Learning and Memory Flashcards

1
Q

Cognition

A

Cognitive states such as motivation, learning and memory were once considered in the realm of psychology rather than physiology

However, cellular events that influence plasticity underlie these cognitive functions

Changes in neuronal connections as a response to experiences is fundamental to learning and memory

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2
Q

Learning definition

A

the acquisition of knowledge about our environment.

Any relative permanent change in behaviour brought about by past experience.

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3
Q

Memory definition

A

the process by which that knowledge is encoded, stored and later retrieved.

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4
Q

Associative learning

A

Forming new association between two events

Includes classical and operant learning

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5
Q

Cognitive (non-associative) learning

A

Interpretation of present information in light of past experience
Includes habituation and sensitisation

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6
Q

Pavlov,classical conditioning

A

learning a simple behavioural response in the presence of a given stimulus.
concerned with reflex behaviour: an unconditional stimulus (US) eg. food leads to an unconditioned response (salivation)
If a novel stimulus (eg. light/bell) is paired with the US, the novel stimulus alone soon elicits the response ie. it becomes a conditioned stimulus and the response becomes a conditioned response

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7
Q

Steps in classical conditioning

A
Neutral stimulus (NS) has no effect on the subject 
Unconditioned stimulus (US) elicits an unconditioned response (UR)

NS is paired repeatedly with
the US; UR occurs

NS is presented alone, UR occurs
Neutral stimulus is now the conditioned stimulus (CS)

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8
Q

Associative learning-operant conditioning

A

Skinner, 1938

Operant conditioning increases the likelihood of a response by following its occurrence with a reinforcer

Involves a voluntary response (behaviour), with which an organism ‘operates’ on its environment;

Initially happens by chance, consequences determine likelihood of doing it again.

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9
Q

Classical conditioning

A

organism is passive, simply responds to stimuli

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10
Q

operant conditioning

A

organism is active, own behaviour brings on reinforcement (e.g. foot pedal causes food to be released).

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11
Q

reinforcement

A

Any event which increases the likelihood of a response
May be positive (reward training) or negative (escape/avoidance training- not punishment)
Primary reinforcer: satisfies a basic drive e.g. food, pain avoidance
Secondary reinforcer: conditioned e.g. money

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12
Q

Structural changes in learning

A

In humans, disruption of brain activity within 10 minutes of learning abolishes the memory, but if greater than 1 hour, it does not.

Structural changes do occur during learning
e.g. rats reared in a visually enriched environment have much thicker visual cortices
Disuse atrophy of neurons occurs.

Inhibition of protein synthesis within 30 minutes of learning disrupts learning.

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13
Q

Habituation-cognitive learning

A

repeated exposure to a stimulus results in reduced responding to that stimulus
generally neutral, non-noxious stimuli

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14
Q

Sensitisation

A

repeated exposure to a stimulus results in increased responding to that stimulus
generally biologically relevant
also refers to augmentation of responding following exposure to a second stimulus

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15
Q

Research on neural mechanism has focused on non-associative learning and classical conditioning.

A

Eric Kandel and his collaborators used Aplysia to unravel synaptic mechanisms for
Short- and long-term habituation
Short- and long-term sensitization
Classical conditioning.

Eric Kandel won the Nobel Prize for Physiology and Medicine 2000 for this work.

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16
Q

Gill withdrawal reflex in Aplysia Californica

A

The gill is used for breathing
The gill can be covered with the mantle shelf
Waste and seawater are released through the siphon
The gill-withdrawal reflex occurs when touching the siphon produces a retraction of the gill

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17
Q

Mechanism for habituation:

A

↑ K+ conductance → hyperpolarisation → ↓Ca2+ influx → ↓NT release

18
Q

Mechanism for sensitisation:

A

5-HT → ↑cAMP → ↓K+ conductance → prolonged depolarisation → ↑ Ca2+ influx → ↑ NT release

19
Q

Habituation in aplysia

A

short term and long term aplysia-refer to notes

20
Q

Sensitisation in aplysia

A

Kandel termed the neural mechanisms that underlie behavioural sensitisation,
“heterosynaptic facilitation,” which is produced by a second (usually stronger) stimulus

21
Q

Memory

A

Refers to the processes of

Acquiring information
Storing it in the brain
Subsequent retrieval and use

22
Q

Declarative (explicit)

A

conscious, expressed by language
Episodic – associated with a time
Semantic – factual knowledge

23
Q

non-declarative (implicit)

A

a memory recalled unconsciously
Procedural or skill learning
Priming: resistant to brain injury, aging and dementia
Conditioning

24
Q

Acquisition and storage of declarative information

A

Short term storage (hippocampus and related structures)->
long term storage ( a variety of cortical sites: Wernickes area for the meaning of words, temporal cortex for the memories of objects and faces etc,

25
Q

Acquisition and storage of nondeclarative information

A

short term memory (sites unknown but presumably widespread)-> long term storage ( cerebellum,basal ganglia, premoter cortex, other sites related to motor behaviour)

26
Q

Short term memory

A

a cognitive system that is used for holding sensory events, movements, and cognitive information, such as digits, words, names, or other items for a brief period of time
Maintenance

27
Q

working memory

A

the maintenance and controlled manipulation of a limited amount of information before recall

28
Q

sensory traces

A

e.g. iconic (visual) and echoic (auditory) ‘after images’ E.g. brief glance at a setting sun
At most a few seconds in duration (example on next slide – negative after image)

Allows an initial evaluation of physical characteristics or psychological meaning, and a decision as to whether to send the info to short term memory i.e. to attend to it (decided by the limbic system)

29
Q

Selective attention

A

Voluntary e.g. studying

Involuntary e.g. we attend to loud noises, moving objects, psychologically-significant words i.e. potentially threatening / rewarding

30
Q

Short term/working memory

A

Information attended to passes into STM

Encoding: mainly acoustic (sound)

Storage: if unrehearsed memory span 7 ± 2 items, for ~30 seconds (Miller, 1956).
Modern estimates are lower: 4 - 5 items.

Forgetting:

a) decay over time
b) displacement of new information

Maintenance rehearsal (repetition) keeps information in ST store

Capacity of short term memory digit / item span (aka working memory load) is ~7 ± 2 items.
However, an “item” can be a single letter or digit, or a CHUNK of several letters or numbers.
Chunking makes more efficient use of short-term memory by recoding information.
Various kinds of memory training systems and mnemonics include training and drill in specially-designed recoding or chunking schemes.

31
Q

Functions of STM

A

Working Memory: what we are ‘thinking’ about

Important for cognitive processes - facilitates conversation, reading, computation, problem solving.

Evaluation of information and a decision as to whether to send it to Long term memory (selected by the limbic system)

32
Q

Characterisation of mechanisms of memory formation

A

Sensory traces
persistent activity in sensory pathways – changes at the level of the synapses

Short-term memory (STM) or working memory
Reverberating circuits
Electrical basis
Limited capacity
Can be disrupted by intrusion of other activity
E.g. Stroop test – example of interference

33
Q

Neural basis of short-term memory

A

Due to reverberating circuits: self-exciting chains of neurons (e.g. wind-up, see lecture on cortical function) in the relevant sensory, association and motor areas (neural networks).

Medial temporal lobe and mammillary bodies form and consolidate verbal memories (Papez circuit) which are stored in the appropriate areas of the cortex.

STM is very susceptible to disruption of the electrical activity of the brain, e.g. during concussion, epileptic fits or general anaesthetics, leading to amnesia for the immediate preceding events.

34
Q

Long term memory

A

Small amount of information in STM transferred to LTM

Ability to store very large amounts of information for very long periods of time

Encoding: mainly semantic (meaning), also visual (faces), auditory (voices), olfactory (scents).

Transfer requires elaborative rehearsal
i.e. coding, relating to stored information, devising associations, organizing.

Storage: probably unlimited capacity, for very long periods of time
Retrieval ‘cues’ ‘unlock’ correct ‘box’ for memories (recognition is easier than recall).
‘Forgetting’ is usually due to retrieval failure from LTM .

Retrieval is increased by elaboration and organisation (information in many ‘boxes’).

Increased if recalled in context
“recall” indicates the ability to retrieve information related to an item in absence of the item
The thalamus is key to memory recall – damage to this area (e.g. Kluver-Bucy syndrome) can result in retrograde amnesia (recalling memories from the past).

Recall is decreased by interference e.g. anxiety

Influence of emotional factors:
Rehearsal of emotionally-charged items leads to increased storage
Negative emotions can interfere with retrieval
Freud: retrieval of traumatic experiences blocked

35
Q

Locating the memory trace (engram)

A

Engram: physical representation or location of a memory
Karl Lashley (1930s) observed the effects of lesions on rats’learning in a maze
The larger the amount of cortex damaged, the more errors the rats made
Lashley believed that the engram was distributed across the cortex
However, the lesions were so large they damaged several cortical regions. Moreover, the rats might solve the maze using sight, smell and feel in addition to memory.

Lashley was incorrect. All cortical regions don’t contribute equally to memory but they are distributed through the cortex.

36
Q

Scoville and Milner,1957

A

Patient H.M. (Henry Molaison)
Sustained a head injury at age 7
Experienced his first major seizure aged 10
Experimental surgery carried out in 1953, (H.M aged 27) where both hippocampus and amygdala removed as a treatment for the seizures
Epilepsy much improved, controlled by medication

However, H.M had great difficulty forming new long-term memories.
STM and working memory remained intact.
Suggested that the hippocampus/amygdala is vital for the formation of new long-term memories.
Memory could be impaired selectively without loss of other cognitive functions
Memory functions localised to the medial temporal lobe

The hippocampus is thought to be a key structure for memory, but impairment may be due to combined damage of the hippocampus and the amygdala- localisation of memory not completely clear.
Impaired ability to form new memories after surgical removal of hippocampi & amygdala - anteretrograde amnesia.

Partially spared: memories formed before onset of amnesia - retrograde amnesia.

** This means that the medial temporal lobe is critical for the initial formation/encoding of new memory but not the place where well established, long-term memories are stored *

37
Q

Neural basis of LTM

A

Depends on permanent structural changes in the relevant sensorimotor and association areas:
Disruption of the brain’s electrical activity does not abolish LTM
Highly specific cortical activation occurs during recall, and retrograde amnesia is specific for cortical area damaged.

Consolidation: process of transfer of information from STM to LTM, when structural changes occur; corresponds to period of elaborate rehearsal, ~1 hr
Interneural hypothesis: changes in synaptic activity in a neural circuit lead to facilitation of that circuit- a ‘memory engram’.
E.g. increased number of presynaptic terminals, vesicle-release sites and transmitter vesicles.
Altered post synaptic dendritic spines

Long Term Potentiation (LTP): well documented mechanism of learning in hippocampus, cerebellum.
Long Term Depression (LTD): long-lasting activity-dependent reduction in the efficacy of synaptic transmission

38
Q

Two common types of brain damage

A

Korsakoff’s syndrome and alzheimer’s disease

39
Q

Korsakoff’s syndrome

A

Prolonged thiamine (vitamin B1) deficiency. Often due to chronic alcoholism
Impedes the ability of the brain to metabolize glucose.
Leads to a loss of or shrinkage of neurons in the brain (mammillary body).
Symptoms include apathy, confusion, and forgetting and confabulation (taking guesses to fill in gaps in memory).

40
Q

Alzheimer’s disease

A

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.

41
Q

Lessons from studying amnesiac patients

A

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.

42
Q

Improving declarative memory

A

Chunking: Grouping items in STM may be recoded, using information from LTM, into larger more meaningful units (chunks) – memory span is still 7±2 items

Elaboration, organisation – hierarchical most efficient

Context: recreating learning situation in imagination

Imagery: meaningful connection between two words e.g. method of loci – mind palace, key-word system, mnemonics

PQ4R (Preview, Question, Read, Reflect, Recite, Review)
Practicing retrieval as one learns ↑↑ retrieval later