Week 4 - Learning/Memory Flashcards

(29 cards)

1
Q

Learning, memory, and Amnesia

Memory as reconstruction

A
  • Memory is a reconstruction shaped by meaning and expectation. We recall the gist more than details.
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2
Q

Learning, memory, and Amnesia

Memory as adaptive

A
  • Memory helps anticipate and prepare for future events; it is prospective, not just retrospective.
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3
Q

Learning, memory, and Amnesia

3 broad types of long-term memory

A
  1. Explicit (conscious): episodic, semantic.
  2. Implicit (unconscious): skills, habits, priming.
  3. Emotional: both conscious and unconscious components.
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4
Q

Learning, memory, and Amnesia

Short-term memory

A

Supports temporary sensory/motor storage.

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5
Q

Learning, memory, and Amnesia

Memory fallibility and bias

A
  • memory errors can arise from favouring one aspect (gist, emotion) over others (details).
  • Priming (implicit memory) = prior exposures sensitises memory, altering perception or recall.
  • Perception influences memory too.
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6
Q

Learning, memory, and Amnesia

Evidence from early cases

Varieties of amnesia

A
  • Confirmed temporal lobes role in memory.
  • Distinct memory contributions from different temporal lobe subregions.
  • Area TE damage interferes with conscious recall, with more damage meaning more severe amnesia.
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7
Q

Learning, memory, and Amnesia

Childhood (infantile) amnesia

Varieties of Amnesia

A

The inability to recall early life events (infancy to early childhood).

Likely causes:
* Memory systems mature at different rates.
* Early episodic memory systems (hippocampus) are not yet developped.
* Neurogenesis in hippocampus may disrupt existing circuits, contributing to memory loss.
* Observed in animals too = species with early hippocampal development do not show infantile amnesia.

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8
Q

Learning, memory, and Amnesia

Amnesias rare and common

Varieties of Amnesia

Fugue state, category-specific Amnesias, everyday forgetting, Alzheimer’s disease.

A

Fugue state:
* Sudden and transient, usually temporary loss of personal identity/history.
* Often leaves language and learned skills intact.
* Possibly due to suppression of medial-temporal-lobe systems.

Category-specific Amnesias:
* Patients may loss memory for nouns but not verbs, or animals but not tools.

Everyday forgetting:
* “Senior moments” - forgetting names, faces, or where things are placed.
* Increases with age and can become severe (AD)

Alzheimer’s disease:
* Starts with medial temporal lobe damage and expands.
* Characterised by progressive memory loss and neuron degeneration.

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9
Q

Learning, memory, and Amnesia

H.M’s case

Anterograde and retrograde Amnesia

A

Anterograde amnesia = inability to form new memories after brain injury.
* Also called global anterograde amnesia when all aspects of memory formation are affected.
* H.M could not remember new people or events post-surgery.
* He is impaired in: spatial and topographical learning, learning personal events and vocabulary acquisition.

Retrograde amnesia = loss of memories before the injury.
* Time-limited: older memories often preserved better than newer ones.
* He remembered who he was, how to read, write, speak, childhood home location, and skills learned before surgery.
* Key point: this improves for events that happened earlier in life but recent memories (close to the injury) are more vulnerable.

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10
Q

Learning, memory, and Amnesia

Time dependent retrograde Amnesia

A

Seen in traumatic brain injury (TBI).

Retrograde memory loss is typically:
* Shrinking over time (older memories are retained more).
* Extent depends on injury severity.

It may include:
* A brief loss of consciousness and confusion.
* Memory gap covering the moments before the injury.
* Often, only a few seconds to minutes of memory are lost long-term.

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11
Q

Learning, memory, and Amnesia

System consolidation theory

Three theories of Amnesia

A

Core idea: the hippocampus consolidates new memories, eventually making them permanent by transferring them to other brain areas (ex: neocortex).

Key points:
* New memories are initially stored in the hippocampus.
* Over time, they’re consolidated elsewhere (ex: neocortex).
* Older memories survive hippocampal damage because they’ve already been transferred.
* Recent memories are more vulnerable because they’re still in the hippocampus.
* Lesion size affects how far back retrograde amnesia extends: small lesion = few years of loss, large lesion = decades of memory loss).

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12
Q

Learning, memory, and Amnesia

Multiple-trace theory

Three theories of Amnesia

A

Core idea: memories of all types are stored in parallel across different brain areas.

Key principles:
* Different memory types -> different brain areas.
* Autobiographical -> hippocampus + frontal lobes.
* Factual semantic -> temporal lobe structures.
* General semantic -> cortical areas.

Memory changes over time:
* Memories are recalled, re-evaluated, and stored again.
* This transforms them from autobiographical -> semantic -> generalised.

Memory is distributed and redundant:
* Older memories have more traces, so they’re more resistant to brain injury.
* Different kinds of memory = differently vulnerable to damage.

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13
Q

Learning, memory, and Amnesia

Reconsolidation theory

Three theories of Amnesia

A

Core idea: every time a memory is recalled, it becomes labile (fragile) and must be reconsolidated, often in a slightly altered form.

What happens during reconsolidation:
* A new memory trace is created each time a memory is used.
* The memory is re-encoded, possibly with distortions.
* Results in many versions of the same memory.

Implications:
* Reconsolidation complicates memory study in amnesia.
* Witnesses, for example, may recall multiple versions of an event.
* Childhood amnesia = hard to tell which memories are original vs reconstructed from repetition or suggestion.

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14
Q

Learning, memory, and Amnesia

Conclusion

Three theories of Amnesia

A
  • Memory is not stored in one place, nor is it static.
  • Each theory captures a different aspect of how anterograde and retrograde amnesia work, and together they explain individual variation in memory loss after trauma.
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15
Q

Learning, memory, and Amnesia

Long-term explicit memory

Long-term explicit memory

A

Explicit memory (declarative memory) is conscious and intentional.

It includes:
* Episodic memory = personal experiences/events.
* Semantic memory = facts and general knowledge.

It relies on top-down processing = how data is organised at encoding influences recall.

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16
Q

Learning, memory, and Amnesia

Episodic (autobiographical memory)

Long-term explicit memory

A
  • Involves personal recall of specific life events.
  • Centered around the self = a timeline of personal life history.
  • It requires autonoetic awareness = the awareness of the self in subjective time (mental time travel).
  • Brain regions: medial temporal lobe, ventral prefrontal cortex, uncinate fasciculus (white matter pathway connecting the two).
17
Q

Learning, memory, and Amnesia

Autonoetic awareness of time

Long-term explicit memory

A

It links episodic memory with a sense of personal continuity over time.

Loss leads to:
* Disconnection from past and future.
* Difficulty imaging future scenarios.

Case study - K.C:
* Severe TBI = damage to medial temporal lobes and surrounding areas.
* Retained IQ, semantic knowledge and short-term memory
* Lost all autobiographical memory (past or future) and the ability to “travel time”.

18
Q

Learning, memory, and Amnesia

Semantic memory

Long-term explicit memory

A
  • Non-personal knowledge: vocab, facts, reading, maths, names of people/faces and recognition of family, historical knowledge.
  • It does not rely on the same network as episodic memory.
  • It is supported by temporal and frontal lobe regions adjacent to (but not the same as) episode system.
19
Q

Learning, memory, and Amnesia

Key brain regions involved

Neural substrates of explicit memory

A

Temporal-frontal system is the proposed core for explicit memory.

Key structures:
* Hippocamus
* Rhinal cortices (entorhinal, perirhinal).
* Prefrontal cortex
* Thalamus (especially medial nuclei).

These regions interact heavily via the thalamus and receive input from:
* Neocortex
* Ascending systems => acetylcholine, serotonin, noradrenaline.

20
Q

Learning, memory, and Amnesia

Hippocampal anatomy

Neural substrates of explicit memory

A

Key structures:
* Ammon’s horn = contains pyramidal cells (CA1, CA2, CA3, CA4).
* Dentate gyrus = contains granule cells.
* Subiculum = acts as output zone.
* Entorhinal cortex = input/output gateway to the hippocampus.

Pathways:
* Perforant pathway = connects neocortex to hippocampus.
* Fimbira fornix = connects hippocampus to the basal ganglia, thalamus, and hypothalamus (lesions here leads to amnesia without direct hippocampal damage).

21
Q

Learning, memory, and Amnesia

Hippocampal function

Neural substrates of explicit memory

A

Core roles from hippocampal patients:
* Anterograde memory is more severely impaired than retrograde memory.
* Episodic memories is mre vulnerable than semantic memories.
* Autobiographical memory (linked to “time travel” is most severely affected.

Supporting evidence:
* Hippocampus integrates multiple inputs to support episodic memory.
* Anterior hippocampus = coarse memory representation.
* Posterior hippocampus = fine-grained details.

22
Q

Learning, memory, and Amnesia

The temporal cortex

Neural substrates of explicit memory

A

Temporal areas bordering the rhinal fissure include:
* The perirhinal cortex and the entorhinal cortex: they provide major route for neocortical input to the hippocampal formation.
* Lesions here affect object recognition and contextual recall.

23
Q

Learning, memory, and Amnesia

Experiment evidence

Neural substrates of explicit memory

A

Monkey experiments:
* Perirhinal cortex = crucial for object recognition (semantic memory)
* Hippocampus = critical for context-based recall (episodic memory).

Human fMRI:
* Perirhinal cortex = active for object recognition.
* Hippocampus = active for recalling personally known facts.

24
Q

Learning, memory, and Amnesia

Hemispheric specialisation of explicit memory

Hemispheric specialisation of explicit memory

A
  • Explicit memory shows lateralised processing across both hemispheres ofthe temporal, parietal, occipital, and frontal lobes.
  • Removal of one hemisphere’s temporal lobe reveals asymmetrical memory deficits.
25
# Learning, memory, and Amnesia Temporal cortex | Hemispheric specialisation of explicit memory
Right temporal lobe damage: * Impaired non-verbal memory = face recognition, spatial position, maze learning etc. Left temporal lobe damage: * Impaired verbal memory = word lists, nonsense syllables, consonant trigrams, verbal associations.
26
# Learning, memory, and Amnesia Parietal and occipital cortex | Hemispheric specialisation of explicit memory
Bilateral lesions = severe topographic amnesia: inability to navigate or recognise spatial location of objects. Also involved in: * Object anomia (naming decifit). * Prosopagnosia (face recognition deficit). Often affects long-term memory for visual/spatial information.
27
# Learning, memory, and Amnesia Prefrontal cortex | Hemispheric specialisation of explicit memory
Left PFC = active during acquisition (learning new words). * Lesions affect encoding more = semantic and episodic. Right PFC = active during retrieval f episodic information. * DLPFC and parietotemporal cortex. * Lesion affects retrieval more = episodic information.
28
# Learning, memory, and Amnesia
29
# Learning, memory, and Amnesia