Lecture 10 - Learning and memory Flashcards

1
Q

Define learning?

A

And adaptive process in which the tendency to perform a particular behaviour is changed by experience
- system tries to adapt to changes in environment
Experiences causes change physiological changes to nervous sytem
- circuits involved in perceiving, performing, thinking and planning are modified

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2
Q

Define long term potentiation

A

Involved in synpatic plasticity
- makes synapses more potent/ strengthens connections
- requires a combination of :
• membrane depolarisation
• activation of NMDA receptors (Ca2+ calcium(

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3
Q

What do learning theories focus on?

A

focus on acquisition processes

  • how infor gets into the system
  • influenced by distraction
  • once info is in, we retrieve it
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4
Q

What do memory theories focus on>

A

focus on retention and retrieval processes, consolidation of info - how we get info back

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5
Q

What are the 4 types of learning?

A
  1. S-R learning
  2. motor learning
  3. perceptual learning
  4. Relational learning
    - all linked to different areas of the brain
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6
Q

Outline SR learning

A

Connects perception/ stimulus to movement/ response, to anticipate stimulus

  • can be automatic (reflex) or a complicated movement
  • CC must regularly offuc prior to presentation of UCS and CS shouldnt regularly occur without UCS
  • operant: Thorndike/ skinner, fruit loops maze thing - we learn via operating on our environment
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7
Q

What did Donald Hebb say/do?

A

he added a physiological basis to SR learning, argued learning involves:
• synaptic plasticity - changes in structure/ biochemicstry that changes how they effect post-synaptic neurons
WHAT FIRES TOGETHER, WIRES TOGETHER

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8
Q

What is Hebbs Rule?

A

If neuron A is active and trying to fire on neuron B, the connection could be strengthened via a plastic change. If Neuron B is receiving strong input from elsewhere (AP’s), it forms a better connection with neuron A as Neuron A is constantly there
- This explains condition/associative learning as neuron A becomes associated with the AP’s of Neuron B

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9
Q

What does Hebb therefore define memory as?

A

Change in synaptic strength/weight

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10
Q

What were Pavlov’s view of the physiology of learning?

A

CC reflected a strengthened connection between a brain area that represented cs and a brain area that represented UCS

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11
Q

What did Lashely (1929,1950) do?

A

Wanted to investigate CC in the brain, removed portions of rat brains. He found:
• More brain removed = more problems with learning
• Doesnt matter where ,always worse at learning
• cut through connecting fibers = gneralised locatlisation about which areas do what
Falsely concluded that:
- memories were widely/ evenly distributed across the brain

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12
Q

What did damage in animal studies prove?

A

Damage to Amygdala = no reinforcement/ conditioning

Damate to PFC = differences in goal directed behaviour which leads to reinforcement - struggle with behaviour that brins us towards a goal

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13
Q

What did animal studies with dopamine show?

A

it Induces synpatic plasticity by facilitating LTP
- does this in the nuclues accumbens, amygdala and PFC
- important for memory consolidation - expecting a reward
Amygdala is important for LTP - it is the physiological version of wiring then firing together

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14
Q

Define perceptual Learning

A

Result of changes in synaptic connections within SENSORY ASSOCIATION CORTEX

  • connections are reinforced, so we know which 2 stimuli go together
  • fMRI shows that memories of pictures, sounds, movements or spatial locations activate the appropriate areas of SAC
  • sounds are in occiptal love - which then goes to inferior temporal and parietal lobe
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15
Q

What does dame to inferior temporal cortex do?

A

Problems in visual discrimination

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16
Q

which areas are important for CC?

A

Info between CS and UCS converges in LATERAL AMYGDALA

  • high frequency stimulation to lateral amygdala leads to LTP
  • blocking NMDA receptors here prevents CC
17
Q

What areas apart from amygdala are important for CC

A
  • Supplementary motor area (learning sequences of movements)
  • Pre motor area - selecting movements to make in response to stimli
  • Basal Ganglia - involved in automated responses - why there is no automated responses in parkinsons
  • ventral Tegmental area - lots of dopamine here
18
Q

Where does VTA project to?

A

• Amygdala/ lateral hypothalamus
- Neurons fire in response to stimuli capable of reinforcing behaviour or pleasurable things

  • PFC - plans for movement, select movement/sequence/bodypart
  • Nucleus accumbens - reinforces behaviour - addiction
19
Q

In terms of perceptual learning, what did DAVIS & SQUIRE (1984) argue?

A

Argues that perceptual learning involves changes in brain chemistry. Found that when animals were trained:
• INcreased productino of chemicals (RNA)
• increased production of proteins

20
Q

Outline SQUIRES MODEL (1987)

A

Info -> visual cortex -> prestriate cortex -> inferior temporal cortex

21
Q

Outline Wernicke-Korsakoff syndrome

A

Extreme ANTEROGRADE amnesia (alcohol amnestic syndrome)
- Fixed n time, cant learn anything new, think youre still young
- OFten caused by alcohol (vitamin B1, Thiamine deficiency)
Caused by damage to:
• thalamus and mamillary bodies (hypothalamus - gets input from hippocampus via fornix)
- areas crucial for learning and memory

22
Q

What are the symptoms of wernickes - korsakoff syndrome?

A
  • Apathy, lack of insight, confusion, confabulation

* Disruption to front lobe functioning (reality checks)

23
Q

Outline patient HM

A

had Severa anterograde amnesia - due to a bilateral removal of temporal lobes to treat epilepsy (including hippocampus)
• couldnt form new, but could remember old, like korsakoff

24
Q

Outline DONALD WEBB (1949)

A

argued that no one mechanism could be rapid enough for immediate memory, but stable enough for permanent memory, argued there must be two things

25
Outline Miller (1956)
7+- 2 chunks - meaningful group of stimuli which can be stored in stm, lasts for 6-12 seconds unless repeated
26
outline MSM
• LTM has huge capacity, touble due to interferance - lasts indenfinitely, mainly semantic coding, organisation is crucial for recall • Sensory registratial stores raw uncoded info • STM is stored acoustically/ visually via rehearsal -Acoustice = auditory loop - Visual - visio-spatial sketchpad
27
OUtline LTM
- Unlimited storage | - relatively permanant biochemical strucutural changes in neurouns resulting ni lasting changes in synaptic change
28
Describe HM's hippocampus damage
- Still had some perceptual learning (if its implicit, not explicit) - as implicit isnt in hippocampus - Still had some S-r learning (e.g. eye blink response) - as its amygdala, not hippocampus - still have some motor learning - e.g. sequence button pressing, mirror drawing
29
What are the 2 types of LTM and who proposed them?
TULVING 1972 | - Semantic, episodic
30
Describe the taxonomy of memory
Knowledge -> split into 2: 1. Non-declaritive/ implicit/ procedural - mental implicit - motor SR learning 2. Relational/explicit/declaritive - episodic (stm-ltm) - semantic (general knowledge)
31
Outline Non-declaritive/ implicit/ procedural
- unconcious, not deliberately learned - SR learning, conditioned emotional response - requires AMYGDALA AND DOPAMINE - Motor learning requires BASAL GANGLIA - Perceptual learning requires INFERIOR TEMPORAL CORTEX
32
outline Relational/explicit/declaritive
- explicit, concious learning about acts, events, people, stimuli - relational requries HIPPOCAMPUS
33
how is the limbic system involved in memory?
- responsible for emotion, memory and motivation - found in border of cortex and subcortical areas Areas include: • FORNIX - conncets hypothalamus to cerebrum • THALAMUS - relay station • HIPPOCAMPUS - memory • SEPTUM - plesure centres (particularly sexual) • AMYGDALA - emotional reactions (fight or flight), at end of hippocampus, rewards, LTP, consolidates hippocampus memories,
34
how is the hippocampus involved in memory?
• olfactory bulb • olfactory tract • mammilliary body - hippocampul circuit - important for alzheimers
35
What are symptoms of alzheimers?
``` - form of dementia, prevalent in old age • progressive memory loss • cognitive problems (planning, language etc) • confusion • depression • hallucinations • sleep pattern changes ```
36
What are the bio causes of alzheimers?
1. Neurons degenerate - dying axons/ dendrites form tangles and plaques. Gets progressively worse - they wither, thin out and die - struggle with LTP, cant consolidate 2. Disrupted ACH production - a NT which helps neurouns communication, sends axons to hippo campus 3. Severe degeneration of hippocampus - 1st effected, causes loss of episodic memories, association cortex of frontal and temporal lobes - SHELINE (2004) - those with depression had smaller hippocampi
37
Which 2 temporal lobe areas are implicated in dementia?
1. Lateral temporal lobe | 2. Medial temporal lobe
38
Outline how the Medial temporal lobe is involved in dementia
- One of the 1st areas damaged by alzheimers - it includes/effects: • hippocampus • episodic memory • anterograde amnesia (later on: retrograde too)
39
OUtline how lateral temporal lobe is involved in dementia
- lateral = outside - damaged by semantic dementia (different type) - loss of memory for facts, episodic is in tact.