Week 4 - Learning/Memory

Question 1

Learning, memory, and Amnesia

Memory as reconstruction

Answer 1

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

Question 2

Learning, memory, and Amnesia

Memory as adaptive

Answer 2

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

Question 3

Learning, memory, and Amnesia

3 broad types of long-term memory

Answer 3

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

Question 4

Learning, memory, and Amnesia

Short-term memory

Answer 4

Supports temporary sensory/motor storage.

Question 5

Learning, memory, and Amnesia

Memory fallibility and bias

Answer 5

• 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.

Question 6

Learning, memory, and Amnesia

Evidence from early cases

Varieties of amnesia

Answer 6

• 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.

Question 7

Learning, memory, and Amnesia

Childhood (infantile) amnesia

Varieties of Amnesia

Answer 7

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.

Question 8

Learning, memory, and Amnesia

Amnesias rare and common

Varieties of Amnesia

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

Answer 8

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.

Question 9

Learning, memory, and Amnesia

H.M’s case

Anterograde and retrograde Amnesia

Answer 9

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.

Question 10

Learning, memory, and Amnesia

Time dependent retrograde Amnesia

Answer 10

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.

Question 11

Learning, memory, and Amnesia

System consolidation theory

Three theories of Amnesia

Answer 11

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).

Question 12

Learning, memory, and Amnesia

Multiple-trace theory

Three theories of Amnesia

Answer 12

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.

Question 13

Learning, memory, and Amnesia

Reconsolidation theory

Three theories of Amnesia

Answer 13

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.

Question 14

Learning, memory, and Amnesia

Conclusion

Three theories of Amnesia

Answer 14

• 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.

Question 15

Explicit memory

Long-term explicit memory

Long-term explicit memory

Answer 15

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.

Question 16

Explicit memory

Episodic (autobiographical memory)

Long-term explicit memory

Answer 16

• 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).

Question 17

Explicit memory

Autonoetic awareness of time

Long-term explicit memory

Answer 17

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”.

Question 18

Explicit memory

Semantic memory

Long-term explicit memory

Answer 18

• 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.

Question 19

Explicit memory

Key brain regions involved

Neural substrates of explicit memory

Answer 19

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.

Question 20

Explicit memory

Hippocampal anatomy

Neural substrates of explicit memory

Answer 20

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).

Question 21

Explicit memory

Hippocampal function

Neural substrates of explicit memory

Answer 21

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.

Question 22

Explicit memory

The temporal cortex

Neural substrates of explicit memory

Answer 22

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.

Question 23

Explicit memory

Experiment evidence

Neural substrates of explicit memory

Answer 23

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.

Question 24

Explicit memory

Hemispheric specialisation of explicit memory

Hemispheric specialisation of explicit memory

Answer 24

• 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.

Question 25

# Explicit memory Temporal cortex | Hemispheric specialisation of explicit memory

Answer 25

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.

Question 26

# Explicit memory Parietal and occipital cortex | Hemispheric specialisation of explicit memory

Answer 26

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.

Question 27

# Explicit memory Prefrontal cortex | Hemispheric specialisation of explicit memory

Answer 27

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.

Question 28

# Implicit memory Long-term implicit memory

Answer 28

Implicit memory: * Unconscious, unintentional memory of skills, habits, conditioned responses and short-term events. * Contrasts with explicit memory which is conscious recall. * Usually preserved in Amnesia.

Question 29

# Implicit memory Long-term implicit memory characteristics

Answer 29

* Encoded and retrieved automatically, without deliberate effort. * Relies on bottom-up (data-driven) processing => depends heavily on sensory input. * Does not require conceptual reorganisation or higher cortical involvement. * Dependent on dorsal stream action pathway.

Question 30

# Implicit memory Sparing of implicit memory in Amnesia | Long-term implicit memory

Answer 30

Priming: * Technique = previous exposure to stimuli facilitates later response without conscious awareness. * Amnesic patients perform equally well as controls, even if they claim not to remember previous exposure. Depth of processing effect: * Explicit memory is enhanced by deeper processing. * Implicit memory is unaffected = scores on priming remain consistent. Study-test modality shift: * If encoding is in one modality (hearing) and testing in another (reading), explicit memory drops but implicit memory remains intact.

Question 31

# Implicit memory Proposed brain circuit | Neural substrates of implicit memory

Answer 31

Involves the entire neocortex and basal ganglia (especially caudate and putamen): * Includes motor cortex, substantia nigra, cerebellum, and ventral thalamus. * The basal ganglia receives projectiosn from all regions in the neocortex as well as from dopamine cells in the subtantia nigra and sends projections to the premotor cortex. * The motor cortex shares connection with the cerebellum. Implicit memory is widely distributed = not localised like explicit memory. * Reflects plastic changes across various brain regions depending on the task.

Question 32

# Implicit memory The basal ganglia | Neural substrates of implicit memory

Answer 32

* Critical for motor learning and implicit memory * Huntington's disease: basal ganglia degeneration = impaired implicit memory and preserved explicit memory. * Parkinson's disease: impaired basal ganglia-dopaminergic pathway = implicit memory deficits but L-dopa treatment improves performance on motor memory tasks.

Question 33

# Implicit memory The cerebellum | Neural substrates of implicit memory

Answer 33

* Involved in classical conditioning. * Plays a key role in non-conscious motor learning. * Lesions in cerebellum remove conditioned responses, but unconditioned responses remain. * Confirms cerebelum's role in adaptive, flexible behaviour.

Question 34

# Emotional memory Long-term Emotional memory

Answer 34

Emotional memory involves affective responses to stimuli or events. * Like implicit memory, it relies on bottom-up processing (sensory-driven), but also involves top-down (intentional) mechanisms like explicit memory. Emotional memories can be: * Implicit (unconscious) = automatic emotioanl responses. * Explicit (conscious) = emotionally charged memories recalled intentionally.

Question 35

# Emotional memory Evoking negative emotions | Long-term emotional memories

Answer 35

Fear conditioning: * Neural stimulus paired with noxious one = conditioned fear without the noxious stimulus. * Amygala = critical for fear conditioning. * Cerebellum = involved in eye-blink conditioning. Emotional memory duality: * Emotional memories have both implicit and explicit components (automatic responses + recollection of emotional experiences). Panic disorder insight: * People with PD exhibit anxiety responses without remembering a triggering event. * This suggests that emotional memory can exist independently of explicit memory - possibly explaining PTSD symptoms where emotional reaction persists without conscious recall of trauma.

Question 36

# Emotional memory Key structure: Amygdala | Neural substrates of emotional memory

Answer 36

Central to emotional learning and memory (especially fear).

Question 37

# Emotional memory Amygdala connectivity | Neural substrates of emotional memory

Answer 37

The amygdala projects to: * Autonomic centers = hypothalamus (hormonal responses), PAG (fight or flight). * Medial temporal cortex (for linking memory circuits). * Basal ganglia (for integrating implicit learning). The amygdala receives input from: * Sensory cortices * Hippocampus * And other limbic areas.

Question 38

# Emotional memory The amygdala's functional role | Neural substrates of emotional memory

Answer 38

* It stores emotional memory, particularly fear related. * Damage to the amygdala = loss of emotional learning, but explicit and implicit memory remain intact. * Emotional memory is evolutionary significant = it triggers survival circuits (freeze/fight/flight).

Question 39

# Emotional memory Unique aspects of emotional memory

Answer 39

Strong encoding: * Emotional events producee vivid memories (both positive and negative ones). * Hormonal and neural systems enhance memory encoding of emotional experiences. Reactivation: * Future emotional events can reactivate these memory circuits. * This is important for fight or flight readiness. Clinical insight: * Demented patients recognise emotionally significant people without consciously knowing them. * Patients consistenty preferred emotionally significant faces = implies intact emotional system.

Question 40

# Short-term memory Short-term memory

Answer 40

Short-term memory (also known as STM, working memory or temporal memory) holds recent sensory, motor, and cognitive events for a brief period of time (seconds). It temporarily stores and organises information.

Question 41

# Short-term memory Streams of processing

Answer 41

1. Ventral steam = object recognition (temporal cortex projects to different areas of the PFC). 2. Dorsal stream = motor-related sensory input (parietal cortex projects to different areas of PFC)

Question 42

# Short-term memory Patient K.F

Answer 42

* Lesion in left posterior temporal lobe = nearly complete loss of verbal STM. * Could not repeat digits, words, or sentences but long-term memory was intact. * Cntrasts with H.M who had normal STM but impaired LTM.

Question 43

# Short-term memory Short-term memory and frontal lobes

Answer 43

Impairs tasks requiring temporary memory for stimulus location. * Poor memory updating.

Question 44

# Neurological diseases and long-term memory Transient global Amnesia

Answer 44

Causes: concussion, migraine, hypoglycaemia, epilepsy, transient ischemic stroke. Symptoms: sudden onset, temporary loss of old memories and inability to form new ones. Usually short-lived but some memory loss can be permanent. Often underreported because recovery seems complete - chronic memory loss is often missed.

Question 45

# Neurological diseases and long-term memory Herpes Simplex Encephalitis

Answer 45

Viral infection damaging the temporal lobes. Damage areas: * Medial temporal cortex = anterograde amnesia. * Lateral temporal cortex, insula and ventromedial prefrontal cortex = retrograde amnesia (insular involvement - activates during retrieval of practiced verbal tasks but not novel ones (may be crucial for accessing old memories)).

Question 46

# Neurological diseases and long-term memory Alzheimer's disease

Answer 46

* Progressive neurodegeneration with widespread cortical loss. * Initial symptom = anterograde amnesia, later followed by retrograde amnesia. * Early damage in the medial temporal cortex = spreads to frontal and temporal association areas. * Affects explicit memory first but implicit memory can declien as disease progresses.

Question 47

# Neurological diseases and long-term memory Korsakoff's syndrome

Answer 47

Linked to chronic alcoholism and thiamine (vitamin B) deficiency. Symptoms: * Anterograde and retrograde amnesia. * Confabulation (plausible but false recollections). * Meagre content in conversation * Lack of insight * Apathy. Classic description: patient seems mentally sound but cannot retain recent memories, asks repeated questions, forgets ongoing conversations etc. Brain areas affected: * Medial diencephalon: medial thalamus, mammillary bodies, frontal lobes. Prognosis: often poor but some recover with B supplementaton, but may never fully regain memory function.

Question 48

# Neurological diseases and long-term memory Neurotransmitter activating systems and memory | Three major systems

Answer 48

Cholinergic systems: * From basal forebrain to frontal and temporal lobes. * Involved in EEG regulation and memory maintenance. * Degeneration associated with Alzheimer's. Serotonergic systems: * Projects from midbrain to limbic and cortical areas. * Maintains waking EEG. Noradrenergic systems: * Works alongside the cholinergic system. * Affects learning, arousal and attention. Loss of two or more system leads to profound amnesia even if the cortex is intact.