Ppt Chap 13

Chapter 13:Biology of Learning and

Memory

Learning, Memory, Amnesia, and Brain Functioning

• An early influential idea was that physical changes occur when something new is learned or a memory is formed.

• Explanations was that connections grew between areas of the brain.– Led to the search for localized

representations of memory


• Ivan Pavlov pioneered classical conditioning in which pairing of two stimuli changes the response to one of them.– A conditioned stimulus (CS) is paired with

an unconditioned stimulus (UCS) which automatically results in an unconditioned response (UCR).

• After several pairings, response can be elicited by the CS without the UCS, – New response is now called a conditioned

response (CR).


• In operant conditioning, responses are followed by reinforcement or punishment that either strengthen or weaken the behavior.– Reinforcers are events that increase the

probability that the response will occur again.

– Punishment are events that decrease the probability that the response will occur again.


• Pavlov believed that conditioning strengthened connections between the CS center and UCS center in the brain.

• Karl Lashley set out to prove this by searching for such engrams, or physical representations of what had been learned.– Believed that a knife cut should abolish the

newly learned response.


• Lashley’s studies attempted to see if disrupting certain connections between cortical brain areas would disrupt abilities to learn associations.

• Found that learning and memory did not depend entirely on connections across the cortex

• Also found that learning did not depend on a single area of the cortex.


• Lashley proposed two key principles about the nervous system:• Equipotentiality – all parts of the cortex

contribute equally to complex functioning behaviors (e.g. learning)

• Mass action – the cortex works as a whole, not as solitary isolated units.


• Richard F. Thompson et. al. suggested that the engram for classical conditioning is located in the cerebellum, not the cortex.

• During conditioning, changes occur in the lateral interpositus nucleus (LIP) of the cerebellum– Responses increase as learning proceeds– necessary for learning and retention

• However, a change in a brain area does not necessarily mean that learning took place in that area.


• Suppression of activity in the LIP led to a condition in which the subject displayed no previous learning.

• As suppression wore off, the animal began to learn at the same speed as animals that had no previous training.

• But suppression of the red nucleus also led to a similar condition.

• Later assumed that the learning did occur in the LIP, as it was the last structure that needed to be awake for learning to occur.


• Psychologist differentiate between learning and memory.

• Hebb (1949) differentiated between two types of memory:

• Short-term memory – memory of events that have just occurred.

• Long-term memory – memory of events from times further back.


• Differences between STM and LTM– Short-term memory has a limited capacity;

long-term memory does not.– Short-term memory fades quickly without

rehearsal; long-term memories persist.– Memories from long-term memory can be

stimulated with a cue/ hint; retrieval of memories lost from STM do not benefit from the presence of a cue.


• Researchers propose all information enters STM where the brain consolidates it into LTM.

• Later research has weakened the distinction between STM and LTM

• Working Memory– Proposed by Baddeley & Hitch as an

alternative to short-term memory.– Emphasis on temporary storage of

information to actively attend to it and work on it for a period of time.


• Common test of working memory is the delayed response task.– Requires responding to something you

heard or saw a short while ago.• Research points to the prefrontal cortex for

the storage of this information• Brain may use elevated levels of calcium to

potentiate later responses


• Older people often have impairments in working memory.

• Changes in the prefrontal cortex assumed to be the cause.

• Declining activity of the prefrontal cortex in the elderly is associated with decreasing memory.

• Increased activity is indicative of compensation for other regions in the brain.


• Amnesia is the loss of memory.• Studies on amnesia help to clarify the

distinctions between and among different kinds of memories and their mechanisms.

• Different areas of the hippocampus are active during memory formation and retrieval.– Damage results in amnesia.


• H.M. is a famous case study in psychology who had his hippocampus removed to prevent epileptic seizures.

• Afterwards H.M. had great difficulty forming new long-term memories.

• STM or working memory remained intact.• Suggested that the hippocampus is vital for

the formation of new long-term memories.


• H.M. showed massive anterograde amnesia after the surgery.

• Two major types of amnesia include:• Anterograde amnesia – the loss of the

ability to form new memory after the brain damage

• Retrograde amnesia – the loss of memory events prior to the occurrence of the brain damage.


• Patient HM also displayed greater “implicit” than “explicit” memory.

• Explicit memory – deliberate recall of information that one recognizes as a memory.

• Implicit memory – the influence of recent experience on behavior without realizing one is using memory.


• H.M. had difficulty with episodic memory and declarative memory.– Episodic memory: ability to recall single

events.– Declarative memory: ability to state a

memory into words.• H.M.’s procedural memory remained intact.

– Procedural memory: ability to develop motor skills (remembering or learning how to do things).


• Research of the function of the hippocampus suggests the following:

1. The hippocampus is critical for declarative memory functioning (especially episodic).

2. The hippocampus is especially important for spatial memory.

3. The hippocampus is especially important for configural learning and binding.


• Research in the role of the hippocampus in episodic memory shows damage impairs abilities on two types of tasks: • Delayed matching-to-sample tasks – a

subject sees an object and must later choose the object that matches.

• Delayed non-matching-to-sample tasks– subject sees an object and must later choose the object that is different than the sample.


• Damage to the hippocampus also impairs abilities on spatial tasks such as:

• Radial mazes – a subject must navigate a maze that has eight or more arms with a reinforcer at the end.

• Morris water maze task – a rat must swim through murky water to find a rest platform just underneath the surface.


• Hippocampus may also be important for contextual learning

• Remembering the detail and context of an event

• suggests that the hippocampus is important in the process of “consolidation”.

• Damage to the hippocampus impairs recent learning more than older learning.– The more consolidated a memory

becomes, the less it depends on the hippocampus.


• Reverberating circuits of neuronal activity were thought to be the mechanisms of consolidation.

• Consolidation is also influenced by the passage of time and emotions.– Small to moderate amounts of cortisol

activate the amygdala and hippocampus where they enhance storage and consolidation of recent experiences.

– Prolonged stress impairs memory.


• Different kinds of brain damage result in different types of amnesia.

• Two common types of brain damage include:

1. Korsakoff’s syndrome

2. Alzheimer’s disease


• Korsakoff’s syndrome – brain damage caused by prolonged thiamine (vitamin B1) deficiency

• impedes the ability of the brain to metabolize glucose.

• Leads to a loss of or shrinkage of neurons in the brain.

• Often due to chronic alcoholism.• Symptoms include apathy, confusion, and

forgetting and confabulation (taking guesses to fill in gaps in memory).


• Alzheimer’s disease is associated with a gradually progressive loss of memory often occurring in old age.

• Affects 50% of people over 85.• Early onset seems to be influenced by

genes, but 99% of cases are late onset.• About half of all patients with late onset

have no known relative with the disease.


• Alzheimer’s disease is associated with an accumulation and clumping of the following brain proteins:• Amyloid beta protein 42 which produces

widespread atrophy of the cerebral cortex, hippocampus and other areas.

• An abnormal form of the tau protein, part of the intracellular support system of neurons.


• Accumulation of the tau protein results in:– Plaques – structures formed from

degenerating neurons.– Tangles – structures formed from

degenerating structures within a neuronal body.


• A major area of damage is the basal forebrain and treatment includes enhancing acetylcholine activity.

• One experimental treatment includes the stimulation of cannabinoid receptors that limits overstimulation by glutamate.

• Research with mice suggests the possibility of immunizing against Alzheimer’s by stimulating the production of antibodies against amyloid beta protein.


• Lessons from studying amnesiac patients include:– There can be deficiencies of very different

aspects of memory.– There are independent kinds of memory.– Various kinds of memory depend on

different brain areas.


• Other subcortical brain areas and the cortex important in learning:

• Amygdala associated with fear learning• Parietal lobe associated with piecing

information together• anterior and inferior region of the temporal

lobe and semantic memory– semantic dementia (loss of semantic

memory)


• Other areas of the cortex important in learning (con’t):

• Prefrontal cortex and learning about rewards and punishments– Basal ganglia, anterior cingulate cortex

also involved

Storing Information in the Nervous System

• Activity in the brain results in physical changes.

• Patterns of activity leave a path of physical changes.

• Not every change is a specific memory as was once originally believed.

• Many ideas originally believed to be true have been refined.


• A Hebbian synapse occurs when the successful stimulation of a cell by an axon leads to the enhanced ability to stimulate that cell in the future.– Increases in effectiveness occur because

of simultaneous activity in the presynaptic and postsynaptic neurons.

– Such synapses may be critical for many kinds of associative learning.


• Studies of how physiology relates to learning often focus on invertebrates and try to generalize to vertebrates.

• The aplysia is a slug-like invertebrate that is often studied due to its large neurons.

• This allows researchers to study basic processes such as:– Habituation– Sensitization


• Habituation is a decrease in response to a stimulus that is presented repeatedly and accompanied by no change in other stimuli.– Depends upon a change in the synapse

between the sensory neurons and the motor neurons.

– Sensory neurons fail to excite motor neurons as they did previously.


• Sensitization is an increase in response to a mild stimulus as a result to previous exposure to more intense stimuli.

• Changes at identified synapses include:– Serotonin released from a facilitating

neuron blocks potassium channels in the presynaptic neuron.

– Prolonged release of transmitter from that neuron results in prolonged sensitization.


• Long-term Potentiation (LTP) occurs when one or more axons bombard a dendrite with stimulation.– Leaves the synapse “potentiated” for a

period of time and the neuron is more responsive


• Properties of LTP that suggest it as a cellular basis of learning and memory include:– Specificity– Cooperativity– Associativity


– Specificity – only synapses onto a cell that have been highly active become strengthened.

– Cooperativity – simultaneous stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by a single axon.

– Associativity – pairing a weak input with a strong input enhances later responses to a weak input.


• Long-term depression (LTD) is a prolonged decrease in response at a synapse that occurs when axons have been active at a low frequency.– The opposite of LTP


• Biochemical mechanisms of LTP are known to depend on changes at glutamate and GABA primarily in the postsynaptic neuron

• This occurs at several types of receptor sites including the ionotropic receptors:

–AMPA receptors–NMDA receptors


• LTP in hippocampal neurons occurs as follows:– Repeated glutamate excitation of AMPA

receptors depolarizes the membrane.– The depolarization removes magnesium

ions that had been blocking NMDA receptors.

– Glutamate is then able to excite the NMDA receptors, opening a channel for calcium ions to enter the neuron.


– Entry of calcium through the NMDA channel triggers further changes.

– Activation of a protein that sets in motion a series of events occurs.

– More AMPA receptors are built and dendritic branching is increased.

• These changes increase the later responsiveness of the dendrite to incoming glutamate.


• Changes in presynaptic neuron can also cause LTP.

• Extensive stimulation of a postsynaptic cell causes the release of a retrograde transmitter that travels back to the presynaptic cell to cause the following changes:– Decrease in action potential threshold– Increase neurotransmitter release of – Expansion of the axons.– Transmitter release from additional sites.


• LTP reflects increased activity by the presynaptic neuron and increased responsiveness by the postsynaptic neuron

• Understanding the mechanisms of changes that enhance or impair LTP may lead to drugs that improve or block memory.– Increasing production of hormones

increased by LTP– Ginkgo biloba– Etc.

Education

Ppt Chap 13