Physiologi Learn

7/28/2019 Physiologi Learn

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Psikologi

Pembelajaran


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How is your brain like(?)

A cabbage

A raisin

A pillowcase A grapefruit

String cheese

A walnut


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Otak Kita

Are like a jungle- nothing runs

the jungle

All parts of the brain participate

with each other, while each hasits own function

There is natural pruning or neural

pruning that occurs when parts are not used (this

may be why sounds not heard or used atrophyover time)

LEARNING IS A DELICATE, BUT IS APOWERFUL DIALOGUE BETWEEN GENETICSAND THE ENVIRONMENT Robert Sylwester, ACelebration of Neuro ns


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Brains Complexity

Cellular level - three pints of liquid, three

pounds of mass, tens of billions of nerve

cells (or neurons), ten times more

numerous glial cells that support, insulateand nourish the neurons

Brain cells - 30 thousand neurons (300,000

glial cells) fit into the space of a pinhead.


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Bagian bagian dari Otak

Brainstem (survival )

Cerebellum ( autonomic nervous system)

Limbic system (emotion) Cortex ( reason/logic)

Brainstem

Cerebellum

Cortex


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Frontal lobe - Cortex

Creativity - Judgment - Optimism - Context

Planning - Problem solving - Pattern

making Upper temporal lobe - Wernickes Area

Comprehension - Relevancy - Link to past(experience) - Hearing - Memory - Meaning

Lower frontal lobe - Cortex Speaking/language - Brocas area

Occipital lobe - Spatial order

Visual processing - Patterns - Discovery

Parietal lobe Motor - Primary Sensory Area - Insights -

Language functions

Cerebellum

Motor/motion - Novelty learning - cognition -balance - posture


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Brocas

area

Pars

opercularis

Motor cortex Somatosensory cortex

Sensory associative

cortex

Primary

Auditory cortex

Wernickesarea

Visual associative

cortex

Visual

cortex

Language and Thought

Grammar

and word

production

Movement and joint positions

Cerebellum


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Neurons

Connect to other neurons,

to muscles, or glands

Send and receive chemical information

(messages) for behaviors

Can be a millimeter in length or as long as

a meter Cells nucleus contains DNA (As long a

meter)


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Neurons contain tubular extensions that aredesigned to communicate quickly withspecific cells in the body network - this is a

transportation system, much like a phonesystem.

The brain has both nerve cells and glialcells. The neurons are cellular agents ofcognition; the glial cells act as a scaffoldingor insulation for impulses. (The insulationincreases the speed of the neural (electrical)

messages.)


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Memory

Place to store information, as in: How muchmemory does your hard drive have?

Information that gets stored, as in: I have fondmemories of my summer vacation.

retention of learned information

Learning: acquisition of knowledge/information


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Memory

Thompson

many structures involved in memory formation;

memory depends on many mechanisms;

classical conditioning of eyelid responses in rabbit

response occurs in cerebellum - lateral

interpositus nucleus (LIP)


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The Modal Model of Human

Memory


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Memory stores

Sensory MemoryShort-Term

Memory

Long-Term

Memory

Capacity Very large 72 items Infinite

DurationVery short (Fraction

of second)

Short (Fraction

of minute)Indefinite

Format(Coding)

Direct

representation ofsensual experience

as action potentials

Spokenlanguage format

Semantic(meaningful)

format


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Processes

Attention

Selects portion of Sensory Memory for further

processing by STM

Ex: Attend to lecture, not sound of ventilation system.

Chunking

Group items into meaningful units

Strategy to increase capacity of STMEx: 270-348-8-0-8-0

Rehearsal

Repeat information until no longer needed.

Strategy to increase duration of STM

Ex: 8080 8080 8080Oops, what was that

number?

EncodingInformation moved from STM to LTM.

Ex: Studying to learn the answers to the test questions.

Retrieval

Information moved from LTM to STM

Ex: Remembering the answer to the question so that

you can write it down.


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Four Theories of Forgetting

from Long-Term Memory

Explanation Description Example

Encoding

Failure

Information never

encoded fromSTM to LTM.

Student studies for exam

while

watching TV, cant rememberanswers to test questions.

Decay

Information encoded in

LTM, but decays over time

with lack of use.

However, some memories

never decay, even though

they are not frequently

used.

Decay can be explained

by interference.

Ebbinghaus memorized

nonsense

words, tested his memory of

these days later, found

forgetting curve.


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Four Theories of Forgetting (contd)

Explanatio

nDescription Example

Interference

Information encoded in

LTM, but cannot be

retrieved because newer

information interferes.

Can be thought of as

retrieval error.Accounts for

Ebbinghauss findings,

without memories

decaying.

Cant remember old phone

number; recall new number

instead.

RepressionAccording to Freud,

painful memories can be

pushed below level of

consciousness.

Very controversial topic;

many psychologists now

argue that repression doesnot occur.

Memories of child abuse

suddenly recalled during

psychotherapy (But are they

accurate?)

Recovered Memory

Syndrome false memories

planted during hypnosis or drugtherapy.


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Types of LTM


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Memory and learning

Types of memory:

declarative

facts and events

conscious recollection easy come easy go

procedural

learning to play an instrument, to ride a bike; no conscious recollection (usually);

need repetition or training;

longer retention


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Memory and learning

Subtypes of declarative memory:

short-termmemory

temporary,

limited capacity,

needs rehearsal (e.g. telephone number)

long-term memory

'permanent' greater capacity

no continual rehearsal needed


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Theories of memory storage

Engram

Engram was a hypothetical structure or

feature inside of the neuron that stored

information

Grandmother cell the neuron that fired

when you see your grandmother

In computers, information (memories) storedin cells or slots of hard drive

But this is not how the nervous system

stores information!


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Theories of memory storage

Long-Term Potentiation (LTP) Recent research indicates that memories are

stored in the synapses between neurons

Learning involves formation and modification of

synapses Neurons that fire together wire together

LTP takes days to complete learning spaced

over several days more effective at inducing LTP

than learning crammed into short period of time Most research on LTP done on sea slugAplysia


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Memory and learning

Plasticity paradigms:

Associative mechanisms:

classical conditioning

pairing of 2 stimuli changes the response to one of them

(Pavlov) conditioned stimulus (CS) - originally neutral (no

response)

unconditioned stimulus (UCS) - automatically evokesresponse unconditioned response (UCR)

after repetitive pairing of CS and UCS presentation ofCS evokes learned response - conditioned response

(CR)

operant conditioning - reinforcement and punishment


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Memory and learning

Nonassociative mechanisms:

habituation

decrease in response to a repeated stimulus not

accompanied by changes in other stimuli

sensitisation

an increase in response to a moderate stimuli as a

result of a previous exposure to a strong stimulus


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Memory and learning

memory consolidation - storing knowledge

in the long-term memory

Hebb - reverberating circuit - prolonged

excitation leads to chemical or structural changes

Memory of meaningful or emotional facts

enhanced

involvement of amygdala (stimulation ofhippocampus and cortex)

damage to amygdala impairs emotional

enhancement of memories


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Memory and learning

working memory - modification of the

concept of short term memory

memory consolidation may take place with or

without use of the short-term memory

a phonological loop a visuo-spatial sketchpad

the central executive - directs attention towards

stimuli; determines what will be stored in the

working memory

working memory test - delayed response task -

higher activity in the prefrontal cortex during the

delay


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Physiology of Memory

Types of amnesia

1. Retrograde amnesia

Loss of memories already formed due to

brain damage

But can still form new LTMs

Example: Patient has stroke and no longer

recognizes family members. Common symptom of Alzheimers disease


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Physiology of Memory

Types of amnesia

2. Anterograde amnesia

Loss of ability to form new long-term

memories

Previously stored memories may still be

intact

Korsakoffs syndrome You meet patient,tell him your name, he can repeat it You

leave room, come back 2 minutes later, he

doesnt know who you are.


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Hippocampus

Thought to play a role in encodinginformation from STM to LTM

Case of H.M.

Both hippocampi removed to control severeepilepsy

No problems with short-term memory

Lost ability to form new long-term memories

(anterograde amnesia) LTM intact for events until shortly beforesurgery

Symptoms similar to Korsakoffs syndrome,

but different area of brain affected


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Memory and learning

Hippocampus

H. M. - removal of hippocampus:

Retrograde amnesia (loss of memory for events

occurring shortly before brain damage)

intact short-term/working memory

acute anterograde amnesia (declarative memory)

(loss of memory for events happening after thebrain damage)

intact procedural memory

better implicit than explicit memory


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Memory and learning

Theories of the hippocampal function:

declarative, explicit memory

supported by the H.M. case

hippocampal damage may impair implicit memory

it does not damage all the memory in nonhumans

in tasks similar those requiring declarative memory

from humans

dependence on the experimental protocol in

delayed matching-to-sample and delayed

nonmatching-to-sample task experiments


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Memory and learning spatial memory

rat maze experiments hippocampus is involved also in nonspatial aspects of the

tasks

configural learning

the meaning of the stimulus depends on what other stimuliare paired with it, e.g. A + food; B + food; AB + no food

hippocampus is involved in nonconfigural learning if its

sufficiently difficult

binding memories

input from many parts of cortex (secondary and tertiary

areas)


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Memory and learning

Brain damage and memory Korsakoff's syndrome brain damage due to

prolonged deficiency in thiamine (B1).

Thiamine deficiency loss of neurons in dorsomedial thalamus

damage to prefrontal cortex

apathy, confusion, retrograde and anterograde

amnesia;

better implicit memory (good at priming tasks);

impaired reasoning about own memories;

confabulation;


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Memory and learning

Alzheimer's disease

forgetfulness, proceeding into serious memory loss

confusion, depression, restlessness

hallucinations

sleeplessness, loss of appetite

impaired procedural memory, explicit memory,

attention.

Genetic involvement;

excessive accumulation of beta-amyloid plaques

atrophy of cerebral cortex (esp. entorhinal),

hippocampus

formation of neurofibrillary tangles


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Memory and learning

Physiology of learning and memory

Hebbian learning

a cell A that successfully stimulated cell B in thepast becomes more successful in the stimulation of

B in the future

Hebbian learning and classical conditioning

Single cell mechanisms of invertebrate

plasticity

Aplysia


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Memory and learning

habituation depends on a change in

synapse between the sensory and motor

neuron


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Memory and learning

Sensitisation

strong skin stimulation

excitation of facilitating interneuron

serotonine release on presynaptic terminals of

sensory neurons

metabotropic effects

prolonged action potential longer opening of voltage-gated calcium channels

greater transmitter release per action potential


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Memory and learning

associative learning

similar to the sensitisation

pairing the CS (conditioned stimulus) and UCS(unconditioned stimulus) increases presence of

calcium in the presynaptic terminal (due to CS)

Intensified metabotropic effects

More transmitter released than in sensitisation


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Memory and learning Physiology of vertebrate plasticity

long term potentiation (LTP)a response enhancement at certain synapses due to rapid

intensive stimulus delivered simultaneously to a neuron by

several axons

underlying mechanisms vary between the brain areas

prominent in hippocampus

attractive as a cellular basis of learning and memory:

Specificity only the active synapses become

strengthened

Cooperativity simultaneous (almost) stimulationproduces LTP

Associativity LTP is hebbian (no need for actionpotential depolarisation sufficient)


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Memory and learning Biochemistry of LTP main actors:

Glutamate receptors

AMPA opens sodium channels

NMDA allows sodium and calcium ions to enter

the neuron

responds to glutamate ONLY when the membrane is

partly depolarised

removal of magnesium ions blocking NMDA

receptors

glutamate excitation of NMDA receptors opens

NMDA-dependent calcium channels


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Memory and learning

large influx of calcium activates protein kinases:

protein kinase C (PKC)

CaMKII (calcium calmodulin-dependent protein

kinase)

alteration the structure (phosphorylation) of

AMPA receptors

conversion of some NMDA receptors into AMPA

receptors creation of more AMPA receptors

increased dendritic branch growth

increased dendritic responsiveness to subsequent

incomin of lutamate


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Memory and learning

Long term depression (LTD)

a prolonged decrease in response to synaptic

input repeatedly paired to another input at alow frequency

LTP (LTD) may be involved in memory

formation - recently questioned


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Memory and learning

Potential problems with LTP/LTD as

correlates of memory formation:

Importance of protein phosphorylation

Protein phosphorylation is not permanent

protein molecules are not permanent (app. 2

weeks lifetime)


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Memory and learningAlternative mechanisms:

continual phosphorylation of proteins

main suspect: persistently active protein kinases (PKC)

large elevation of calcium activates calpain (enzyme)

breaking the peptide bond between regulatory and

catalytic parts of PKC

freeing the catalytic region (remains active) leading to

continual proteins phosphorylation problem with PKC solution limited time (minutes to

hoursbut Bruces work)


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Memory and learning

protein synthesis

evidence from experiments with protein synthesis

inhibitors

animals injected with these inhibitors learn normally

but fail to recall during later testing

structural changes

change in the number of synapses

morphological reorganisation

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