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27
Q

what happens to the cells repsonse to stimulus?

A

it is sent to the brain

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28
Q

as you go down the __ __ __, info processing becomes more ____.

A

ventral visual stream

complex

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29
Q

receiptor field is like a ___.

A

line

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30
Q

If someone knows where something is but not what it is what has gone wrong?

A

some signalls are getting to the pariental lobe through the alternate V5 route rather than the damaged V1 route.

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31
Q

what is V5s job?

A

to tell if something is moving.

If there is something moving it can tell where it is but not what it is unless it has been through the V1 stream.

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32
Q

what is achromatopsia?

A

absense of colour vision (damage to V4)

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33
Q

what is akinetopsia?

A

absense of motion vision (damage to V5) eg snapshot vision.

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34
Q

Name 4 characteristics of apperceptive agnosia:

A
  • failure of object recognition due to failure of visual perception
  • preserved elementary visual function
  • poor matching/copying
  • colour vision is still good
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35
Q

was kind of effects do different damages to the V1 have?

A

poison could damage V1 without destroying it completely, resulting in partial blindess or visual impairment such as agnosia.
trauma such as the V1 being removed or destroyed completely will result in full blindness.

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36
Q

what does scatoma mean?

A

blind spots (small or large eg. peppery vision making it hard to recognise objects.

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37
Q

what are the 4 types of visual agnosia?

A
  1. apperceptive agnsia
  2. dorsal simultagnosia
  3. ventral simultagnosia
  4. associative agnosia
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38
Q

what is dorsal simultagnosia?

A
  • failure to recognise obects due to spatial perceptual impairment.
  • can recognise objects but not more than one at a time
  • cant see where the object is.
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39
Q

what is ventral simultagnosia?

A
  • failure of object recognition due to a complex perceptual impauirment
  • can recognise one obect at a time but can see more
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40
Q

what is associative agnosia?

A

failure of object recognition due to a higher-order complex perceptual impairment

  • seemingly normal copying however perception isnt normal and copying they do is from shapes not recognition of the actual obects.
    eg. Dr. P
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41
Q

what did Rene Descartes do?

A

was the first to introduce the idea that there had to be some central/connected part of the brain that each side of the vision met at.

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42
Q

what did Gall + spurzheim do?

A

introduced the idea that there were localised faculties in the brain.
thought that because a part of someone skull is big that must mean that they are particually good at the skill that the part of the brain is associated with.

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43
Q

what did Broca do?

A

(patient Tan)
introduced ‘broca aphasia’ in which he predicted and showed that speech difficulties were linked to damaged tissue in a certain part of the brain, proving localisation.

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44
Q

what did Wernicke do?

A

challenged Brocas localisation of speech impairment (speaking) by showing that another part of the brain also was responsible for speech (hearing). They were both right that those different parts were both linked to speech impairments.

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45
Q

what did Fritsch + Hitzig do?

A

discovered that the brain used electrical impulses.
found out that if you stimulate part of the brain then part of the body will move, proving that localised parts of the brain are associated with physical movement in the body.

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46
Q

how much of the brain is for visual?

A

around 1/3

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47
Q

what is a sulcus?

A

groove in brain

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48
Q

what is a gyrus?

A

the ridge between sulci in the brain.

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49
Q

what does damage to the occipital lobe mostly cause?

A

blindess/blightsight and apperceptive agnosia

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50
Q

what are the parts of the temporal lobe?

A

lateral surface - superior gyrus, middle gyrus, inferior gyrus.
medial surface - medial temporal lobe

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51
Q

what shape is the temporal lobe like?

A

a tube

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52
Q

what does the superior temporal gyrus do, and what happens if you damage it?

A 
auditory.
if damaged (especially in the A1) it can cause deafness, wernickes aphasia (hearing to speaking), and auditory agnosia (similar to visual)
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53
Q

what does the middle and inferior gyrus do?

A

ventral visual system

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54
Q

what does damage to the middle/inferior temporal gyrus do?

A
  • achromotopsia (colour) A4
  • akinetopsia (motion) A5
  • ventral similultagnosia
  • associative agnosia
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55
Q

what kind of impairment happens when the medial temporal lobe is damaged?

A

memory impairment

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56
Q

what is the main structure of the MTL?

A

the hipocampus

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57
Q

when the right of the MTL is damaged how does the impairment present itself?

A

visual:
they can copy fine but cannot recall an image.
verbal:
they can hear and recall a story well (no verbal impairment)

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58
Q

when the left of the MTL is damaged how does the impairment present itself?

A

visual:
they can copy and recall fine (no visual impairment)
verbal:
they can hear but cannot recall a story

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59
Q

what impairments are caused by the removal of the MTL

A

retrograde amnesia and anterograde amnesia.

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60
Q

what is retrograde amnesia and anterograde amnesia?

A

retrograde: cant recall past memeories
anterograde: cant make new memories

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61
Q

what does temporally graded amnesia mean?

A

when they can remember memories far in the past (already stored) but not recent memories.

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62
Q

what does temporally graded amnesia tell us?

A

that the MTL recieves memories b ut does not store them. they are stored in higher places of the visual and auditory streams.

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63
Q

what is the exception of anterograde amnesia?

A

people cant remember 90% of the memories but they are able to impove in simple tasks over time which shows that they must have some memory. this proves that there must be many memory systems in the brain.

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64
Q

what are the two types of memory?

A

declaritive: explicit, eg. a thing that happened to them
nondeclaritive: implicit eg. a skill

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65
Q

which type of memory is impaired by MTL damage?

A

declaritive

66
Q

what does the parietal lobe deal with?

A

spacial (dorsal stream)

67
Q

Where is the parietal lobe?

A

in the dorsal stream:

  • behind central sulcus
  • above lateral sulcus
  • in front of the occipital lobe
68
Q

what does damage to the parietal lobe do?

A

causes impairment in:

  • intergrating sensory info
  • control of movement
  • guiding movements to points in space
  • abstract concepts
  • directing attention
69
Q

what are the impairments that damage to the left parietal lobe cause?

A
  • agraphia (difficulty writing)
  • acalculia (difficulty in maths)
    things that you cant always see brain damage in:
  • right/left confusion
  • dyslexia
  • difficulty in drawing details
70
Q

what is contralateral neglect?

A

not being able to see half of your feild of vision eg. left side. absolutely no concept of the left side - cant turn, cant reach.

71
Q

is neglect perceptual or non-perceptual? explain.

A

due to the tests done so far it is assumed that neglect is non-perceptual. People that cant see the left still make judgements about things based on info gathered from the left of the picture without consciouslly seeing the left side.

72
Q

what is the difference between perceptual and non-perceptual?

A

perceptual: they dont register the left side

non-perceptual: they register but just dont (/cant?) pay attention to the information that theyre recieving.

73
Q

what si the difference between ego centred neglect and object centred neglect?

A

ego centred: ignoring what is on the left of you

object centred: ignoring what is on the left sie of each individual object.

74
Q

what are the 4 parts of the frontal lobe?

A
  1. motor cortex
  2. premotor cortex
  3. prefrontal cortex
  4. orbitofrontal cortex
75
Q

what happens in the frontal lobe?

A

all the systems converge (this also happens at the parietal lobe) to put the info together and then act based on that information.

76
Q

what are the 2 types of IQ?

A

convergant: one answer qs (what is the closest planet to the sun)
divergent: multianswer/abstract questions (eg what can you use a phone for)

77
Q

Which kind of IQ is impaired by damage to the frontal lobe?

A

divergent

78
Q

impairments to motor function are caused by damage to what part of the brain?

A

the motor cortex and the premotorcortex

79
Q

what are the impairments caused by damage to motor function?

A

loss of fine movements, speed, strength

broca’s aphasia (difficulty speaking)

80
Q

loss of divergent thinking can be shown through what test?

A

the word fluency test:
eg. name as many 4 letter words as you can in a a minute. People with the impairment are able to do the test but a lot slower and they will break the rule of 4 letter words.

81
Q

damage to the frontal lobe can cause:

A

failure of response inhibition (they arent able to change thought process/game stratergy quick at all) eg. wisconsin card sorting test.

82
Q

what are the 3 changes in behaviour caused by temporal lobe damage?

A

imitation behavior
utilisation behaviour
change in personality/change in temprament

83
Q

explain imitation behaviour and when it occurs:

A

when: damage to temporal lobe
what: patients copy what the people around them are doing without using indivual throughts do matter how strange or unlogical it is eg. picking up random glasses and putting them on top of your existing glasses.

84
Q

explain utilization behaviour and when it occurs:

A

when: damage to temporal lobe:
what: when handed an object, patients use it for the purpose it was made for, even when not instructed to. eg. are handed a envelope, will lick and seal, if given medical equipment, they will do a check up to theur best ability despite not being doctors.

85
Q

explain changes to patients temprament when they sustain temporal lobe damage.

A

patients become child/animal/like or very limited in emotions.

86
Q

the brain is the organ of:

A

interpretation and prediction

87
Q

what does the brain interpret and what does this say about the putside world?

A

the brain interprets stimulus such as colopur and smell. the world isnt necessarily telling us certain things eg. that flowers smell good, it is just that our brain interpret the molecules it recieves in a certain way.

88
Q

what is the tendancy to see faces called?

A

Pareidolia

89
Q

what kind of process helps the brain with predictions and what predictions does it make

A

the brain makes predictions on what we need to prioritise our focus (vision, memory, hearing) on based on what we have needed in the past eg. escaping large animal, the brain focusses on animal, not plants behind it. this results in change blindness

90
Q

what are the 2 parts of the human nervous system?

A

central NS and Peripheral NS

91
Q

how many specialsed brain nerve cells do we have?

A

85 billion

92
Q

explain the main structure of a neuron

A

dedrites, cellbody + neucleus, axon, presynatpic terminals.

93
Q

inside the neuron is ____ chargedcompared to outside.

A

negatively

94
Q

what is the resting membrane potential?

A

-70mV

95
Q

how does the action potential change?

A

when exposed to certain stimuli, ion channels open changing the ion concentration which causes depolarisation creating action potential/casuing it to increase.

96
Q

what does spacial summation mean?

A

when 2 potentials (from stimuli)from different parts of the body meet together at the same time at the same dendrite creating an even bigger change in membrane potential at the dendrite.

97
Q

what is temporal summation?

A

when 2 potential (from stimuli) arrive at the dendrite at quick sucsession of each other.

98
Q

what computes the potentials?

A

the neuron

99
Q

explain the ‘all or nothing’ nature of action potential in the axon.

A

the action potential will not change until it reaches a certaan level of stimulation. if it is then stimulated more, it will not increase even more - it only increases that certain amount.

100
Q

how does the body gage how hard/loud the stimulation is?

A

not by how much AP is created, but by how many pulses of AP is recieves. eg. low stimulus = little amount of AP impulses
high stimulus = many bursts of AP.

101
Q

what happens when you disrupt the production of AP and how?

A

some toxins stop the ion channels from opening so ions cannot change the concentration, so AP can not be generated, so all transmition of info stops.

102
Q

what is a toxin that can cause the closing of ion channels and what if the impact?

A

tetrodotoxin (TTX) 50% death rate, 200 cases a year ww. Causes paralysis and eventually death.

103
Q

briefly explain how neurons ‘talk’ to each other.

A

stimulus nerve signal sent to brain. Ap comes from brain, travels to neuron, then from one neuron to the other, the AP goes to the axon terminal, and converts to chemical signal in the form of neurotransmitters which are contained in vesicles that drop them into the synaptic cleft where they are picked up by dendrites, converting them back to AP (electrical).

104
Q

what is reuptake?

A

some neurotransmitters that havent binded to dendrites are accepted back into the axon terminal for reuse.

105
Q

what types of effects can drugs have neurotransmitters?

A

synthesis - produce more/less NTs
storage - vesicles leaky, therefore deliver less NTs
release - more or less release of NTs
binding - the NTs may not even have an effect on the dendrite
reuptake - stay in cleft longer, not reused efficiently

106
Q

what are the two impacts drugs can have on NTs? and what do they do?

A

Agonists - facilitate/increase transmission of info by mimicing (direct) naturally occuring substances, or by enhancing (indirect) the natural substances (release or action)
Antagonists - block or suppress NTs

107
Q

what is temporal summation?

A

2 APs that arrive close enough together that they build on each other and reach the threshold for NTs to be released

108
Q

what are the 5 neurotransmitters?

A
  1. acetylcholine (ACh) - CNS memory, PNS movement
  2. dopamine
  3. noradrenaline - fight or flight
  4. glutemate - rapid response, thinking
  5. seratonin - mood
109
Q

what are some examples of agonists and antagonists that impact a cholingentic synapse (uses ACh)?

A

agonist - nicotine, black widow spider

antagonist - botulinum toxin, scopolamine (sea sickness antidote - reduces stimuli).

110
Q

what are the symptoms of parkinsons?

what is a treatment for it (drug and other)?

A

slowness (bradykinesia), tremors, muscular rigidly, postural instability (dysronia, dskinesia) , festination.
drugs - dopamine agonists
surgery - deep brain stimulation (inserting electrodes into the brain attached to pulse generator that provide appropriate stimulus at the right time)

111
Q

what are the symptoms of schizophrenia?

A

positive: delusion, hallucination (auditory/visual) disorganised thinking
negative: blunted effects, poverty of speech + thought, apathy
cognitive symptons: poor memory, disruption of ettention and function.

112
Q

what is the treatment for schizophrenia?

A

dopamine antagonists, can result in parkinson like symptons because parkinsons is linked to a lack of dopamine caused by the degeneration of substantia migra (mid brain nucelus that produces dopamine).

113
Q

explain drug induced schizophrenia:

A

drugs such as cocaine and amphetamines are dopamine agonists and so increase the levels of dopamine neurotransmitters received. this can cause schizophernical like symptons.

114
Q

what are some examples of dopamine agonists?

A

L - Dopa, bromocripline, cocaine, amphetamines.

115
Q

what is the neurotransmitter most involved in drugs of abuse? is it an agonist or antagonist?

A

drugs of abuse are dopamine agonists.

116
Q

explain what intercranial self stimulation is:

A

ICSS is when an electrode is inserted into the ‘human reward’ part of the brain (sex, food, money) and attached to a electrical stimulator. ICSS activates dopaminergic pathways inducing the nucleus accumbens and VTA (ventral tegmental area).

117
Q

what were the findings of ICSS with rats?

A

the rats chose to press the button to recieve a shock to the brain excessively, to point where they were so addicted, they chose the button over, food, water, sex, and even risked pain and danger for it.

118
Q

what is the VTA?

A

Ventral tegmental area is 50% dopaminergic (producing?) neurons which project out to the nucelus accumbens and to the wider prefrontal cortex.

119
Q

what parts of the brain are the ‘human reward system’?

A

the nucleus accumbens and the VTA ventral tegmental area.

120
Q

what has DBS been used for?

A

on top of stopping trmeors in parkinsons disease, it has been used before in treatment resisten depression patients. putting the elctrodes ijnto the nucleus accumbens to stimuklate dopamine producing areas.

121
Q

neurons are the:

A

basic functional units of the nervous system

122
Q

the reflex is the:

A

simplest behaviour producing network. a simple automatic repsonse to a stimulus

123
Q

what are the 4 charactistics on a reflex?

A

stereotyped - not much variation
subconcious
unlearned
you are able to override/take control of most reflexes eg.blinking, not dropping hot coffee.

124
Q

what are some examples of reflexes?

A

eye blink, swallowing, pupil dilation, pilerection (hair raising), photic sneeze (10% population)

125
Q

what are alpha motor neurons?

A

neurons that are involved in muscle contraction

126
Q

what is monosynaptic stretch reflex?

A

monosynaptic (one synapse)
when you one muscle concentrically, signalls are sent back to the brain so the brain can eccentricly activate other muscles to counterbalance it. it is a reflex so it can be fast and not a conscious decision.

127
Q

what is a interneuron?

A

a local nueron that doesnt project far.

128
Q

what is synaptic inhibition?

A

there are some inputs from one cell to another that inhibit the overall making of transmission of AP and therefore make the overall change in membrane potential much less significant. when there are strong positive APs arriving at the synapse, and a negative AP, the negative AP will cancel out part of the positive AP.

129
Q

how do the body stop muscles from working against each other?

A

the reflexes inhibit certain muscles so they arent working against each other.

130
Q

what is the withdrawal reflex?

A

if you are touching something painful, the nervous system triggers an instant alpha motor neuron repsonse to move you out of harms way before the pain signal even has a chance to reach the brain

131
Q

explain a baby’s reflexes and why we no longer have them:

A

babies have a grasping (stimulation to hand, fingers close) and suckling (brush cheek, mouth suckles) reflexes to aid in survival. As the nervous system develops, higher order parts of our brain inhibit these reflexes.

132
Q

under what circumstances would the baby reflexes be disinhibited and why would doctors check this?

A

intoxication can cause disinhibition of the parts of the brain that inhibit the baby reflexes.
doctors may test these reflexes, as if the body shows the baby reflexes, that means that the more complex parts of the brain that inhibit them are damaged.

133
Q

what does VOR stand for?

A

Vestibulo Ocular Reflex

134
Q

what is the Vestibulo Ocular Reflex?

A

the VO is an inner ear system that detects head movement, and controls muscles that do eye movement.
the reflex means that our eyes can focus on a moving thing without us consciously deciding to. this maintains stable gaze.

135
Q

where are memories stored physiologically?

A

in the networks of the neurons. when an experience happens AP goes through a certain sequence of neurons (because certain neurons are triggered by different stimulus). the more an experience happens, the more synapses are between the neurons in this sequence so it is easier for AP to follow that trail. Memories are the reactivation of those neuron pathways so it is as if you are experiences that stimulus again.

136
Q

what are the 3 things that can increase the strength of synapses?

A
  • increase in neurotransmitter release
  • increase in postynaptic response
  • increase in physical synapses between neurons
137
Q

what test shows that memories are stored in synaptic pathways of neurons?

A

Rats were kept in an impoverished conditions (no stimulus) and were found to have very little synapses between neurons. they gained up to 2000 when they were moved to enriched conditions for 6mnths (even if they were already developed adults).

138
Q

what does IC, SC, EC mean?

A

impoverished conditon - no social, no toys
social condition - other rats, so toys
enriched condition -other rats and toys, most beneficial for creating memories.

139
Q

what did the 2000 synapse rat experiment show?

A
  • number of synapses can be changes, even in adults that have had stunted growth early on.
  • mental exercise strengthens brain and neural pathways.
140
Q

what is genetic memory?

A

inherited behaviours eg. agnostic displays/ facial expressions. we know that frown = sad/angry even though we havent been taught.

141
Q

what are the 4 memory levels?

A
  1. biological - brain systems, neurochem, genetics
  2. individual - perception, cognitive behaviour
  3. social - interpersonal behaviour, social cognition.
  4. cultural - thoughts, actions, behaviours
142
Q

memory on the individual level includes:

A
  1. encoding - conversion info/stimulus into a form that can be stored in memory.
  2. storage - the creation of a trace of this info within the nervous system
  3. retrieval - an attempt to recover a memory trace
143
Q

what is the order in which a memory is processed and how are memories lost?

A 
input > 
encoding 
v 
storage
v 
retrieval ......> forgetting
< output

forgetting can happen throughout the encoding and storage parts of the process.

144
Q

the memory system is capaple of:

A 
long retention (under certain cirsumstances)
massive capacity.
145
Q

who was the first person to investigate memeory?

A

Ebbinghaus 1850 -1909

146
Q

what did Ebbinghaus say?

A

Ebbinghaus’ forgetting curve:

  • the longer people have to retain something the more likely they are to forget it.
  • 40% less remember after 20 mins
  • 9hrs - 31 days is pretty much the same rate of remembrance.
147
Q

what kind of memeory is easier to remember?

A

things that are familiar/can be associated with something, we are reminded of them daily.

148
Q

what was the Peterson + Peterson experiment?

A
  • distraction reduces memory retension to the point that most people cannot remember 3 number after 18 seconds when concetrating on somethung else.
  • counting backwards from a number, trying to remember 3 letters at the same time.
149
Q

what was the miller experiment and when did it occur?

A

1956
you can only hold around 7 random numbers in your memory when instanting tested.
this shows that were can only remember things for years under certsin circumstances.

150
Q

memory can be split into the sub groups of:

A

short term/working memory, and long term memory.

151
Q

long term memory:

A

massive capacity, very slow (or no) forgetting

152
Q

short term/working memory:

A

processes for around 20s
only has certain processessing capacity
rapid forgetting

153
Q

what is the serial position effect/curve?

A

given 15 words each with a coresponding number, asked to remeber the words in order.
- closest to 1 and 15 were the easiest because words near the start had had the chance to reach long term memory and also at the start there were only a few words to remember. near the middle the STM proccessing capacity has reached max. near the end is STM.

154
Q

what are the 2 words to dscribe how long it has bee since the stimulus?

A

primacy and recency.

155
Q

when you distract people during the serial position tests what happens?

A

it inhibits their short term memory so they can remember the primary ones but not the recency ones.

156
Q

what is the evidence of existance of the 2 memory systems?

A
  • differential manipulation of primary + recency effects (delay before recency)
  • bias in encoding (phonetic - STM worse, semantic LTM worse)
  • medial temporal libe damage produces anterograde amnesia (LTM) with intact STM (H.M., may be able to remember long term after the damage but cant retain any new memories)
157
Q

what is maintenance reheasrsal?

A

repeatedly verbalizing something. not effective for LTM.

158
Q

Why is STM compared to a work bench?

A

because it has a certain processing limit but not a capacity limit.
active manipulation rather than passive maintanence

159
Q

what is AL and VSS?

A

2/3 of the STM
AL - phonological or articulatory loop (sounds)
VSS - visuo-spatial sketchpad (visual)

160
Q

explain the most recent theory on the process of memory:

A 
attention > 
AL + VSS + central executive 
v^
rehearsal 
retrieval

LTM

PYSCOLOGY (1 decks)

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