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NESC 3670: Genes, Brain & Behaviour > Lec 11: Cognition, Learning & Memory > Flashcards

Lec 11: Cognition, Learning & Memory Flashcards

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1
Q

what are Piaget’s 4 stages of cognitive development

A

Sensorimotor (birth–> 2 years)

preoperational (2-6 years)

concrete operational (6-11 years)

formal operational (12–> adult)

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2
Q

characteristics of the sensorimotor period (piaget)

A
  • use senses and motor abilities to understand world,
  • active learning
  • no conceptual/reflective thought
  • object permanence= learn object exists when out of sight
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3
Q

characteristics of the preoperational period (piaget)

A
  • think magically and poetically
  • use language to understand world
  • egocentric thinking
  • language becomes significant means of self-expression and of influence from others
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4
Q

characteristics of concrete operational period (piaget)

A
  • understand and apply logical operations,
  • interpret experiences objectively and rationally
  • thinking is limited to what can personally see, hear, touch, experience
  • learn to understand concepts of conservation, number, classification
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5
Q

characteristics of formal operational period (piaget)

A
  • think about abstractions and hypothetical concepts and reason analytically
  • can be logical about things they have never experienced
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6
Q

name some factors that influence human physical, cognitive and social-emotional development

A
  • epigenetics and early nutrition
  • genetics
  • age
  • pre-natal care
  • parenting
  • neurophysiology
  • disability
  • neural circuitry
  • stress factors
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7
Q

what did Karl Lashley study??

A

how is memory organized in the brain
- scraped mice cortex, more cortex removed= more problems getting through maze

  • law of mass action
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8
Q

what is the law of mass action?

A

the severity of the memory imparimentfor maze performance correlated with the size of the cortical area removed and NOT with its specific location

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9
Q

who was William Scoville and Brenda Milner?

A

Scoville= neurosurgeon, ‘psychosurgery’

Milner= neuropsychologist

–> Patient H.M.

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10
Q

describe patient HM

A
  • head injury at 7
  • first seizure at 10
  • first generalized convulsion at 16
    between 16-27 seizures became more frequent and severe (debilitating)
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11
Q

what was the treatment for HM?

A
  • hippocampus is epileptogenic= damage/lesions to one hippocampi as cure for epilepsy
  • experimental surgery performed by Scoville when HM was 27
  • both parts of L and R medial temporal loves (hippocampi) removed and amygdala
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12
Q

what brain tissue was removed form patient HM?

A

bilateral resection of medial temporal lobe

= hippocampus, amygdala, rhinal cortical areas

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13
Q

what was result following the surgery for HM?

A
  • massive anterograde amnesia following surgery
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14
Q

2 types of amnesia and were they spared or impaired for HM?

A

1) retrograde amnesia
- partially spared
- loss of memory events prior to the occurrence of the brain damage

2) anterograde amnesia
- impaired
- loss of ability to form new memory after brain damage occured

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15
Q

conclusions made about medial temporal lobe following surgery of HM?

A

critical for initial formation/encoding of new memory

  • not location where well-established long-term memories are stored
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16
Q

what was HM’s problem after?

A
  • unable to form new long term memories (anterograde amnesia)
  • difficulty with episodic and declarative memory

-

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17
Q

did HM still have short term memory?

this suggests??/

A

yes

STM/working memory remained intact

  • suggesting that hippocampus is vital for formation of new long term memories
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18
Q

what is episodic memory?

A

ability to recall single events

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19
Q

what is declarative memory

A
  • conscious memory
  • e.g. personal history
  • ability to put memory into words
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20
Q

what happened to HM’s procedural memory

A

remained intact

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21
Q

what is motor procedural memory

A

ability to develop motor skills (remembering or learning how to do things)

do not need MTL

e.g. mirror-tracing task

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22
Q

T/F the hippocampus is needed to process procedural memories

A

FALSE

  • it is NOT needed
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23
Q

name 3 locations where long-term procedural memories are strored

A
  • basal ganglia
  • cerebellum
  • motor cortices
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24
Q

what were the major findings of patient HM

A
  • memory could be impaired selectively without loss of other cognitive functions
  • memory function localized in the MTL
  • hippocampus key structure for memory
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25
Q

discuss impaired anterograde amnesia

A

inability to form new memories after onset of disorder

  • cannot learn new declarative memories (memories that are consciously recalled from the time of impairment)
    e. g. learn list of names, remember what happened yesterday
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26
Q

discuss spared retrograde amnesia

A

loss of memories formed before onset of amnesia

  • dont have memory before impairment
  • HM: childhood memories leading to surgery
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27
Q

how long are consolidation periods?

A
  • several years long

- lots of repetition before memory becomes hippocampal dependant

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28
Q

what are the 2 main kinds of long term memory?

A

declarative

nondeclarative (procedural

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29
Q

what is declarative memory?

A

things you know that you can TELL others

  • can be tested in humans because they talk
  • HM unable to form new declarative memories
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30
Q

what is nondeclarative memories

A
  • procedural
  • things you know that you can show by DOING
  • tested in other animals/humans
  • HM capable of this, exemplified by mirror-tracing
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31
Q

which form of long-term memory is MTL dependent?

A

declarative

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32
Q

what are the 2 subtypes of declarative memory

A

episodic

semantic

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33
Q

what is episodic memory?

A

events

  • autobiographical
  • e.g. remembering the first day of school
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34
Q

what is semantic memory

A

memory of facts

  • e.g. knowing capital of france
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35
Q

is episodic and semantic memory impaired by HM?

A

yes both are impaired

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36
Q

3 subtypes of nondeclarative memory

A
  • skill learning (learn to ride bicycle)
  • priming (more likely to use word you heard recently)
  • conditioning (salivating when see fave food)
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37
Q

explain 3 conditions in Pavlov’s experiment

A

1) unconditioned stimulus–> food–> dog salivates
2) conditioned stimulus–> bell + food –> dog salivates
3) dog associates bell with food–> bell–> dog salivates

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38
Q

what is skill learning (non-declarative)

A

learning to perform task requiring motor coordination

  • e.g. mirror drawing/mirror reading
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39
Q

what is conditioning?

non-declarative

A
  • association of 2 stimuli or of a stimulis and a response

e. g. Pavlov’s dog

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40
Q

brain structure critical for conditioning=

A

cerebellum

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41
Q

brain structure critical for fear conditioning?

A

amygdala

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42
Q

brain structure involved with episodic (declarative) memory

A
  • storage in cortex

- right frontal and temporal regions

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43
Q

brain structure involved with semantic (declarative) memory

A
  • storage in cortex

- temporal lobes

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44
Q

3 brain structures involved with skill learning (nondeclarative)

A
  • basal ganglia
  • motor cortex
  • cerebellum
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45
Q

2 subtypes of priming memory (nondeclarative)

A
  • perceptual

- conceptual

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46
Q

brain areas associated with perceptual (priming- nondeclarative) memory

A

reduces activity in bilateral occipito-temporal cortex

47
Q

brain area associated with conceptual (priming-nondeclarative) memory

A

reduces activity in left frontal cortex

48
Q

2 subtypes of condition (nondeclarative) memory

A

simple conditioning

complex conditioning

49
Q

brain areas associated with simple conditioning (conditioning-nondeclarative) memory

A

cerebellar circuit

50
Q

2 brain areas associated with complex conditioning (conditioning-nondeclarative) memory

A

hippocampus and cortex

51
Q

what is a method to test declarative memories in monkeys??

A

delayed non-matching to sample task

52
Q

what is the delayed non-matching to sample task??

A

test of object recognition memory

  • subject must choose object that was NOT seen previously
53
Q

if MTL is damaged is there impairment on delayed non-matching-to-sample task?

A

YES impaired

54
Q

describe steps in the delayed non-matching-to-sample task

A
  • monkey orignally presented with sample object
  • when he moves it, finds food under
  • after delay, monkey is presented with original object and another object
  • over series of trials with diff pairs of objects, monkey learns that food is present under the object that differs from the sample
55
Q

what happens if monkey had amygdala-hippocampus lesion?

A

reproduced similar lesion to HM

  • performance was close to chance
  • anterograde amnesia impairment in performance
56
Q

what happens if have separate amygdala or hippocampus lesion?

A

A= little impairment

H= little impairment

57
Q

what is the overall conclusion regarding the hippocampus??

A

it is key to anterograde memory impairment

58
Q

what was discovered with patient RB?

A

specific areas of the hippocampus (CA1 region) were involved in memory

59
Q

describe patient RB

A
  • age 50, diagnosed with angina
  • ischemica brain injury during heart bypass surgery
  • killed cells in CA1 subfield of hippocampus
60
Q

what area of hippocampus was patient RB cells killed?

A

CA1 subfield of hippocampus (bilateral damage)

61
Q

what happened to patient RB’s memory???

A

impaired anterograde memory (Declarative memory) and partially impaired retrograde memory (similar to HM)

62
Q

theory of consolidation

A

describes how LTM is stored in the brain

  • MTL is important for variable amounts of time as memories “consolidate” or strength with practice
63
Q

which 4 areas participate in plasticity that underlies fact and event memories that are dependent on cortical stuctures

A
  • hippocampus
  • cortical circuit
  • perirhinal cortex
  • entorhinal cortex
64
Q

list 6 stages of NT transport/function in neuron

A

1) AP reach terminal
2) voltage-gated Ca channels open
3) Ca enters axon terminal
4) NT is released and diffuses into cleft
5) NT binds to postsynaptic rec
6) NT removed from synaptic cleft

65
Q

Charles Sherrington speculated that….

A

alterations in SYNAPSES were basis for learning

66
Q

what were the changes that Charles Sherrington found?

A
  • changes in presynaptic or postsynaptic (or both)
  • changes can include NT release, or effectiveness of receptors
  • structural changes at synapse may provide long-term storage
  • new synapses could form or some could be eliminated with training
  • training/experience might lead to synaptic reorganization
67
Q

as memory training occurs= inc/dec in post synaptic potential?

A

INC

68
Q

what are other outcomes that appear after training??

A
  • changes involving synaptic transmitters
  • changes involving interneuron modulation
  • formulation of new synapses
  • rearrangement of synaptic input
69
Q

what occurred when used animals to measure brain changes?

A

lab animals living in complex environment demonstrated biochemical and anatomical brain changes from those living in simpler environments

70
Q

list the 3 housing conditions while testing lab animals

A
  • standard condition (SC)
  • impoverished/isolated condition (IC)
  • enriched condition (EC)
71
Q

animals housed in EC (vs IC) developed:….. (3)

A

1) heavier, thicker cortex
2) enhanced cholinergic activity
3) more dendritic branch with more dendritic spines= more synapses

72
Q

where does the inc in dendritic branches (in EC mice) occur?

A

basal dendrites

** near cell body

73
Q

what is Hebb’s Law??

A

when an axon of cell A is near enough to excite cell B and repeatedly/persistently takes part in firing it

some growth process or metabolic change takes place in oen or both cells

such that A’s efficiency as one of the cells firing B, is inc….

*** synapses grow stronger when the presynaptic neuron repeatedly causes postsynaptic cell to fire

74
Q

phrase that Hebb made famous?

A

neurons that fire together, wire together

75
Q

what are cell assemblies/

A

ensembles of neurons

linked via Hebbian synapses

could store memory traces

76
Q

Hebbs Law: synapses grow ____ when presynaptic neuron ____ causes the postsynaptic cell to ____

A

Synapses grow STRONGER when the presynaptic neuron REPEATEDLY causes the postsynaptic cell to FIRE.

77
Q

what is a Hebbian synapse?

A

occurs when the successful stimulation of a cell by an axon leads to the enhanced ability to stimulate that cell in the future

  • INC in effectiveness occur b/c simultaneous activity in presynaptic and postsynaptic neurons (critical for associative learning)
78
Q

which invertebrate is commonly used to study how physiology relates to learning

A

aplysia (slug-like)

–> large neurons

79
Q

what is habituation?

A

dec in response to stimulus that is presented repeatedly and accompanied by no change in other stimuli

80
Q

what is the result of habituation?

A

change in synapse between sensory neurons and motor neuron s

  • sensory neurons fail to exite motor neurons
81
Q

what is sensitization?

A

inc in response to mild stimulus, result to previous exposure to more intense stimulus

82
Q

chronic stimulation of receptors leads to ….???

A

habituation

83
Q

name 2 changes at identified synapses due to sensitization

A
  • 5HT released from facilitating neuron blocks K channels in presynaptic neuron
  • prolonged release of transmitter from neuron results in prolonged sensitization
84
Q

name 2 advantages to using Aplysia

A
  • fewer nerve cells (large neurons)

- can create detailed circuit maps for particular behaviours (little variation between individuals)

85
Q

explain how habituaiton is studied in Aplysia

A
  • squirt water on siphon, causes it to retract its gill
  • after repeated squirts, animal retracts gills less; learned water poses no danger

** short-term habituation

86
Q

habituation in Aplysia is caused by …

A

synaptic changes between sensory cell in the siphon and the motoneuron that retracts the gill

  • less transmitter released in the synapse results in less retraction
87
Q

habituation of Aplysia over several days results in ….

A

animal habituates faster

= long term habituation

  • # of synapses between sensory cell and motoneuron is reduced
88
Q

long-term habituation in Aplysia is due to

A
  • squirted repeatedly over days
  • fast habituation
  • retraction of synaptic terminals from sensory neurons onto motoneurons
89
Q

LTP means??

A

long-term potentiation

90
Q

LTP was first described by??

A

Bliss and Lomo 1973

91
Q

where was LTP first discovered?

A

at glutametergic synapses in hippocampal formation

dorsal hippocampus of anaesthetized rabbit was exposed

92
Q

high freq stimulation of perforant pathway fibers (inputs) to dentate gyrus cells produces…

A

INC in amplitude of excitatory postsynaptic potentials (EPSP) lasting hours/days

93
Q

short term habituation = more/less NT release?

A

LESS

94
Q

synaptic plasticity can be measured in….

A

hippocampal circuits

95
Q

modification to the postsynaptic site due to training results in

A

higher post synaptic potentials

  • cells have more rec= more responsive to less signal
96
Q

what is PEPSP?

A

population excitatory postsynaptic potential

97
Q

PEPSP is important for (2)

A

learning and memory

98
Q

what is facilitation?

A

amplitude of postsynaptic response inc when postsynaptic cell is activated several times in quick succession

99
Q

what is tetanus?

A

brief inc of electrical stimulation that triggers 1000s of axon potentials

100
Q

what is LTP?

A

long term potentiation

stable and enduring inc in effectiveness of synapses

101
Q

LTP occurs where??

A

hippocampus

102
Q

describe 3 ways in which synapses in LTP behave like Hebbian synapses

A
  • tetanus drives repeated firing
  • postsynaptic targets fire repeatedly due to the stimulation
  • synapses are stronger than before
103
Q

when does LTP occur?

A

when 1+ axon bombard dendrite with stimulation

104
Q

result of LTP (to the synapse)

A

leaves synapse “potentiated” for period of time and neuron is more responsive

105
Q

3 properties of LTP suggesting it as a cellular basis of learning and memory

A

1) specificity
2) co-operativity
3) associativity

106
Q

what is specificity (LTP)?

A

only synapses onto a cell that have been highly active become strengthened

107
Q

what is co-operativity (LTP)?

A

simultaneous stimulation by 2+ axons produce LTP much more strongly than does repeated stimulation by a single axon

108
Q

what is associativity (LTP)

A

pairing a weak input with a strong input enhances later responses to a weak input

109
Q

LTP occurs at several sites in the ____ ___ which is formed by what 3 areas/

A

hippocampal formation

  • hippocampus
  • dentate gyrus
  • subiculum
110
Q

name 3 regions of the hippocampus

A

CA1
CA2
CA3

CA= cornus ammon

111
Q

what is long-term depression?

A

prolonged dec in response at a synapse that occurs when axnns have been active at a low freq

** opposite of LTP

112
Q

biochemical mechanisms of LTP depend on changes in ____ synapses on postsynaptic neuron

A

glutamate synapse

113
Q

changes in glutamate synapses due to LTP occur at which ionotrophic rec?

A

AMPA receptors

NMDA receptors

NESC 3670: Genes, Brain & Behaviour (12 decks)

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