CHAPTER 12 Learning and Memory Learning as the Storage of Memories Brain Changes in Learning Learning deficiencies and Disorders

CHAPTER 12CHAPTER 12

Learning Learning

and Memoryand Memory

Learning as the Storage of MemoriesLearning as the Storage of Memories

Brain Changes in LearningBrain Changes in Learning

Learning deficiencies and DisordersLearning 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 Slobber

CR

Slobber with less Digestive enzymes

Conditioned emotional response:

• CER: Conditioned Emotional Response – 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. PunishersPositive 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

ReinforcementPunishment

Positive Positive Reinforcement (Positive) PunishmentAdd make bed-->10cent hit sister->spankedStimulus

Negative Negative Reinforcement Negative Punishment

Remove make bed-> Mom stops hit sister->lose TV

Stimulus nagging


• 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? 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

• 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


• 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


• 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

• 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

Changes in the structure of the Changes in the structure of the synapse during Learningsynapse during Learning

• 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 circuitsSpread 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 circuitsSpread of learning circuits

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.

• In most locations the neurotransmitter involved in LTP is glutamate.

• There are two types of glutamate receptors:1. The AMPA receptor2. The NMDA receptor

How does LTP and LTD happen?How does LTP and LTD happen?

• 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.

• .


• 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:– 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.

• The final stage of LTP:– involves alteration of gene activity – and the synthesis of proteins.

• Changes responsible for structural modifications in the dendrites

• These changes produce longer-lasting increases in synaptic strength:– Neurons develop increased numbers of dendritic spines:

• partially bridge the synaptic cleft • make the synapse more sensitive.

– Later, additional AMPA receptors are transported from the dendrites into the spines.


• Plays fundamental role in learning.

• Decreasing number of NMDA receptors in mice results in: – reduced LTP in the hippocampus – impaired learning.

• Learning improved by chemically increasing LTP

• Humans may possess genes related to various proteins involved in LTP.

• 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!

Research suggestsResearch suggestsLong term potentiationLong term potentiation

• 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.

Learning while we sleep??Learning while we 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

Brain Changes during sleepBrain Changes during sleep

• 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!

Learning as consolidationLearning as consolidation

• 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

Three stages of memoryThree stages of memory

• 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.

Storage of Memories Storage of Memories in brainin brain

• 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 memoryTypes of memory

• variety of declarative memory subtypes:– 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.

Types of memoryTypes of 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 Declarative vs. nondeclarative memorymemory

• 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.


• 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.


• Amygdala = significant role in nondeclarative emotional learning.– 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.

Role of amygdala inRole of amygdala inStorage of MemoriesStorage of Memories

• 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

STM or working memorySTM or working memory

• 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

Working memory = prefrontal Working memory = prefrontal functionfunction

• A memory must be both– 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

Forgetting? Forgetting? Brain Changes in LearningBrain Changes in Learning

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.The Case of H.M.

• At the age of 7, – 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

• 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

Why is H.M. interesting? Why is H.M. interesting?

Types of amnesiaTypes 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

• 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 Hippocampal formation and memoryformation and memory

• 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.

Hippocampal CA1 Hippocampal CA1

• 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!

Forgetting? Forgetting? Brain Changes in LearningBrain Changes in Learning

• 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

Traumatic Brain injury and Traumatic Brain injury and MemoryMemory

• 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 TBI: Traumatic Brain injury and MemoryMemory

• Memory involves 4 sequential, interrelated processes:– Paying attention– Encoding– Storage– Retrieval

• Memory impairment in TBI may involve some or all of these processes– 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

TBI: Traumatic Brain injury and TBI: Traumatic Brain injury and MemoryMemory

• 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

Impact on daily lifeImpact on daily life

• Must compensate or bypass memory problems and use residual skills more effectively

• Memory compensatory strategies include– 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”

Compensation strategiesCompensation strategies

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CHAPTER 12 Learning and Memory Learning as the Storage of Memories Brain Changes in Learning Learning deficiencies and Disorders