Memory Representation in the Temporal Neocortex Flashcards

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1
Q

What does the Hippocampus allow?

A

recollection of episodes
-> our ability to join together the different elements of memory in order to allow us to recollect memory later

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2
Q

what can recollective experiences be known as?

A

mental time travel

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3
Q

According to Tulving (1972), there are two types of declarative/explicit long-term memory available to consciousness. What are these?

A
  • event/episodic memory
  • semantic memory
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4
Q

episodic memory

A

dependent on hippocampus and impaired with amnesia

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5
Q

what is the other type of LTM as suggested by Tulving (1972)?

A

non-declarative / implicit

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6
Q

semantic memory

A

factual knowledge about the world and preserved in amnesia

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7
Q

episodic memory (according to Tulving, 1972)

A
  • events
  • mental time travel (temporarily bound memory about a mode in time)
  • self-referential -> you are the centre of information (self moves through time and space, and when you recollect events you see them from your own perspective)
  • fragile, easily forgetten
  • Affected in amnesia
  • Better when young (declines in older adults)
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8
Q

semantic memory (according to Tulving, 1972)

A
  • facts
  • time/place NOT coded
  • NOT self-referential -> separate from oneself - the concept of who you are doesn’t contribute very much
  • more consolidated / durable
  • not affected in amnesia (spared)
  • better when old (i.e. Ronnlund et al. (2005) -> better time to accumulate knowledge about the world
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9
Q

Patient KC developed amnesia after a motorbike accident, what were their episodic memory like?

A
  • inability to remember recent and new events
  • severely impaired retrograde -> inability to remember events before the accident [this includes the period of time where he was working as a skilled machinist] -> he has a rich vocab and concepts about these tools but cannot remember using these tools or requiring them
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10
Q

Patient KC developed amnesia after a motorbike accident, what were his semantic memory like?

A
  • retained some concepts gained as a machinist i.e concepts about tools like keyway shank and feed screw
  • knowledgeable about how to change a tire but cannot remember ever changing one (episodic)
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11
Q

KC tasks about his accent, what is this an example of?

A

personalised semantic memory (learning a new piece of information about themselves but its not a rich detail or recollection of an experience)

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12
Q

what is KC an example of?

A

single dissociation
-> deficit of one domain (episodic) and preservation of another (semantic)

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13
Q

how can we argue that there are two separate systems supporting different aspects of knowledge?

A

a double dissociation -> you need other patients who show the reverse impairment (impairment of semantic but not episodic memory)

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14
Q

why is a single dissociation viewed as insufficient to demonstrate separate systems?

A

episodic memory might be more vulnerable to damage than semantic memory within a single system

  • having a single dissociation is thought to be insufficient to show you’ve got two separate systems because some tasks are harder than others
  • if you have some degree of brain injury then some of the harder tasks might be more easily impaired than easy tasks -> or perhaps episodic memory is just more difficult (perhaps all memory captured in the hippocampus but episodic impairs first because it’s harder)
    -> to prove this is not the case, we need to find individual’s who hippocampus is spared yet has problem with semantic memory in different brain region)
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15
Q

why do people often show issues with episodic and semantic memory?

A

anterior temporal lobe and hippocampus are exceedingly close together

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16
Q

what types of double dissociations can we look at to test if semantic and episodic memory are from two different systems?

A

amnesia (episodic impaired, semantic preserved) and semantic detention (semantic impaired, episodic preserved)

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17
Q

what is a key deficit in semantic dementia?

A

poor understanding of words and objects
-> semantic memories deficits encompasses all aspects of knowledge about the world (i.e. concepts etc)

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18
Q

what is semantic dementia?

A
  • subtype of frontotemporal dementia (FTD) -> bilateral atrophy in the anterior temporal lobe (peak of atrophy is in the ventral of anterior temporal lobe -> right next to/beside the anterior part of the hippocampus)
  • progressive loss of conceptual knowledge across modalities
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19
Q

What did Jefferies et al. (2006) find about episodic memory in semantic dementia patients in a double dissociation with amnesia?

A

relatively intact memory for recent events (able to recall experiences) and impaired semantic memory (cannot name particular concepts)

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20
Q

(Graham et al., 2000)
Patients with SD were asked to recognise objects and later on were asked to pick out which of the three objects they had seen previously
* Condition 1: was exactly the same (had to pick up perceptually identical object)
* Condition 2: had to pick a perceptually non-identical version of the object (same concept of the one you studied earlier)

Looked at which words people could still use: picture naming and picture matching as well -> sort items into two types: semantically known and semantically unknown
-> In SD: As their semantic memory degrades, particularly ideas are affected. And these particular ideas are affected across all tasks and modalities -> reliable fashion, consistent with the idea the concept itself is degrading (i.e. persevered concept of a telephone but not a television)

A
  • SD patients can recognise objects when they are identical
  • for non-identical objects meaning is important. Performance is predicted by which items are still understood on semantic tests
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21
Q

What did Graham et al. (2000) find (in detail)

A
  • If item is still known, able to recognise all of the objects -> they could do if they knew the idea in both conditions when it was perceptually identical and perceptually different
  • When they didn’t know the idea (semantic impairment), their episodic memory for the perceptual identical items were still good but they do struggle for perceptually non-identical ideas
    â—‹ Shows episodic memory in many ways is preserved in semantic dementia (3/4 of these conditions) -> people can have normal visual recognition performance
    ○ BUT this is not the case for amnesia because they wouldn’t even remember looking at the pictures
  • Shows semantic memory does contribute to certain types of memory if you cant rely on perceptual features to recognise an object then you have to rely on semantic, and if it’s degrading then performance will be impaired
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22
Q

What do Patient KC and studies of semantic detention provide us with?

A

a double disocciation between episodic and semantic memory
* difference between hippocampus and anterior temporal lobe

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23
Q

what is the hippocampus responsible for?

A

encodes and recreates unique multimodal experiences of people/places/objects in events (i.e. episodic memory)
-> allows us to separate experiences from all the other experiences we’ve had (by binding them together, the unique elements allow us to separate memories

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24
Q

what is the ATL responsible for?

A

extraction of similarities between multimodal experiences to create concepts (i.e. semantic memory)
-> may be critical for seeing similarities between different experiences, extract information which is common across these experiences in order to form conceptual information that can predict things which will be similar in the future

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25
Q

what is the complementary learning system hypothesis?

A
  • building complementation model which can stimulate brain responses and the effect of brain injury -> shows you can build computer models that stimulate the effect of learning in the hippocampus and ATL
    -> hypothesis suggests that the hippocampus and ATL work differently

-> idea that hippocampus and ATL have different memory jobs and complementary roles to play in our cognition links to this

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26
Q

what does hypothesis suggest about the hippocampus?

A

FAST learning in the hippocampius

  • hippocampus neurons learn really quickly and bind together elements from unique episodes -> capture episodic memories in one go for unique memory that occurs on time
  • uses sparse code (relatively few neurones for each item, allowing us to separate unique memories -> as different neurones are involved)
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27
Q

What does the hypothesis suggest about the ATL?

A

SLOWER learning in the neocortex to extract similar features which happen across multiple experiences

  • similar features shared by multiple experiences are encoded strongly
  • useful for semantic category learning
  • prevents catastrophic interference -> loss of old memories when new material is learned (way cortex learns to avoid this problem)
  • by turning down learning rate, the model overcomes catastrophic interferences allowing memories to be formed from multiple experiences that happen over a long period of time
  • This slow learning allows us to then understand why memories are better for more frequent things
  • Can also explain why semantic concepts have features which are very strong part of the concept which tend to occur in all the different learning exemplars and then peripheral features which are sometimes true (dogs are brown, but they aren’t all brown)
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28
Q

what is emotional memory?

A

emotional valence is formed quite slowly as a concept and something largely intact during amnesia
* more semantic than episodic

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29
Q

what is the opposite view to two distinct systems for episodic and semantic memory?

A

transfer of information from hippocampus to neocortex in memory consolidation during sleep

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30
Q

what does Squire suggest about episodic and semantic memory?

A

hippocampus has time-limited role
-> system consolidation (information being transferred to the neocortex)

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31
Q

Kim & Fanselow (1992). What are the differences between synaptic consolidation and system consolidation.
Synaptic consolidation:

  • looking at inhibiting the synthesis of proteins at the synapse in the hippocampus and at the impact of inhibiting protein system on the duration of memory
    i.e. a drug prevents any structural changes happening as a consequence of learning
A

Inhibition of protein synthesis which allows structural changes at the synapse in long-term potentiation
-> disrupts memory for 1hr

  • if you impair protein synthesis an 60 or 90 minutes after learning, it visually has no impact on how much the rat remembers later on
    -> suggesting most changes happening at the synapse are down to LTP and happening in the first hour after learning
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32
Q

Kim & Fanselow (1992). What are the differences between synaptic consolidation and system consolidation.
System consolidation:

A
  • if you lesion the hippocampus immediately after learning something, memory will be really poor
  • if you lesion / damage hippocampus, two weeks after the memory has been formed, the rat only forgets 50% of what was encoded -> some but not all of the information has been transformed out of the hippocampus
  • a month after encoding, a little bit of memory loss but it’s memory will be pretty good -> perhaps the hippocampus is still playing some kind of role which is why a tiny bit of memory is lost
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33
Q

what can we conclude about hippocampus damage after learning occurs?

A

when hippocampus is damaged AFTEr learning has occurred, memories are especially vulnerable if they were only recently acquired. While older memories are more preserved.

34
Q

What happens to the older memories for them still be preserved?

A

perhaps they travel out of the hippocampus

35
Q

there is a similar ‘temporal gradient’ in amnesia. What does this refer to?

A

Poorer retrograde amnesia for recent than more distant events

36
Q

what is the gradient of retrograde amnesia?

A

if you have case of amnesia, there will be an impairment of all the newly acquire memories since the brain injury (anterograde amnesia)
-> as well as loss of memories that happened before the brain injuries (retrograde) -> but won’t tend to affect younger, earlier acquired memories, instead it gets more severe the close you get to the brain injury date and time

37
Q

what is the gradient of retrograde amnesia? / layout

A
  • events that happened well before brain injury are spared
  • BUT events that happened just before brain injury are impaired
  • ongoing events that happened after brain injury are severely impaired (anterograde amnesia)
38
Q

what might happen to these older memories?

A

may transfer information out of the hippocampus
-> if memories are dependent on hippocampus for some time, then they will be lost if there is injury BUT those which have already been transported out will be spared

39
Q

Graham & Hodges (1997) looked at temporal gradient in amnesia.
* Control and Alzheimer disease patients were compared to SD patients
* had to come up with an autobiographical memory where they saw a river.

What did they find for the control?

A

good at coming up with autobiographical memories

-> mental time travel, with people and objects
-> specific events all coming together

40
Q

Graham & Hodges (1997) looked at temporal gradient in amnesia.
* Control and Alzheimer disease patients were compared to SD patients
* had to come up with an autobiographical memory where they saw a river.

What did they find for AD/amnesia?

A

Better preserving childhood memories

  • impairment with temporal gradient -> recall more childhood and early adult memories but fewer more recent memories

-> consistent with the idea that the hippocampus is important for maintaining recent memories, for learning but older memories may be spared in this conditions

41
Q

Graham & Hodges (1997) looked at temporal gradient in amnesia.
* Control and Alzheimer disease patients were compared to SD patients
* had to come up with an autobiographical memory where they saw a river.

What did they find for SD?

A

Better perserved recent memories (around 4 years)

  • severely impaired at recalling childhood and early adulthood events

-> old memories transferred out of hippocampus into temporal neocortex (anterior temporal lobe becomes dependent on the semantic system)
-> semantic system declines = childhood memories more affected

42
Q

Temporal Gradient in Amnesia (Cermak and O’Connor, 1983)

A

Older memories have been retrieved more times -> changes their quality (and neural basis); they become more story-like and reliant on semantics
-> becomes like antedote and loses it episodic quality and is all dependent on semantics

43
Q

why may recent and remote memories have different quality?

A

can recall your breakfast in vivid detail but trying to recall a birthday party as a child may be really hazy -> can recall some things but not the whole experience (little fragments)

44
Q

what do older memories become more reliant on? (explaining temporal gradient in amnesia - Squire, 1992)

A

neocortex and less dependent on the hippocampus overtime, following consolidation

45
Q

How does encoding work?

A

place (parahippocampal), object (inferior temporal cortex) and familiar character (anterior temporal lobe) co-occur in time so they are bound together in the hippocampus

46
Q

What happens with encoding in patients with amnesia?

A

impaired -> poor learning of new events

47
Q

why is encoding impaired in amnesia

A

events co-occur in time so they are bound together in the hippocampus
-> those with hippocampal damage (amnesia) cannot learn new events because they cannot bound together in the hippocampus

48
Q

how does retrieval work before consolidation?

A

Go back to the location it happened
-> hippocampal memory activates and reconstruct the object and the person who was there at the time

49
Q

when will retrieval in amnesia patients to impaired?

A

poor retrieval of events just prior to the brain injury because that memory will be dependent on the hippocampus which is important for reconstruction of memory

50
Q

what happens to retrieval after consolidation has happened?

A

a direct cortical pathway has been constructed between same elements which don’t rely on the hippocampus

i.e. link place to object via cortical connections

51
Q

what happens to retrieval after consolidation in patients with amnesia?

A

not impaired -> normal recall of childhood events

52
Q

how do memories connections work?

A

connections start to form between the cortical areas allowing the hippocampal connections to weaken
-> can still recover the memory
-> eventually you’ll have a dense connection in the context which captures the memory very well and the original hippocampal connectivity becomes unnecessary

53
Q

what drives consolidation? (as suggested by Gaskell)

A

slow-wave sleep (SWS) is important for declarative memory consolidation

54
Q

what phase of sleep is important for declarative memory consolidation?

A

slow-wave sleep

55
Q

what is awake cortical activity like?

A

associated with lots of high frequency oscillations and lots of brain activity

56
Q

what happens when you enter sleep?

A

activity slows down, oscillations become slower (Stage I and II) and deeper until you get to SWS (Stage III and IV)
* REM -> associated with movement and dreaming

57
Q

what is SWS characterised by?

A

Stage III and IV

-> very deep and slow oscillations important for structuring communication between the hippocampus and neocortex -> allowing consolidation to occur

58
Q

what is also associated with aspects of consolidation?

A

high frequency spindle activities

59
Q

what did Marshall et al. (2006) find?

A

electrical stimulation that enhances slow wave rhythm boosts verbal learning
-> SWS plays a huge role in memory consolidation

60
Q

Friedrich et al. (2014) suggest sleep helps babies generalise word meaning.
* event-related potentials to words ; look for comprehension markers
* if babies learned a word and then had a sleep, and then tested to see if they could generalise this new word form to other exemplars

What did they find?

A

babies aged 9-18 months who napped for 1.5h were better at generalising meaning beyond the exemplar that was learned [to other exemplars in the same category] (compared to babies who stayed awake)
-> correlated with sleep-based electrical activity (‘sleep spindles’ - associated with hippocampal activity)

61
Q

Wilson & McNaugton (1994) looked at reactivation of place cells during sleep in rats

What did they find?

A

Same sequence of neurones (place cells coding for specific locations) that code for route through maze reactivate in that order during SWS

-> memory stored in the hippocampus is reactivated during sleep

62
Q

Diekelmann et al. (2011)
One group awake, One group slept -> both exposed to odors they were exposed to in the card locations
* Then made it harder by introducing a new card task
* Looked at their ability to remember the first set of card locations when they presented the odor cues and when they didn’t -> odours represented during sleep or awake. then inference learning

what did they find?

A

better memory for odour cue, and increase hippocampal engagement
* better in those who went to sleep, when trying trying to remember the card location
* better memory for card location when exposed to the odour
* those who stayed awake had the worse memory

ALSO FOUND MORE ACTIVATION IN THE HIPPOCAMPUS WHEN RECOVERING CARD LOCATIONS IN SLEEP GROUP (group which slept) -> hippocampus may be reactivated and strengthened during the sleep phase

/odours might be interfering in this situation, being presented with the odours and not the card locations might be harmful to the memory because it’s only part of the episode?/

63
Q

what can we conclude about the role of memory?

A
  • SWS plays an active role in stabilising memories
  • During SWS, there may be reactivation of hippocampal-dependent memories
  • may promote their consolidation - integration with similar memories -> representation of the cortex and understand how they link to other similar memories
  • there is lots still to understand: other sleep stages (REM) might be important in a different way
64
Q

what did Tulving suggest?

A

episodic vs. semantic

65
Q

what does squire suggest?

A

episodic then semantic

66
Q

what can we suggest about memory consolidation

A

clearly two dissociable memory stores

67
Q

what does system consolidation suggest?

A

interdependence between these two dissociable systems

68
Q

Hippocampus may remain important for some old memories. What is Multiple Trace Theory (Nadel & Moscovitch, 1997)

A

hippocampus re-encodes during retrieval to create multiple traces and remains important for all ‘recollection’ experiences (even though most information is transferred to the cortex)

-> create multiple traces with partly explain why older memories have a different flavour to them
* Once you’ve got multiple traces, hippocampal representations are more durable and can remain important for memories even that are very old
-> critical thing that is characteristic of the hippocampus’s engagement in memory is true recollective experience [you need hippocampus for mental timetravel and reconstructing the whole environment as neocortex is not a true recollective experience]

69
Q

What is a critique of Squire’s account? does acquisition of semantic information dependent on episodic memory?

A

Evidence you can still learn without the hippocampus being intact -> Squire proposed acquisition depends..
* Might do -> i.e. ability to understand words which have come into vocab since a brain injury
* These words are not usually comprehended in amnesia (entering the lexicon after the brain injury)

70
Q

Developmental Amnesia (Vargha-Khadem) looked at 3 children who have acquired and had clear bilateral hippocampal injury during birth (hypoxia due to complications in birth). Through their childhood into their adulthood
* 44% reduction in hippocampus volume relative to the control

What did they find?

A
  • Amnesic - poor at verbal and non-verbal learning
    -> poor performance on episodic memory tasks and poor recollection on events going on around them

BUT these children had relatively normal IQ and academic attainment, reading comprehension, working memory, semantic memory all developed normally
-> Did really well at school -> a surprise because semantic informaiton is meant to be required from episodic information
-> But instead it suggests that you can learn semantic information even in the absence of an intact hippocampus

71
Q

How does the semantic system acquire information?

A

we don’t exactly understand but research suggests some regions adjacent to the hippocampus might be particular important in supporting this pattern of development
i.e. neocortex might be important in supporting this parahippocampal, perhinal and entorhinal -> which is why their semantic learning is relatively in tact

  • entorhinal and perihinal cortex are relatively spared in development amnesia -> this might provide basis for semantic learning
72
Q

the hippocampus and adjacent neocortex provide two distinct systems foe what?

A

episodic recollections and capturing similarities between experiences (i.e. semantic)

73
Q

how is information transferred from hippocampus to neocortex?

A

with sleep - giving rise to system consolidation

74
Q

According to Tulving, which type of long-term memory is self-referential?

A

Episodic

75
Q

In the autobiographical memory interview, which era of memories are most impaired in semantic dementia?

A

Childhood -> dependent on the semantic systems so transferred to anterior temporal cortex and get impaired with semantic information

76
Q

What is the name given to this effect on time on memory in semantic dementia?

A

Reverse Temporal Gradient

77
Q

Which form of consolidation occurs over a time-frame of weeks, not hours?

A

System consolidation

78
Q

Which phase of sleep is particularly associated with strengthened declarative memories?

A

Slow-Wave Sleep

79
Q

What is one method that can be used to show a causal effect on SWS on memory?

A

Electrical Stimulation

80
Q

What important insight particularly comes from the study of developmental amnesia?

A

The hippocampus is not necessary for declarative learning