PSY102: BIOLOGICAL BASIS OF BEHAVIOUR

LEARNING AND MEMORY

LEARNING OBJECTIVES
WHAT IS MEMORY?

 Structures and processes involved in the

storage and subsequent retrieval of information
 Forms basis of experiences and perceptions of
self
 3 stages
 Encoding

 Storage

 Retrieval
WHAT IS MEMORY?

 (1) Short-term/working memory  (2) long

term memory  (3) short-term/working
memory
MEMORY

 Amnesia
 Failureof storage and retrieval
 Anterograde Amnesia

 Retrograde Amnesia
MEMORY

 Amnesia
 H.M
 Bilateral
removal of medial temporal lobes at 27
 Severe anterograde amnesia

 Retrograde amnesia – age 16

MEMORY

 Hippocampus
 Damage to entire area – severe anterograde
amnesia, retrograde amnesia 15 years or more
 Damage to CA1 area – moderate anterograde
amnesia, and minimal retrograde amnesia
MEMORY

 Consolidation
 Form physical representation of information
 Fragile process

 Older memories vulnerable to intense experiences

 Hippocampus is critical
MEMORY

 Retrieval
 Hippocampus involved
 Prefrontal area also involved
 Directs search strategy
MEMORY

 Storage
 Memories are stored in the area of first processing
 Hippocampus offers temporary storage
MEMORY

 Storage
 Place cells - hippocampus
 Increase firing when in a specific location
 Map of the environment – spatial memory
MEMORY

 Long Term Memory

 Declarative Memory
 Facts, people, events that can be verbalised

 Nondeclarative Memory
 Proceduresand skills, emotional learning, stimulus-
response conditioning
MEMORY

 Long Term Memory

 Differentpatterns of activation
 Hippocampus – declarative memory

 Striatum – nondeclarative memory

 Amygdala
 nondeclarativememory (emotional learning)
 Strengthens declarative memory about emotional events
MEMORY

 Working Memory
 Temporary register for information while it is being
used
 Uses attention and executive functions

 Dynamic system – online manipulations

 Limited capacity
MEMORY

 Working memory
 Prefrontal area
 Centralexecutive for learning
 Manages behavioural strategies and decision making

 Coordinates activity
LEARNING AND THE BRAIN

 Learning
 Form of neural plasticity
 Changes behaviour by remodelling neural
connections
LEARNING AND THE BRAIN

 Hebb Rule
 Ifan axon of a presynaptic neuron is active while
the postsynaptic neuron is firing, the synapse
between them will be strengthened
LEARNING AND THE BRAIN

 Long term potentiation (LTP)

 Increasein synaptic strength resulting from the
simultaneous activation of presynaptic neurons and
postsynaptic neurons
LEARNING AND THE BRAIN

 LTP
 Characteristic in hippocampus and other neural
tissue involved in learning
 Can last for months in animals
LEARNING AND THE BRAIN

 LTP
 Triggered by theta EEG activity
 Frequencyrange of 4-7Hz
 Hippocampus – exposed to a novel situation
LEARNING AND THE BRAIN

 LTP
 Glutamate
 Initially
activates AMPA receptors but not NMDA
receptors (blocked by magnesium ions)
 LTP induction  depolarises membrane  dislodges
magnesium ions
 NMDA receptors activated influx of Na+ and Ca+ 
further depolarises neuron
 Ca+ activates enzyme critical for LTP
LEARNING AND THE BRAIN

 Long term depression (LTD)

 Decrease in strength of synapses that occur when
stimulation of presynaptic neuron is insufficient to
activate postsynaptic neurons
LEARNING AND THE BRAIN

 LTD
 Modifiesmemories and clears old memories to
create space for new information
LEARNING AND THE BRAIN

 Associative LTP
 Weak synapse and strong synapse on the same
postsynaptic neuron are active simultaneously 
weak synapse is potentiated/strengthened
 Eg. Classical conditioning
LEARNING AND THE BRAIN

 Neural Growth
 LTP Induction  functional changes in synapses
 Gene activation, gene silencing, synthesis of proteins
LEARNING AND THE BRAIN

 Neural Growth
 Nitric oxide
 Released when postsynaptic neuron is activated
 Diffuses to synaptic cleft  induces neuron to release
more neurotransmitter
 Brief duration  long effects
LEARNING AND THE BRAIN

 Neural Growth
 Dendritic Spines
 Outgrowths from dendrites that partially bridge synaptic
cleft
 Make synapse more sensitive

 Transport additional AMDA receptors

 Increased dopamine  initiates growth of new synapses

LEARNING AND THE BRAIN

 Neural Growth
 New neurons in hippocampus
 Low rate
 Integrate into already established networks

 Increased volume
LEARNING AND THE BRAIN

 Memory Changes
 Memories are not cast in stone
 Memories can be unreliable

 3 mechanisms to make memories stable but

malleable
 Extinction

 Forgetting

 Reconsolidation
LEARNING AND THE BRAIN

 Extinction
 Conditioned stimulus no longer produces
conditioned response  no ucs
 Memory is not gone

 Requires activation of NMDA receptors

LEARNING AND THE BRAIN

 Forgetting
 Failure to recall/retrieve information
 Removal of useless information

 Efficient memory requires balance between

remembering and forgetting
LEARNING AND THE BRAIN

 Reconsolidation
 Each time memory is retrieved  reconsolidated
 Modification of memories happens

 Strengthens memory traces

 Reconstructed memories
MEMORY DEFICITS AND DISORDERS

 Ageing and memory

 Some cognitive decline associated with ageing
 Circuits in hippocampus lose synapses and NMDA
receptors
 Learning is slower, forgetting is more rapid
 Degeneration in basal forebrain area
MEMORY DEFICITS AND DISORDERS

 Alzheimer’s Disease
 Dementia – Substantial loss of memory and other
cognitive functions
 Most common dementia

 Progressive brain deterioration

 Impaired memory and other cognitive abilites

MEMORY DEFICITS AND DISORDERS

 Alzheimer’s Disease
 Usually a late onset
 Declarative memory – earliest and most severe
symptom
 Affects language, visuo-spatial functioning, and
reasoning
MEMORY DEFICITS AND DISORDERS

 Alzheimer’s Disease
 Neural Characteristics
 Amyloid Plaques – clumps of proteins around the axon
terminals
 Neurofibrillary tangles – protein tangles inside neuron

 Tangles associated with brain cell death

MEMORY DEFICITS AND DISORDERS

 Alzheimer’s Disease
 Heredity
 Genes affect amyloid production or deposits in the brain
 APP gene mutation - increases plaques  impairs LTP
and spatial learning
 APOE gene (ε4 allele) – increases Alzheimer’s risk
MEMORY DEFICITS AND DISORDERS

 Alzheimer’s Disease
 Treatment
 Increase levels of acetylcholine – prevent breaking down
at synapse
 Limits neuron sensitivity to glutamate

 Stem cell and gene therapy – still at early stages

MEMORY DEFICITS AND DISORDERS

 Alzheimer’s Disease
 Detection
 Conclusive diagnosis only possible at autopsy
 Rule out other forms of dementia – probable Alzheimer’s

 PET scans correlate highly with autopsy

 Difficult to predict from MCI

 Biomarkers in blood and CSF

MEMORY DEFICITS AND DISORDERS

 Alzheimer’s Disease
 Reserve hypothesis
 Individualswith greater cognitive reserves are able to
compensate for brain changes due to ageing, brain
damage, or disorders
 Delays onset of cognitive decline

 Correlational
MEMORY DEFICITS AND DISORDERS

 Korsakoff’s Syndrome
 Brain deterioration caused by chronic alcoholism
 Deficiency of vitamin B1 (thiamine)
 Not enough nutrients in diet
 Alcohol reduces absorption of thiamine in stomach
MEMORY DEFICITS AND DISORDERS

 Korsakoff’s Syndrome
 Severe anterograde amnesia is common
 Retrograde amnesia also severe

 Impaired declarative memory; nondeclarative

memory intact
MEMORY DEFICITS AND DISORDERS

 Korsakoff’s Syndrome
 Hippocampus and temporal lobes intact
 Mammillary bodies and medial thalamus – reduced

 Frontal lobes – structural and functional

abnormalities
MEMORY DEFICITS AND DISORDERS

 Korsakoff’s Syndrome
 Confabulation
 Fabricate stories and facts to make up for lost memories
 Damage to area in frontal lobes

 Difficulty suppressing irrelevant information