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AA - COG NEURO > the remembering brain - part one > Flashcards

the remembering brain - part one Flashcards

1
Q

What is the function structure relationship?

A
  • do not match exactly
  • structure can participate in multiple functions
  • function may rely on many structures
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2
Q

What is episodic memory?

A
  • mental time travel: Tulving emphasised re-experience
  • ability to create links between unrelated bits of info, making a coherent episode = emphasis on relational memory
  • placing past experience within particular time and place = emphasis on context
  • autobiographical memory: events from past, semantic personal past
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3
Q

What is the MTL system composed of? (7)

A
  • fornix
  • thalamus
  • mammillary body
  • hypothalamus
  • amygdala
  • rhinal cortex
  • hippocampus
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4
Q

What is the parahippocampal gyrus?

A
  • grey matter cortical region of the brain that surrounds the hippocampus and is part of the limbic system
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5
Q

What does the parahippocampal gyrus consist of?

A
  • rhinal sulcus
  • perirhinal cortex
  • parahippocampal cortex
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6
Q

What is the hippocampus?

A
  • named due to seahorse shape
  • role in memory
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7
Q

What structures composes the hippocampus?

A
  • dentate gyrus
  • cornu ammonis (CA) subfields C1,2,3
  • subiculum
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8
Q

How does information flow within the MTL?

A
  • hierarchical organisation: info initially collected through perirhinal and parahippocampal cortices
  • passes to entorhinal cortex to hippocampus
  • cortical regions do not only funnel info to hippocampus: large network of connections within and among subregions of MTL cortical regions perform extensive info processing
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9
Q

What are the two types of amnesia?

A
  • anterograde
  • retrograde
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10
Q

What is anterograde amnesia?

A
  • difficulties in acquiring new memories
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11
Q

What is retrograde amnesia?

A
  • issues in remembering events before injury
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12
Q

Who was Henry Molaison?

A
  • intractable epilepsy in medial temporal lobes
  • treated by bilateral medial temporal lobectomy, including hippocampus and amygdala removal
  • preserved memory of the past and had good STM and WM but couldn’t form new LTM
  • global amnesia - affecting all sensory modalities
  • problems linked to mainly declarative/explicit memory
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13
Q

What were the good outcomes of HM’s surgery?

A
  • reduced convulsions in severity and frequency
  • improved IQ from 104-118 perhaps due to seizures no longer impacting cognitive processes
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14
Q

What were the bad outcomes of HM’s surgery?

A
  • minor retrograde amnesia for events within 2 years before
  • profound anterograde amnesia: could not STM->LTM
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15
Q

What is the digit span + 1 task? How did HM perform in this task?

A
  • normal subjects remember up to 18
  • after 25 trials, HM could only remember up to 7 (capacity of STM)
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16
Q

What is the mirror drawing task?

A
  • implicit memory
  • asked to draw shape by looking at mirror reflection
  • continuous experience improves performance
  • HM could not remember having done the task before but still improved and began each time with lower error rates initially
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17
Q

What did HM’s performance the digit span + 1 and mirror drawing task show?

A
  • implicit memory remains intact in anterograde amnesia, explicit memory is damaged
  • damage in the MTL produced anterograde amnesia and variable levels of retrograde amnesia = MTL critical for making new memories and retrieving old
18
Q

What is the aim of the subsequent memory paradigm?

A
  • aims to evaluate the encoding-phase activity leading to unsuccessful and successful memory

= which brain regions relevant for learning new things that supports info retrieval from LTM

(brain bases of remembered vs. forgotten events)

19
Q

What is the subsequent memory paradigm?

A
  • expose Ps to stimuli e.g. word lists and use fMRI = encoding task
  • perform recog memory test
  • compare to fMRI data of remembered vs forgotten events
20
Q

What was the Wagner et al 1998 subsequent memory paradigm study?

A
  • activity in left ventrolateral PFC and left MTL predicted later remembered vs. forgotten stimuli
  • hippocampus involved in encoding and remembering events
21
Q

What two processes support recognition?

A
  • familiarity
  • recollection
22
Q

What is familiarity?

A
  • sense of memory that a stimulus has been encountered before
  • no recall
23
Q

What is recollection?

A
  • memory for the context or other associative info about a previous encounter with a stimulus
  • cued recall
24
Q

What is the role of the hippocampus as a binder of relational memories?

A
  • Eichenbaum 2017 model: proposed a degree of functional specialty for familiar and recollection processes
  • the perirhinal cortex processes item representations (important for familiarity)
    –>
  • parahippocampal cortex assumed to process context including scene perception (context representation)

–> entohinal cortex –>

  • hippocampus binds items together in context: assoc of event and its context = recollection needs the hippocampus activation
25
Q

What was the Ranganath et al 2004 familiarity and recollection memory effects study?

A
  • words presented in green or red: can say it has been presented before but fail to remember which context = familiar
  • familiarity based recognition predicted by perirhinal cortex activation
  • familiarity reported in confidence scale = increased perirhinal cortex
  • recollection based recognition predicts activity in hippocampus: recog of colour and item, higher activity with higher confidence scores
26
Q

What did Kafkas et al 2017 study show about familiarity and recollection effects at retrieval in the MTL?

A
  • used faces, words, pics and asked to provide F and R ratings after training
  • in hippocampus, recollection based recognition is independent of stimulus type
  • hippocampus always active for recollection despite stimulus type = global activity
  • rest of MTL (cortices): familiarity recog had a degree of stimuli material specialisation = more specific roles depending on type of stimuli
  • Concluded that hippocampus was essential for storage of associations and recollection of these associations, but the rest of the MTL involved with generalised familiarity
27
Q

What is consolidation?

A

process that stabilises a memory over time after it is acquired

28
Q

What are the two types of consolidation?

A
  • synaptic
  • system
29
Q

What is synaptic consolidation?

A
  • structural changes in synaptic connections between neurons = faster
  • may take hours to days to complete
  • supported by neural plasticity - long term potentiation
  • learning at synaptic level
30
Q

What is system consolidation?

A
  • gradual shift of memories from hippocampus to neocortex
  • reorganisation of neural circuit = slow
31
Q

What are the two theories of consolidation?

A
  • standard consolidation theory
  • multiple trace theory
32
Q

What is the standard consolidation theory?

A
  • memories do not change once they are put into long-term memory
  • temporary role of hippocampus
  • hippocampus links together different kinds of info = active role
  • over time plays less of a role as the memory becomes independent from the hippocampus and is only represented by the neocortical arras
33
Q

What is Ribot’s Law?

A
  • memory loss following brain damage = temporal gradient in how memory is strored
  • law = more recent memories more likely to be lost, demonstrated in amnesias
  • remote memories have undergone system consolidation = do not rely on MTL anymore
34
Q

What is the temporal gradient of amnesia as seen in PZ?
(Support for Ribot’s Law and standard consolidation model)

A
  • university professor with Korsakoff’s syndorme
  • wrote research papers and books, autiobiography 2 years before onset
  • unable to learn new paired associates
  • remembered some famous people from 30s-40s but not after amnesia onset

supports temporary role of HC in memory

35
Q

How do dementia patients such as HM support Ribot’s Law and the standard consolidation model?

A

Support from dementia patients:
Semantic dementia who have lesions to anterior temporal lobes but typically spare the hippocampus - these patients can have a reverse temporal gradient and can only remember new items - reversal suggested to be due to the fact that memories haven’t been transferred from the hippocampus to neocortex meaning they’re intact.
Patients with hippocampal damage (Alzhemia’s dementia) it is recent memories which are lost as they have not been consolidated.
HM
Most remote memories not compromised because these memories were consolidated and therefore do not rely on the hippocampus anymore as they have been solidified in other neocortical regions (NB: hippocampus was damaged in surgery)

36
Q

How are memories retrieved if they are nonconsolidated vs when they are consolidated, according to the standard consolidation model?

A
  • event with different info types e.g. visual, auditory, spatial
  • hippocampus contains unified representation of the event
  • when retrieval cue containing only S and V info encountered before consolidation = hippocampus plays crucial role
  • after consolidation hippocampus not needed = retrieval cue accesses memory directly from the unified representation of the memory in the cortex
37
Q

What is memory reactivaton?

A
  • core mechanism
  • reactivation leads to reinstatement patterns of neural activity in cortex
  • results in stabilisation and refinement of cortical traces
  • iterative process -> storage and recall become completely dependent on the cortex, independent of hippocampus
38
Q

What is the temporal gradient of amnesia and semantic dementia? How does this support the standard consolidation model?

A
  • SD: damage to ATL, intact hippocampus (can remember recent but not old)
  • AD: damage to hippocampus and related structures (can remember old but not recent)
  • SD patients can remember recent but not old events: memories not yet consolidated and not transferred out of hippocampus
39
Q

How does retrograde amnesia support system consolidation?

A
  • assume old memories not fully consolidated at time of injury,
40
Q

What is the multiple trace theory?

A

Nadel and Moscovitch

  • hippocampus never stops having role in episodic memory recall
  • older memories have been reactivated more times
  • each reactivation creates new MTL traces
  • the older the memory is, the more reactivation it has had, the more traces and accessibility it has
  • to the extent that damage is not global and has not affected entire hippocampus, older memories more likely to be remembered due to having multiple traces
  • System consolidation of remote memories is not a transferring of memories, but rather a transformation from episodic-like to semantic like information (causing them to rely less and less on the hippocampus, and other areas), but remote/recent memories which episodic vividness continue to rely on the hippocampus.
41
Q

What study by Gilboa et al 2004 supports the multiple trace theory?

A
  • fMRI of remote personal memories
  • family members of Ps provided pictures of autobiographical events from remote past to recent times (5 photos for 5 periods)
  • Ps scanned while thinking about the event and rating vividness
  • hippocampus activated for recent and remote
  • hippocampus activation related to richness episodic nature/vividness rather than memory age

AA - COG NEURO (11 decks)

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