Transcript Chapter 1

CHAPTER 12
Learning
and Memory
Learning as the Storage of Memories
Brain Changes in Learning
Learning deficiencies and Disorders
Classical Conditioning
• Classical conditioning is learning to react to a predictive
stimulus
– The predictive stimulus predicts the eliciting stimulus
– The eliciting stimulus elicits the reflex
– Learn to anticipate the reflex behavior so that it occurs to the
predictive stimulus
– Notice: NO response is required; response is anticipatory to another
response
– This is S-R learning
Labeled each
part of these events:
• Unconditioned stimulus or US:
– The stimulus that automatically elicited the behavior (usually innate)
– E.g., the food elicited the slobber
• Unconditioned response or UR
– The behavior that is automatically elicited
– Unlearned; often reflexive
• Conditioned stimulus or CS:
– The stimulus that predicts the US
– Is a learned (thus conditioned) stimulus
• Conditioned response or CR:
– The behavior that occurs to the CS
– Often very similar to the unconditioned response
– Occurs because the CS predicts the US
Classical Conditioning
Procedure
CS  US  UR
Bell
Food
CR
Slobber with less
Digestive enzymes
Slobber
Conditioned
emotional response:
• CER: Conditioned Emotional Response
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US or UCS: foot shock
CS: tone
UCR: fear response, or a non-specific “emotional “ response
CR: learn to fear the tone as it PREDICTS the foot shock
• LATERAL nucleus of the AMYGDALA processes this
CER
Conditioned
emotional response:
The Law of Effect
• Thorndike (1911): Animal Intelligence
– Experimented with cats in a puzzle box
– Put cats in the box
– Cats had to figure out how to pull/push/move lever to get out;
when out got reward
– The cats got faster and faster with each trial
• Law of Effect emerged from this research:
– When a response is followed by a satisfying state of affairs, that
response will increase in frequency.
– And, when a response is followed by an unsatisfying state of affairs,
that response will decrease in frequency
• Note: a response is REQUIRED: forms a contingency
• R-S learning
Skinner’S verSion of
Law of Effect
• Had two problems with Thorndike’s law:
– Defining “satisfying state of affairs”
– Defining “increase” in behavior
• Rewrote the law to be more specific:
– Used words reinforcer and punisher
– Idea of reinforcer is strengthening of relation between a R and Sr
• Now defined reinforcement and punishment:
– A reinforcer is any stimulus which increases the probability of a
response when delivered contingently
– A punisher is any stimulus which decreases the probability of a
response when delivered contingently
– Also noted could deliver reinforcers and punishers in TWO ways:
• Add something: positive
• Take away something: negative
Reinforcers vs. Punishers
Positive vs. Negative
• Reinforcer = rate of response INCREASES
• Punisher = rate of response DECREASES
• Positive: something is ADDED to environment
• Negative: something is TAKEN AWAY from
environment
• Can make a 4x4 contingency table
Reinforcement
Punishment
Positive
Punishment
Add
>spanked
Stimulus
Positive Reinforcement
(Positive)
make bed-->10cent
hit sister-
Negative
Punishment
Negative Reinforcement
Negative
Remove
make bed-> Mom stops
hit sister->lose TV
Stimulus
nagging
Brain Changes in Learning
• Over 50 years ago Donald Hebb (1940) stated what
has become known as the Hebb rule:
– If an axon of a presynaptic neuron is active while the
postsynaptic neuron is firing, the synapse between
them will be strengthened.
– Note: Hebb made this statement in the absence of much
knowledge regarding neural architecture or decent
anatomical evidence!
experience is critical?
• Stimulation continues to shape synaptic
construction and reconstruction throughout the
individual’s life.
• Reorganization
– a shift in connections that changes the function of an area of the
brain.
– Much of the change resulting from experience in the mature brain
involves
Enrichment vs. deprivation
• Data show that type of environment an individual grows up in can
significantly affect the ability to learn, remember and function intellectually
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Rosenzweig (1960) compared single rats in normal cages, and those reared
in social groups with toys, ladders, tunnels, and running wheels.
– enriched environments affected enzyme cholinesterase (AChE) activity
– enrichment increased cerebral cortex volume
– this due to increased cerebral cortex thickness and greater synapse and glial numbers
• Lakin, Heidenreich and Farmer-Dougan found that too much can be bad,
too!
– Raised rats in highly enriched, solitary with group play sessions, and alone
– Rats reared in highly enriched showed lower DA, learned quickly but became bored
more quickly
– had poorer reward sensitivity: insensitive to reward
– Rats isolation learned more slowly but were highly sensitive to reward
Enrichment vs. deprivation
• environmental richness effects may improve brain function
whether it is experienced
– immediately following birth
– after weaning/during childhood
– during maturity.
• When synapse numbers increased in adults:
– can remain high in number even when the adults are returned to
impoverished environment for 30 days
– thus not necessarily temporary.
• Enrichment can also affect neurons outside the brain such as in
the retina and the cochlea
Enrichment vs. deprivation
• Localized cerebral cortex changes documented in humans via
– MRI studies
– Institutional deprivation: lack of early stimulation
– Cognitive reserve and resilience: Education and continuing to learn
throughout lifetime is a neural protectant!
• Children that receive impoverished stimulation due to being
confined to cribs/deprived of social interaction or reliable caretakers
in orphanages:
– Showed severe delays in cognitive and social development
– 12% of them if adopted after 6 months of age show autistic or mildly
autistic traits later at four years of age
– Can catch up in many cognitive functioning is adopted before age 2
– Show marked differences in their brains, consistent with research upon
experiment animals
Changes in the structure of
the synapse during Learning
• Long-term potentiation (LTP):
– increase in synaptic strength following repeated high-frequency stimulation
– Increase in dendritic growth
– Changes in receptor sites in synapse
• Long-term depression (LTD):
– decrease in synaptic strength when an axon of a neuron is active while the
postsynaptic neuron is not depolarized.
– May result in decreased dendritic growth
– Also changes in receptor sites in synapse
Spread of learning circuits
• Associative long-term potentiation:
– synapse is stimulated weakly while another synapse on the same
postsynaptic neuron is being stimulated strongly; both are
poteniated
– Helps build generalization or secondary associations
• Associative long-term depression
– weakening of a synapse that is active when the postsynaptic
neuron is not depolarized
– is inactive when the postsynaptic neuron is depolarized.
• LTP, LTD, associative LTP, and associative LTD can all be summed up
in the expression, “Cells that fire together wire together.”
Spread of learning circuits
• Associative long-term potentiation:
– synapse is stimulated weakly while another synapse on the same
postsynaptic neuron is being stimulated strongly; both are
poteniated
– Helps build generalization or secondary associations
• Associative long-term depression
– weakening of a synapse that is active when the postsynaptic
neuron is not depolarized
– is inactive when the postsynaptic neuron is depolarized.
• LTP, LTD, associative LTP, and associative LTD can all be summed up
in the expression, “Cells that fire together wire together.”
The graphs show excitatory postsynaptic potentials in response to a
test stimulus before and after repeated stimulation.
(a) 100-Hz stimulation produced long-term potentiation that
was evident 25 minutes later.
(b) 5-Hz stimulation produced long-term depression that
blocked potentiation established earlier.
How does LTP and LTD
happen?
• In most locations the neurotransmitter involved in
LTP is glutamate.
• There are two types of glutamate receptors:
1. The AMPA receptor
2. The NMDA receptor
Brain Changes in Learning
• During initial trials:
– Glutamate activates AMPA receptors but not NMDA receptors,
– NMDA receptors NOT activated because they are blocked by
magnesium (Mg) ions.
• During LTP induction:
– activation of the AMPA receptors by the first few pulses of
stimulation partially depolarizes the membrane
– This dislodges the magnesium ions
– Dislodging of magnesium ions allows NMDA receptors to begin being
activated.
• .
Brain Changes in Learning
• Thus: critical NMDA receptor activated with repetition
– This NMDA activation result = influx of sodium (Na+) and calcium
(Ca+) ions.
– Action of Ca+ ions allows release of Mg
• Release of Mg ions and thus stimulation of NMDA receptor:
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Influx of Na+ and Ca+ further depolarizes the neuron AND
Calcium activates CaMKII.
CaMKII: is an enzyme that is necessary for LTP;
acts as a binary switch to change the strength of a synapse.
Allows growth at the synapse of dendrite
(a) Initially, glutamate activates the AMPA receptors but not the NMDA
receptors, (blocked by magnesium ions)
(b) IF activation is strong enough to partially depolarize the postsynaptic
membrane- magnesium ions are ejected.
The NMDA receptor can then be activated, allowing sodium and calcium ions to
enter.
Brain Changes in Learning
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The final stage of LTP:
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involves alteration of gene activity
and the synthesis of proteins.
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Changes responsible for structural modifications in the
dendrites
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These changes produce longer-lasting increases in synaptic
strength:
– Neurons develop increased numbers of dendritic spines:
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partially bridge the synaptic cleft
make the synapse more sensitive.
– Later, additional AMPA receptors are transported from the dendrites
into the spines.
Research suggests
Long term potentiation
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Plays fundamental role in learning.
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Decreasing number of NMDA receptors in mice results in:
– reduced LTP in the hippocampus
– impaired learning.
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Learning improved by chemically increasing LTP
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Humans may possess genes related to various proteins involved in LTP.
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Also supports data suggesting that what “works” to remember:
– repetition
– massed trials
– Or other similar practice/rehearsal strategies
– Mastery learning: Practice makes perfect
– Practice grows your brain!
Learning while we sleep??
• Hippocampus has ability to acquire learning “on the fly”
– That is, while the event is in progress
– Why would this be important?
• In contrast, longer time needed for long-term storage of
declarative memories in the cortex.
• Hippocampus appears to transfers information to the cortex
during times when the hippocampus is less occupied,
– for example, during sleep
– May be function of dreaming.
Brain Changes during sleep
• Neurons in rat hippocampus and involved cortical areas
– repeat pattern of firing sequences that occurred during awake
learning
– Presumably: “offline” replay provides cortex opportunity to undergo
long-term potentiation
• Cortex requires more time to develop LTP, perhaps due to
complexity: Takes time for changes in synapse; dendrites
• Hippocampus = STM store; cortex is your hard drive
Learning as consolidation
• Consolidation
– process by which brain forms a more or less permanent physical
representation of a memory.
– Memory is formed via consolidation
– We will explain this later (LTP processes)
• Retrieval = process of accessing stored memories.
• Hippocampal formation plays a lead role in
consolidation,
– damage to that area accounts for difficulty learning new material
– No consolidation, no memory!
Three stages of memory
• Formation of memory
– Remember, “memory” is a process, not a “thing
– Takes time to form permanent memory
• Cognitive psychologists: 3 stages of memory
– Sensory register memory: recognizing info as important
– Short term memory:
• Is short in duration- no more than 20 sec typically
• Has limited capacity: 7+/-2
• Must engage in active effort to transfer to long term memory
– Long Term memory:
• Unlimited duration; Unlimited capacity
• Why forgetting? Interference or tissue loss
Storage of Memories
in brain
• STM: hippocampus stores information temporarily in
the hippocampal formation.
• LTM: Over time, a more permanent memory is
consolidated elsewhere in the brain.
• Memories are not stored in a single area
• But: memory also NOT distributed throughout the brain.
– different memories are located in different cortical areas
– Tend to be located according to where the information they are based on
was processed.
Types of memory
• Declarative memory
– involves memories of facts, people, and events, which a person can
verbalize, or declare.
• Hippocampus is CRITICAL
– Has inputs to it and regions that receive outputs as well
• Also LIMBIC Cortex or TEMPORAL LOBE
– Includes parahippocampal cortex
– Perirhinal and entorhinal cortices
– Damage = impaired memory
Types of memory
• variety of declarative memory subtypes:
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episodic memory (events)
factual memory
autobiographical memory
spatial memory (the location of the individual and of objects in space).
• Nondeclarative memory involves memories for
behaviors.
– Memories for procedural or skills learning: motor memory
– emotional learning
– stimulus-response conditioning.
Declarative vs.
nondeclarative memory
• Why distinguish?
– have different origins in the brain.
– Represent very different behaviors/functions
• How know which area processes which type of memory?
– Animal tests: can conduct lesions
– Testing rats in the radial arm maze
– Determine which brain areas were involved in learning tasks
corresponding to non-declarative and declarative learning
• Damage particular brain areas
• Test/retest rats and examine change in performance.
Declarative vs.
nondeclarative memory
• Why distinguish?
– have different origins in the brain.
– Represent very different behaviors/functions
• How know which area processes which type of memory?
– Animal tests: can conduct lesions
– Testing rats in the radial arm maze
– Determine which brain areas were involved in learning tasks
corresponding to non-declarative and declarative learning
• Damage particular brain areas
• Test/retest rats and examine change in performance.
Declarative vs.
nondeclarative memory
• Research Evidence supports importance of hippocampus
• Rats with damage to both hippocampi could learn the simple
conditioning task of going to any lighted arm for food.
– When every arm was baited with food:
– Rats would skip over “new” arms
– repeatedly returned to arms where the food had already been eaten.
• Rats with damage to the striatum
– could remember which arms they had visited
– could not learn to enter lighted arms.
Role of amygdala in
Storage of Memories
• Amygdala = significant role in nondeclarative
emotional learning.
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Nonverbal learning
Procedural, spatial, visual
Particularly emotional learning
But also involved in some procedural (motor) learning
• Amygdala strengthens declarative memories about
emotional events:
– increases activity in the hippocampus.
– If electrically stimulate amygdala: activates the hippocampus,
– enhances learning of a non-emotional task, such as a choice maze.
STM or working memory
• Remember: Working memory: temporary “register”
for information while it is being used.
– Working memory: phone number you just looked up
– holds information retrieved from long-term memory while
it is integrated with other information
– Or used in problem solving and decision making.
• Is short in duration and capacity!
– Like your working memory for files in computer
– If you don’t save, it is gone
Working memory =
prefrontal function
• Prefrontal area = working memory’s central
executive.
– manages behavioral strategies and decision making;
– coordinates activity in brain areas involved in perceptual
and response functions in a task; and
– directs the neural traffic in working memory.
• Damage to prefrontal area
– Increased impulsivity
– Lack of control for emotions
– Poor short term memory
Forgetting?
Brain Changes in Learning
• A memory must be both
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stable to be useful
Malleable to be adaptable
Need to remember new information
But must also be able to forget irrelevant/worthless information
• Several ways the brain accomplishes this:
– Extinction
– Forgetting
Spatial learning
• Like Classical conditioning, in that associate a location
with an event
• Typically use a maze such as a radial arm maze
– Has many arms
– Task is to find the food
– Must remember where you haven’t been and where you have been
so as to avoid going to same arm more than once
• Damage to hippocampus = poor learning and
performance
– Place cells: activity increases in response to looking or being in a
particular place
– Allows spatial learning and memory
The Case of H.M.
• At the age of 7,
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HM was knocked down by a bicycle
unconscious for five minutes.
Three years later: minor seizures
First major seizure occurred on his 16th birthday.
• As he got older: increased intensity/frequency of seizures
– averaged 10 small seizures a day
– one major seizure per week.
• When he was 27: surgeon did bilateral removal of temporal
lobes where the seizure activity was originating.
• Familiar story of severe seizure disorders, except for the
bilateral removal of temporal lobes- this was exceptional
Why is H.M. interesting?
• HM’s intelligence was not impaired by the operation.
– His IQ test performance even went up,
– Why? probably because post surgery was no interference from seizures.
• Although H.M. could recall past events, couldn’t learn new
things:
– can recall personal and public events and remember songs from his earlier life,
– difficulty learning and retaining new information.
• Only hold new information in memory for a short while
– , if distracted loses memory
– Memory dissipates within few minutes
– Almost COMPLETE loss of STM
Types of amnesia
• Anterograde amnesia
– an impairment in forming new memories
– HM’s symptoms one of first documented cases
• Retrograde amnesia
– inability to remember events prior to impairment
– Also found with HM’
– the surgery also caused considerable retrograde amnesia
• Typically: etiology of amnesia unknown
– H.M. unique because definitive cause of amnesia
– Rare chance to look at how brain forms memories
Hippocampal
formation and memory
• HM’s surgery damaged or destroyed the hippocampal
formation
– Structures near by along with hippocampus form this formation, nearby
structures
– Amygdala also important in this circuit (remember emotions!)
• Why important?
– The hippocampus consists of several substructures
– Each has different functions
– Which area damaged = what kind of damage
Hippocampal CA1
• Hippocampal CA1: provides the primary output from the
hippocampus to other brain areas.
• Damage in CA1 part of both hippocampi results = moderate
anterograde amnesia
– only minimal retrograde amnesia.
• If the damage includes the rest of the hippocampus,
anterograde amnesia is severe.
Forgetting?
Brain Changes in Learning
• Extinction
– involves new learning
– Like LTP, extinction requires activation of NMDA receptors;
– blocking these receptors eliminates extinction.
• Forgetting is a problem, but is also adaptive
– Prevents saturation of synapses with information that is not used regularly
– Eliminates information that not made connections with other stored memories
– Thus importance of elaborative rehearsal.
• A number of studies indicate: Any time memory is retrieved it must be
reconsolidated: During that time the memory becomes vulnerable again to disruption.
• Bottom line:
– Use it or lose it
– Use it and risk losing it!
Traumatic Brain injury
and Memory
• TBI is leading cause of death and disability in young adults
– 200-300/100,000 young adults admitted to hospital with TBI each year
– Most are males
• Mortality peaks from 15-24 years of age
– Risk peaks between 15 and 30
– 70% result of motor vehicle accident
TBI: Traumatic Brain
injury and Memory
• Memory deficits = most marked sequels in TBI
– Often persist beyond period of immediate recovery
– Most frequent site of injury: temporal and basal-frontal regions of cortex
– Areas highly associated with memory
• Memory deficits occur in 69-80% of individuals with TBI
– 36% show severe deficits
– 73% of those with severe TBI show long term deficits
– Predictors: degree of severity (marked by duration of loss of
consciousness) and duration of amnesia
TBI: Traumatic Brain
injury and Memory
• Memory involves 4 sequential, interrelated processes:
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Paying attention
Encoding
Storage
Retrieval
• Memory impairment in TBI may involve some or all of these
processes
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25% of TBI patients show difficulty with encoding or storage
Often lasts for months or years
Milder cases show disruption in attention, retrieval or combo of both
Difficulty with new learning, retrieval of new information
Impact on daily life
• Memory deficits
– Impair daily functioning
– Prevent return to work/school
– Impact ability to engage in daily living skills (bathing, eating, carrying
out daily chores)
• Depression often co-existing condition
– May be biologically related
– May be result of awareness of disability and loss
Compensation strategies
• Must compensate or bypass memory problems and use residual skills
more effectively
• Memory compensatory strategies include
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Use of mnemonics and memory aids
Cognitive training and memory building
Self-awareness of limitations and feedback
Memory groups
• External memory aids:
– Alarms for taking medication
– Electronic memory aids
– Neuropage alphanumeric paging system:
• Important events entered into computer
• Phone system pages the individual with reminder
• Issue of ecological validity: is this “normal”