Learning And Memory Flashcards

(25 cards)

1
Q

What is learning?

A

Behavioural experience associated with change

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2
Q

What is memory?

A

Encoding of learning experience

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3
Q

2 types of learning:

A
  1. Associative learning
  2. Non-associate Learning
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4
Q

Associate learning:

A
  • based on associations between different phenomena
  • Pavlov classical conditioning - dog experiments
  • operant conditioning&raquo_space; responce followed by reinforcement or punishment
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5
Q

Non- associate learning

A
  • not based on association
  • habituation&raquo_space; repeated exposure to stimulus that offers no threat/ benefit
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6
Q

Where does learning occur?

A

Lateral Interpostius Nucleus (LIP) in cerebellum = area for learning

Red nucleus = preformance of learnt behaviour

PAVLOV- classical conditioning rusted in streghthed connection between 2 areas

LASHLEY- made multiple deep cuts in brain, learning not impaired, only impaired by large lesions in multiple areas&raquo_space;> all parts of cote contribute equally to complex behaviours

Later experiments: red nucleus= crucial for preformance of conditioned response, bit NOT learning

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7
Q

Types of memory:

A
  1. Short-term memory&raquo_space; limited capacity, least faer few seconds
  2. Long-term memory&raquo_space; unlimited capacity, hints help reconstruct it
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8
Q

What is working memory for?

A

Stores info that is still in use
Stores info that’s still relevant
Stores info crucial for complex cognitive activities

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9
Q

How to test what areas are used for working memory?

A

Delayed responce task
- testing ppl’s responces to stimuli they saw/ heard short while before
- record brain activity during delay

Info stored in: prefrontal cortex

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10
Q

What changes at cellular level during learning?

A

Habituation:
- decrease in repsonce to stimulus that’s presented repeatedly

Sensitisation:
- increased responce to unpleasant stimulus after shock
- highly sensitive to sudden noises
- chnages in synaptic activity produces behavioural placticty (allows to respond to environment appropriately)

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11
Q

Cellular level

A
  • stimultaneuous activity in pre-synaptic + post synaptic neurons increase effectiveness of each action potential
  • so, if axon stimulates cell that’s recently been stimulates, responce = increased
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12
Q

Long-term potential (LIP)

A

Axons bombard dendrites with rapid series of stimuli
Leaves synapse more responsive for period of time

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13
Q

Lon-term depression

A

When axons are active at low frequency, responce reduces

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14
Q

Hippocampus and Amnesia

A

Case study: sever epilepsy, removal of hippocampus reduces seizures, but every memory loss

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15
Q

What is Anterograde Amnesia ?

A

Loss of memory for events that happened AFTER brain damage

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16
Q

What is Retrograde amnesia ?

A

Loss of memory for events that happened a few years BEFORE brain damage

17
Q

What is the hippocampus important for?

A

New memories
Declarative, explicit memories

18
Q

Hippocampus- specialised for decelerate memory

A
  • crucial for dcelarite, episodic memory + remembering specific/ personal events
  • if you damage hippocampus in animals + test their abilities = preformance impaired
19
Q

Hippocampus - specialised for spatial memory

A
  • hipp= crucial for remembering places + locations
  • London taxi drives have larger hipp than non-taxi drivers
  • those driving for longer had even larger hippocampus
  • experience leads to growth
20
Q

Hippocampus - specialised for configural learning

A
  • hipp records configural info quickly and cortex detects repeated patterns
  • hipp ‘binds’ info in order (smell or smoke with sound of fire cracking)
  • cortex establishes this memeory as important- later connected it with memory of fire
21
Q

Korsakoff’s Syndrome

A

Brain damage, leading to amnesia.
Mainly in alcoholics- drink lots and don’t eat enough, brain starved of vitamins.
Vitamin B1 deficiency.
Causes shrinkage of neurons in brain.
Pathway to cortex damaged= executive functions effected
Loose executive control over memories- try fill in gaps with confabulations.

22
Q

What are confabulations?

A

Due to memory loss, make guess to fill their memeory loss. Over time begin to believe these ‘guesses’ as true memories.

23
Q

Alzheimer’s Disease

A

Accumulation of amyloid—> causes washing away of cerebral cortex, hippocampus + others.
Starts with minor forgetfulness > progresses to severe memory loss.
Can configure new skills, but don’t remember learning them.
Better implicit than explicit memeory, but both impaired.

24
Q

What causes Alzheimer’s?

A
  1. Genetic — ppl with Down’s syndrome almost always get it in Middle Age
  2. Environment— bad diet?
25
Alzheimer’s and Krsakoffs:
Both involve hippocampus and cortical damage. Both= widespread damage Similarities: lose prev memories + ability to form new ones Differences: confabulation