Psikologi Pembelajaran

How is your brain like(?)

A cabbage A raisin A pillowcase A grapefruit String cheese A walnut

Otak Kita
Are like a jungle- nothing runs the jungle All parts of the brain participate with each other, while each has its 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 atrophy over time) LEARNING IS A DELICATE, BUT IS A POWERFUL DIALOGUE BETWEEN GENETICS AND THE ENVIRONMENT Robert Sylwester, A
Celebration of Neurons

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, insulate and nourish the neurons Brain cells - 30 thousand neurons (300,000 glial cells) fit into the space of a pinhead.

Bagian bagian dari Otak

Brainstem (survival ) Cerebellum ( autonomic nervous system) Limbic system (emotion) Cortex ( reason/logic)
Cortex

Cerebellum
Brainstem

 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

Motor cortex

Somatosensory cortex

Movement and joint positions

Pars opercularis Sensory associative cortex

Visual associative cortex

Brocas area

Grammar and word production

Primary Auditory cortex

Visual cortex

Wernickes area

Cerebellum

Language and Thought

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)

 Neurons contain tubular extensions that are designed to communicate quickly with specific cells in the body network - this is a transportation system, much like a phone system.
The brain has both nerve cells and glial cells. The neurons are cellular agents of cognition; the glial cells act as a scaffolding or insulation for impulses. (The insulation increases the speed of the neural (electrical) messages.)

Memory
Place to store information, as in: How much memory does your hard drive have? Information that gets stored, as in: I have fond memories of my summer vacation. retention of learned information Learning: acquisition of knowledge/information

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)

The Modal Model of Human Memory

Memory stores
Sensory Memory Short-Term Memory 72 items Long-Term Memory Infinite

Capacity

Very large

Duration

Very short (Fraction Short (Fraction of second) of minute)

Indefinite

Format (Coding)

Direct Semantic representation of Spoken (meaningful) sensual experience language format format as action potentials

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 STM Ex: 270-348-8-0-8-0

Repeat information until no longer needed. Strategy to increase duration of STM Rehearsal Ex: 8080 8080 8080Oops, what was that number? Encoding Retrieval Information moved from STM to LTM. Ex: Studying to learn the answers to the test questions. Information moved from LTM to STM Ex: Remembering the answer to the question so that you can write it down.

Four Theories of Forgetting from Long-Term Memory

Explanation Description Example Student studies for exam while watching TV, cant remember answers to test questions. Information never encoded from STM to LTM. 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.

Encoding Failure

Decay

Ebbinghaus memorized nonsense words, tested his memory of these days later, found forgetting curve.

Four Theories of Forgetting (contd)

Explanatio n
Description
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.
According to Freud,

Example

Cant remember old phone

Interference

number; recall new number instead.

Repression

Memories of child abuse

painful memories can be pushed below level of consciousness. Very controversial topic; many psychologists now argue that repression does not occur.

suddenly recalled during psychotherapy (But are they accurate?) Recovered Memory Syndrome false memories planted during hypnosis or drug therapy.

Types of LTM

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

Memory and learning

Subtypes of declarative memory: short-term memory
temporary, limited capacity, needs rehearsal (e.g. telephone number)

long-term memory
'permanent' greater capacity no continual rehearsal needed

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) stored in cells or slots of hard drive But this is not how the nervous system stores information!

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 slug Aplysia

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 evokes response unconditioned response (UCR) after repetitive pairing of CS and UCS presentation of CS evokes learned response - conditioned response (CR) operant conditioning - reinforcement and punishment

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

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 of hippocampus and cortex) damage to amygdala impairs emotional enhancement of memories

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

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

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.

Hippocampus
Thought to play a role in encoding information from STM to LTM Case of H.M.
Both hippocampi removed to control severe epilepsy No problems with short-term memory Lost ability to form new long-term memories (anterograde amnesia) LTM intact for events until shortly before surgery Symptoms similar to Korsakoffs syndrome, but different area of brain affected

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 the brain damage) intact procedural memory better implicit than explicit memory

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

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 stimuli are 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)

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;

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

Memory and learning

Physiology of learning and memory
Hebbian learning
a cell A that successfully stimulated cell B in the past becomes more successful in the stimulation of B in the future

Hebbian learning and classical conditioning

Single
plasticity
Aplysia

cell

mechanisms

of

invertebrate

Memory and learning

habituation depends on a change in synapse between the sensory and motor neuron

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

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

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) stimulation produces LTP Associativity LTP is hebbian (no need for action potential depolarisation sufficient)

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 receptors magnesium ions blocking NMDA

glutamate excitation of NMDA receptors opens NMDA-dependent calcium channels

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 incoming of glutamate

Memory and learning

Long term depression (LTD) a prolonged decrease in response to synaptic input repeatedly paired to another input at a

low frequency
LTP (LTD) may be involved in memory

formation - recently questioned

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)

Memory and learning

Alternative 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 hours but Bruces work)

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