Chapter 18 Learning and Memory

18.1 Memory and Amnesia

- Famous Case: H.M.
o Surgery to relieve epilepsy; bilateral medial-temporal lobe resection
o Less frequent seizures, but severe amnesia
o Unable to acquire new memories
o Impaired spatial and topographic learning
o Sparse learning of new words, events, people
o Able to learn new motor skills
o Multiple memory theory
- Amnesias can be very specific:
o Specific in time
o Cannot remember events, but can remember facts; cannot remember events, can learn motor skills;
cannot remember objects, can remember locations; recognition of nouns but not verbs, or fruits vs
birds, etc.

Varieties of Memory
Multiple memory theory: proposes that we have a number of different kinds of memory, each of which is dependent
upon different neural structures.

Different types of memory (recap), where memory is the ability to recall previous experiences (from slides)
- Long-term memory (LTM)
o Explicit: conscious memory [(temporal/frontal) cortex and hippocampus]
▪ Episodic: personal, autobiographical
▪ Semantic: facts, knowledge, languages
o Implicit: nonconscious (although can perform well, little recall of how they were acquired); learned
skills, habits, priming, conditioned responses (basal ganglia)
o Emotional: conscious and nonconscious; attraction, avoidance, fear (amygdala)
- Short-term memory (PFC/DLPFC)
o Sensory, motor, cognitive
- Working memory
o Sequence learning, planning
Varieties of Amnesia
Amnesia: the loss of memories or inability to form new memories: (from slides)
- Amnesia and time-span (from slides)
o Anterograde amnesia
▪ Inability to form new memories
▪ Problems with storage of new information in LTM
(consolidation)
o Retrograde amnesia
▪ Inability to retrieve old memories
▪ Problems with retrieving information from existing LTM
▪ Specific time-span
▪ Time-dependent retrograde amnesia: injury resulting in
loss of more recently acquired memory, while
memories from distant past are retained
- Childhood amnesia (inability to remember events from first 4 years of
life)
o Adult’s memory of infancy and childhood is constrained by
memory processes maturing at various ages; early memories
can influence later life, but details of how they were acquired
are forgotten as they occurred before all memory systems were
fully matured
o Brain actively ‘deletes’ memories to make room for new
memories
o Maturation of memory systems:

- Forgetfulness when getting older

- Traumatic brain injury (TBI)
o Often causes time-dependent retrograde amnesia
o Can be transient loss of consciousness
o Also impairments with prospective memory (memory for things that one intends to do, eg. keeping
appointment or attending lass)
▪ Consistent with anteograde amnesia
o Also impairments with destination memory (memory of past interactions, eg. remembering who we
told a story; if don’t remember then will be reminded)
▪ Consistent with retrograde amnesia
- Rare and Common Amnesias
o Fugue state: memory loss of personal history that is sudden and usually transient
▪ Dissociative state
o ‘Everyday’ amnesias: forgetting names or faces or where we put keys
▪ Increases with advancing age
- Can also occur due to:
o Surgery
o Infections of the brain (herpes simplex encephalitis)
o Alzheimer’s disease (degenerative)
 o Korsafkoff (alcohol-related)
o Concussion (short term, recoverable)

18.2 Explicit Memory

Explicit memory (declarative, conscious, top-down, demands attention, depends on active processing): remembering
and recognising facts and general knowledge (from slides)

Episodic Memory
Episodic (autobiographic) memory: time- and place-locked (from slides)
- Depends on ability to mentally displace oneself in time
- Important role of medial temporal lobe (including hippocampus), ventral PFC, and connection between these
areas
- Patient G.O. with episodic autobiographical amnesia
- Autonoetic awareness of time:
o Autonoetic awareness: self-knowledge that allows us to bind together the awareness of our self as a
continuous entity through time
o Allows travelling in subjective time (to past or future); hippocampal and frontal cortical injury lose
self-knowledge and have difficulty due to deficit of behavioral self-regulation and ability to profit
from past experience in making future decisions
o “Time-travelling”
o Autobiographical memory: medial temporal lobe, ventral PFC and connections between them by
uncinate fasciculus

Semantic Memory
- Semantic memory: specific facts (eg. persons,
events) and general knowledge (eg.
language, arithmetic) (from slides)
o Important role of temporal, posterior
parietal, and occipital cortex

Neural Substrates of Explicit Memory (from

slides)
- Explicit LTM is a result of processing
(consolidation) of cortical information
(temporal, parietal, occipital)
- Consolidation is necessary to store information as an explicit memory
- Structures involved in consolidation of explicit information:
o Hippocampus: important for consolidation of types of explicit memory (spatial context is particularly
important for episodic memory)
▪ Consolidation more severely affected by hippocampal damage than retrieval (hippocampus
important for retaining memory after learning)-> relate this to anterograde/retrograde
amnesia
• Patient V.C.: complete loss of hippocampus -> complete retrograde and anterograde
amnesia for explicit information from all age periods of life
▪ Episodic (autobiographical) memory more affected than semantic memory; “time travel” (to
past and future) is diminished
▪ Connected to rest of brain through two major pathways, that allows hippocampus to
function as a way station between posterior neocortex and frontal cortex, basal ganglia, and
brainstem:
• Perforant pathway: connects hippocampus to posterior parietal and temporal cotex
• Fimbria fornix (“arch fringe”): connects hippocampus to thalamus, PFC, basal ganglia,
and hypothalamus
▪ Concluding hippocampal function:
• Anterograde memory more severely affected than retrograde memory
• Episodic memories more severely affected than semantic memory
• Autobiographical memory especially severely affected
• “Time travel” is diminished
• Damage to hippocampus or any of its pathways that connect temporal lobes to other
brain regions results in memory impairment
o Paralimbic cortex (perirhinal, entorhinal, parahippocampal):
“interface” of hippocampus – neocortex; important for
consolidation of episodic and semantic memory information
o Amygdala: crucial for emotional memory; responsible for
emotional ‘coloring’ of new stimuli or events that are stored
in memory (in slides, not in TB)
o PFC (including connections with temporal cortex and medial
TL): involved in encoding and retrieval of episodic and
semantic memory (in slides, not in TB)
▪ Assumptions about lateralisation:
• Left PFC involved in encoding > retrieving
semantic and episodic information
• Retrieving episodic information right PFC >
left PFC
 o Medial thalamus: important for consolidation in general; increased connectivity with PFC and
hippocampus during consolidation -> Wernicke-Korsakoff syndrome (in slides, not in TB)
- Following consolidation, memory information is more or less permanently stored within various cortical
association areas, although there is evidence that consolidation is not always permanent: (in slides, not in
TB)
o Information retrieved from LTM may be influenced by new experiences
o And may, in a modified form, be stored again in LTM (reconsolidation), sometimes in other location

Cortical lesions may lead to problems with explicit LTM: (in slides, not in TB)
- Lesions temporal cortex:
o R-sided lesions: on average more problems with nonverbal material (like faces, objects, spatial
locations, maze learning tasks, geometrical figures, tones/melodies)
o L-sided lesions: on average more problems with verbal material (like stories, words, numbers)
- Lesions posterior parietal cortex: topographic amnesia (memory loss for spatial locations of objects and their
relationships, CH 21)

LTM: Explicit (in slides, not in TB)

- Remember: information requires consolidation to be stored in explicit LTM
- Distinct regions that make up circuit for explicit memory receive activating input from the neocortex and
from a combination of ascending projections:
o Acetylcholine (Ach) systems: cholinergic projections from nuclei in basal forebrain (CH 5)
o Serotonin (SE) and noradrenaline (NA) systems: projections form nuclei in brainstem
- Degenerative disorders: often loss of neurons in cholinergic, serotonergic and/or noradrenergic systems (CH
5), eg. Alzheimer’s disease

Dementia: Alzheimer’s Disease (AD) (in slides, not in TB)

- Degenrative form of dementia with progressive loss of cells/ synaptic connections
- Early stages: prominent damage to (medial) temporal lobe
- (Neo-)cortex: association areas are primarily affected
o Posterior parietal; spatial memory, spatial orientation, apraxia
o Inferior temporal; object and face recognition, and memory
o Limbic cortex (especially entorhinal); STM and LTM (mainly episodic)
o Primary sensory and motor areas are spared for relatively long time
- Memory dysfunction in AD
o Initial loss of explicit memory (hence anterograde amnesia), but later on, also loss of implicit
memory (all kinds of daily life skills)
o Memory dysfunction = both anterograde and retrograde
▪ Anterograde amnesia in earlier stages: initial degeneration of medial temporal lobe
(entorhinal cortex, hippocampus)
▪ Retrograde amnesia due to inevitable degeneration of lateral temporal cortex, other parts of
posterior association cortex, and frontal cortex in later stages of disease

Other Neurological Diseases associated with LTM (in slides, not in TB)
- Herpes simplex encephalitis of temporal lobe
o Produces serious retrograde amnesia (effects on lateral temporal cortex and insula) and anterograde
amnesia (effects on medial temporal lobe: hippocampus and paralimbic cortex)
o Patient C.W., an established musician with 30 second episodic memory (‘just awoke’)
- Korsakoff’s syndrome (due to chronic alcoholism): complete anterograde amnesia and increasing retrograde
amnesia
o Characterised by confabulation, apathy, and indifference
o Damage in medial thalamic nucleus (or mamillo-thalamic tract) together with general cerebral
atrophy (particularly frontal) due to vitamin B1 (thiamine) deficiency

Hemispheric Specialization for Explicit Memory

Asymmetries in explicit memory exist in all neocortical lobes
- Temporal Cortex:
 o Right removal: facial recognition, spatial-position, maze learning tests impairments; demonstrated by
Corsi block-tapping test (tapping sequence on board) -> impaired will learn very slowly or not learn
at all
o Left lesions: impairments in recalling word lists, consonant trigrams, and nonspatial associations;
Hebb recurring-digits test (repeat list of digits) -> fail to learn repeated digit sequence
▪ Little effect on nonverbal tests
o LH memory for verbal material, RH memory for nonverbal material
- Parietal and Occipital Cortex
o Lesions cause LTM difficulties, eg. color amnesia, prosopagnosia, object anomia (inability to recall
object names), and topographic amnesia (inability to recall location of object in environment)
o Deficits appear in bilateral lesions only
- Frontal Cortex: autobiographical memory
o HERA (hemispheric encoding and retrieval asymmetry) pattern predicts:
▪ Left PFC more encoding semantic information than retrieval
▪ Left PFC more encoding episodic information than retrieval
▪ Right PFC more episodic memory retrieval than left PFC

18.3 Implicit Memory

Implicit (or procedural) memory (nondeclarative, non-conscious, bottom-up, does not demand attention or active
processing) (from slides)
- Motor and cognitive skills (eg. grammar rules, categorising)
- Daily habits
- Classically conditioned responses
- Priming (Faster recognition of stimuli following earlier presentation; relies on activation of immediate (i.e.,
short-term) memory within sensory cortical areas)

LTM (from slides)

- Explicit LTM: actively created, fast, unreliable, flexible
- Implicit LTM: passively created, slow, reliable, inflexible
- Both types of memory function are relatively independent of each other, as seen in studies of patients

Sparing of Implicit Memory in Amnesia

- Patient HM: typical learning curve on
mirror-drawing task, but don’t
remember doing it
- Priming also survives in amnesic
patients, despite reporting no
conscious recollection of ever seeing it
- Gollin Incomplete-Figures Test
 - Depth-of-processing effect: thinking about meaning of word greatly improves recall
- Study-test modality shift in healthy controls: modalities for learning and recalling different -> explicit recall
not affected

Neural Substrates of Implicit Memory

Two competing views about neural systems that support implicit memory: (1) all brain regions, other than circuitry,
involved in explicit memory, is involved in implicit memory, or (2) implicit memory has its own dedicated neural
circuit
- Motor and cognitive skills and daily habits: role of “loop” between cortex and basal ganglia (from slides)

o Classical conditioning of
▪ Motor responses: role of cerebellum
▪ Emotional responses: role of amygdala
o Priming: role of primary and secondary sensory cortex
- Basal ganglia: important for implicit memory -> Huntington’s patients impaired on implicit tasks but
unimpaired on explicit memory tasks
- Motor cortex and basal ganglia damage -> impaired learning of abilities such as mirror drawing (from slides)
o Subject remembers practicing, but does not get better at task
o In contrast with patient H.M. (anterograde amnesia), who would not remember practicing but would
get better at task
o Same applies to priming -> amnestic subjects (explicit) perform on similar level as control subjects
- Patients with Huntington’s or Parkinsons Disease most likely to have problems with implicit memory (motor
and cognitive skills) (from slides)
- Neurotransmitter Activating Systems and Memory
o Four neurotransmitter systems (cholinergic, serotonergic, noradrenergic, dopaminergic) implicated in
memory
o Loss of cholinergic cells: amnesia of Alzheimer disease
o Both serotonergic and cholinergic cells damaged together: profound amnesia
o Both noradrenergic and cholinergic blocked together -> impairment of learning tasks

18.4 Emotional Memory

Emotional memory: like implicit memory, acts are “bottom-up”; emotional associations are automatically elicited by
a stimulus of memory item (cue) (from slides)

Evoking Negative Emotions

- Fear conditioning
- Panic disorder: anxiety but cannot identify specific cause -> emotional memory can be seen as separate from
explicit and implicit memory

Neural Substrates of Emotional Memory (from slides)

- Emotional memory for affective properties of stimuli or events is vivid and arousing
- Can have explicit and implicit properties
 - Evoking negative emotions in fear conditioning -> relies on different parts of brain than non-emotional (eg.
motor) conditioning (both Pavlovian)
- Amygdala damage removes emotional memory, but little effect on implicit/explicit memory

Unique Aspects of Emotional Memory

- Emotionally significant experiences reactivate hormonal and brain systems to stamp in vivid memories,
through modulation of memory circuits in rest of brain
- Future experiences can reactivate these circuits

18.5 Short-Term Memory

- Neural record of recent events and their order: use STM to hold sensory events, movements and cognitive
information such as digits, words, names for brief period; Ventral stream – dorsal stream and PFC (from
slides)
- STM for location (dorsal) vs objects (ventral) (from slides)
- Problems with STM may be effect of damage of: (from slides)
o Temporal or parietal association areas
▪ Dependent on type of damage, problems may be modality-specific (eg. auditory or visual) or
be related to verbal or nonverbal material
o Different regions of PFC, having specific effects on WM (WM is important type of STM)
▪ PFC involved in WM for (a) identity of objects, (b) their spatial locations, and (c) the order of
presentation
o How to test for problems with STM?
▪ WM tasks, eg. digit span task; backword, or N-back task

Short-Term Memory and the Temporal and Parietal Lobes

- STM deficits from damage to polymodal sensory areas of posterior parietal and posterior temporal cortex

Short-Term Memory and the Frontal Lobes

- Frontal cortex damage: STM impairments for tasks where subjects must temporarily remember locations of
stimuli

Neuropsychological Testing for Short-Term Memory Function

- Interference tasks: recalling 12 words each from 4 lists
o Proactive interference: earlier lists interfered with learning new information
o Release from proactive interference (man why cant you just call it retroactive interference): can recall
as many words in list 5 as in list 1
o Frontal lobe patients: strong proactive interference, failed to show release from proactive
interference
- Movement copying task: ask to copy a series of three discrete facial movements
o Patients: error of omission (leave one movement out) or error of intrusion (added movement from
previous sequence)
18.6 Special Memory Abilities
- Savant Syndrome
- Superior autobiographical memory

18.7 Issues in Relating Memory to Neural Structures

- System consolidation theory: states that one role for hippocampus is consolidating new memories, a process
that makes memories permanent. Upon completion of consolidation, memories moved and stored
elsewhere in brain
o Explains why older memories survive hippocampal damage
- Multiple-trace theory: memories encoded in number of brain regions concurrently
o Single memory event, autobiographical aspects encoded in hippocampus and frontal lobes
o Factual semantic memory of event encoded in temporal-lobe structures
o General semantic memory encoded in remaining cortical areas
- Reconsolidation theory: memories rarely consist of a single trace or neural substrate
o Each time memory is used, it is reconsolidated
- Trace transformation theory of memory: perceptual features of events are richly represented in posterior
hippocampus, and shifted to anterior hippocampus, which represents the gist of memory, with time.
Memory then further encoded in medial PFC that houses schemas (groups of similar memories)

Memory and Daily Life

- Associative inference: ability to associate existing knowledge with novel information, another method to
reconstruct memory
- Gist
o Adaptive purpose of anticipating and responding to future situations in ways that benefit from past
experiences
o Eg. witness accident -> can give gist but not details of what happened, or recall details not
remembered by others. Recollections also can be distorted -> Possible priming effect of hearing
stories by other people