Learning and Memory Flashcards

1
Q

Describe the multi-store model of memory by Atkinson and Shiffrin (1968).

A
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2
Q

What were the important points from the multi-store model of memory?

A
  • Process such as rehersal or retrieval were distinct from storage boxes.
  • Each type of storage box in memory were thought to have characteristic what information they took (encoding), how long they kept the information (duration) and howmuch information could be put into the stores (capacity).
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3
Q

Describe sensory memory.

A
  • Duration - 1/4 - 1/2 second.
  • Capacity - all sensory experience (very large capacity).
  • Encoding - sense specific (e.g. different stores for each sense).
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4
Q

Describe short-term memory.

A
  • Duration - 0-18 seconds.
  • Capacity - 7+/- 2 items.
  • Encoding - mainly auditory.
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5
Q

Describe long term memory.

A
  • Duration - unlimited.
  • Capacity - unlimited.
  • Encoding - mainly semantic (but can be visual and auditory).
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6
Q

What is the primacy and recency effect?

A
  • Glanzer and Cunitz showed that when participants are presented with a list of words, they tend to remember the first few and last few words and are more likely to forget those in the middle of the list, i.e. the serial position effect.
  • Supports the existence of separate LTM and STM stores because they observed a primacy and recency effect.
  • Words early on in the list were put into long term memory (primacy effect) because the person has time to rehearse the word, and words from the end went into short term memory (recency effect).
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7
Q

What happens to the primacy and recency effects in disease?

A
  • They start to go in various brain diseases, rather like reflexes will diminish in neurodegenerative diseases.
  • Primacy and recency diminish in AD or tauopathy, in the cognitive impairment in Autism or some traumatic brain injury.
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8
Q

Outline the hypothesis of Craig and Lockhart (1972).

What happens to this hypothesis in disease?

A
  • How we could predict forgetting?
  • The ‘levels of processing’ model said that the more meaningful the material encoded and stored, the more likely they would be to be recalled and not forgotten.
  • The deeper you processed your memories the more likely they would be to be recalled.
  • Memories which are self-referent, personally meaningful, are better remembered.
  • In disease, this rule fails:
    • You will find that personally meaningful memories will be forgotten just as easily as less important memories.
    • Some with mental health problems will fail to recall hugely important things, or helplessly over attend to the minutia.
    • The rule that we tend to remember and not forget what is meaningful to us does not apply.
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9
Q

Outline the hypothesis of Baddeley and Hitch (1974).

A
  • Their working memory model was developed because the short term memory model did not explain all the factors in STM.
  • They further split short term memory into verbal and non-verbal components, controlled and overseen by a ‘central executive’.
  • Why? Because the previous model did not explain how we learned to play chess, how we could not sometimes cope with 2 things at once, such that talking about fishing while you are trying to memorise a song will slow you up.
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10
Q

Describe the working memory model - how we get short term to long term memory.

A
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11
Q

Outline the supervisory attentional system (Norman and Shallice, 1980).

A
  • Proposed (a bit like the central executive) there was something that controlled what we attended to in order to remember new things, and what was so ‘overlearned’ that we recalled how to do this or that without full conscious awareness (‘I could do that in my sleep’ sort of tasks).
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12
Q

Describe the idea of ‘supervisory’ control of attention and memory.

A
  • They figured some sort of system had to control when we needed to ‘consciously attend’ when information was new, emotional or more complex.
  • So, when we are in danger or threatened, when we are learning something new, when something changes requiring different action than habit, the SAS switches out of automatic into conscious attention.
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13
Q

What brain structures are involved in different sorts of memory?

A
  • Mapping different sorts of memory onto different part of the brain involves these sorts of different memory processes.
  • Memory for events and facts = episodic memory.
  • Memory for automatic ‘how to do things’ = procedural memory.
  • This research also uses the concepts of short and long term memory and attention (as we have been discussing).
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14
Q

What aspects of memory are controlled by the prefrontal cortex?

A
  • The prefrontal cortex is involved in attention, short term memory and is implied in retention of long term memory.
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15
Q

What aspect of memory is controlled by the medial temporal lobe?

A
  • The medial temporal lobes are onvolved in conscious learning and ‘episodic’ memory.
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16
Q

Describe the circuit of Papez.

A
  • Everything which affects the medial temporal areas affects memory.
17
Q

Describe the role of the medial temporal lobe in memory.

A
  • The medial temporal lobe feature of the limbic system, which has the hippocampus, the amygdala, the cingulate gyrus, the thalamus, the hypothalamus, the mamillary body and other organs, are all involved in processing memory of one kind or another.
  • The hippocampus, for example, is essential for the transference from short term memory, and for the control of spatial memory and behaviour. The hippocampus, unusually, can grow new neurons, although this ability is impaired by stress-related glucocorticoid.
  • The amygdala also performs a primary role in the processing and memory of emotional reactions and social and sexual behaviour, as well as regulating smell.
  • The basal ganglia is a sub-cortical system (inside the cerebral cortex) essential to memory function, particularly the striatum (or neostriatum) which is important in the formation and retrieval of procedural memory.
18
Q

Describe Wernicke-Korsakoff’s syndrome.

A
  • Amnesia, confabulation, no insight, usually alcohol related, maybe eye movement abnormalities (ophthalmoplegia, confusion, ataxia = Wernicke’s encephalopathy.