Learning and Memory Flashcards

1
Q

What is learning?

A

an attempt to create a memory that lasts

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2
Q

What is memory?

A

how you encode, store, and retrieve information

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3
Q

What is an engram?

A

the physical basis of memory - a pathway of cells/memory trace

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4
Q

How are memories established?

A

the formation of neuronal interconnections, susceptible to change

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5
Q

Distinguish between anterograde amnesia and retrograde amnesia

A

Anterograde - failure to store memories after trauma

Retrograde - failure to recall memories before trauma

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6
Q

What are the 3 stages of memory?

A
  1. Encoding
  2. Storage
  3. Retrieval
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7
Q

What is plasticity?

A

the brain’s ability to adjust its structure to reflect life’s experiences

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8
Q

Describe the process of neurogenesis (4)

A
  1. nerve cells form more synapses
  2. blood capillaries increase in the brain
  3. glial cells increase in size and number
  4. myelin sheath increases
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9
Q

Define neurogenesis

A

the process by which new neurons are formed in the brain

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10
Q

How does learning occur according to Pavlov and Skinner? (2)

A

Pavlov - classical conditioning (involuntary responses)

Skinner - operant conditioning (voluntary responses)

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11
Q

Describe classical conditioning (2)

A

conditioned stimulus is paired with an unconditioned stimulus to produce an unconditioned response

after several pairings, the conditioned stimulus alone produces a conditioned response

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12
Q

Describe operant conditioning

A

Responses are followed by reinforcement or punishment to strengthen or weaken behaviour respectively

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13
Q

Distinguish between positive and negative reinforcement, and punishment (3)

A

Positive - addition of positive stimuli to strengthen a behaviour

Negative - removal of negative stimuli to strengthen a behaviour

Punishment - addition of negative stimuli to weaken a behaviour

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14
Q

What was Lashley’s 1st hypothesis? (2)
Was it true or false?

A

learning depends on new/strengthened connections between 2 brain areas

hence, a cut somewhere in the brain interrupts that connection and destroys the learned response

Result: false

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15
Q

What was Lashley’s 2nd hypothesis? (2)

Was it true or false? Explain

A

certain portions of the cerebral cortex are more important than other for learning

hence, removing chunks of the cerebral cortex impairs learning

Result: false
Explanation: amount of tissue removed mattered, not from where it was removed

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16
Q

What did Lashley’s studies conclude? (2)

A

Learning and memory do not depend only on connections

Learning doesn’t depend only on one area

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17
Q

Explain Lashley’s principle of equipotentiality? (3)

A

all parts of the cortex contribute equally to learning

hence one part of the cortex can take over the function of another part

therefore, to destroy 1 function, the whole area must be destroyed

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18
Q

Explain Lashley’s principle of mass action (2)

A

the cortex works as a whole

hence if cortical tissue is destroyed after learning a complex task, deterioration of performance is determined by the amount of tissue destroyed

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19
Q

Where is engram found according to Thompson?

A

in the lateral interpositus nucleus of the cerebellum

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20
Q

Explain Thompson’s experiment regarding the LIP (3)

A

Classical conditioning:
tone (CS) + airpuff (UCS) –> eyeblink (UCR)

learnt response:
tone (CS) –> eyeblink (CR)

Pathway taken to the LIP:
facial nucleus –> red nucleus –> LIP

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21
Q

What results did Thompson’s experiment yield? (2)

A

Temporary inactivation of LIP blocked learning completely

Temporary inactivation of red nucleus blocked learning only during inactivation

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22
Q

What are the 3 types of memory?

A

Short term memory
Working memory
Long term memory

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23
Q

Define working memory

A

memory for temporary information required for carrying out cognitive tasks (e.g., learning)

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24
Q

What are the 2 types of long term memory?

A

Declarative (explicit) memory
Procedural (implicit) memory

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25
Q

What are the 2 types of declarative memory?

A

Episodic memory
Semantic memory

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26
Q

What are the 2 types of procedural memory?

A

Skills
Habits

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27
Q

Describe episodic memory

A

autobiographical memories - things that have happened to you

28
Q

Describe semantic memory

A

the conscious recollection of factual information and general knowledge

29
Q

Describe procedural memory
Give an example

A

memory of skills and procedures that can be used without conscious thought

e.g., playing an instrument

30
Q

What is the hippocampus responsible for? (4)

A

formation of long term declarative memories, especially episodic memories

spatial memory

context association

memory consolidation

31
Q

What are 2 properties of the hippocampus?

A

located in medial temporal lobe

shaped like a seahorse

32
Q

What 2 regions is the hippocampus made up of?

A

Dentate gyrus
Cornu ammonis

33
Q

What results from the removal of the hippocampus? (3)

A

moderate retrograde amnesia

severe anterograde amnesia

better procedural/implicit memory than declarative/explicit memory

34
Q

Which brain structures are associated with procedural (implicit) (3) and declarative (explicit) memory?

A

Procedural: amygdala, medial temporal lobe, basal ganglia

Declarative: hippocampus

35
Q

Compare the learning functions of the basal ganglia and the hippocampus (2)

A

Basal ganglia:
produces habits
learns on reinforcement/punishment

Hippocampus:
produces flexible responses
learns through making connections

36
Q

What is the hippocampus’s role in context association?

A

binding information to context by synchronizing the many brain areas a memory is spread across

37
Q

What is the hippocampus’s role in memory consolidation

A

guides the reorganization of information stored in the neocortex, so that it becomes independent of the hippocampus

38
Q

What are 2 types of brain damage that result in amnesia?

A

Korsakoff’s syndrome
Alzheimer’s disease

39
Q

What is Korsakoff’s syndrome caused by? (2)

A

Thiamine deficiency
Chronic alcohol consumption

40
Q

Distinguish between Wernicke’s encephalopathy and Korsakoff’s syndrome

A

Wernicke’s encephalopathy - reversible

Korsakoff’s syndrome - non-reversible

41
Q

How does Korsakoff’s syndrome lead to amnesia?

A

the brain needs thiamine to metabolize glucose - without thiamine, there is decreased energy, leading to loss or shrinkage of brain neurons

42
Q

Which brain area is most affected by Korsakoff’s syndrome?

A

thalamus

43
Q

What are symptoms of of Korsakoff’s syndrome? (5)

A

apathy
retrograde amnesia
anterograde amnesia
ataxic gait (cerebellar dysfunction)
confabulation

44
Q

What is confabulation?

A

wild guessing mixed with correct information to hide memory gaps

45
Q

Distinguish between dementia and Alzheimer’s (2)

A

Dementia - umbrella term
Alzheimer’s - disease that falls under dementia

Therefore, not every type of dementia is Alzheimer’s, but every case of Alzheimer’s is dementia

46
Q

Describe the 3 stages of Alzheimer’s? (9)

A

Mild - getting lost, taking longer to complete daily tasks, repeating questions

Moderate - problems recognizing family, inability to learn new things, paranoia

Severe - cannot communicate, bedridden, dependent on others

47
Q

What is found in the brain of people with Alzheimer’s? (3)

A

amyloid plaques (outside neurons)
neurofibrillary tangles (inside neurons)
broken neural connections

48
Q

What causes amyloid plaques and neurofibrillary tangles?

A

Amyloid plaques: accumulation of amyloid beta protein 42

Neurofibrillary tangles: altered tau function - destabilization of microtubules

49
Q

What is the treatment for Alzheimer’s? (2)

A

Donepezil - inhibits acetylcholinesterase - prevents breakdown of acetylcholine

Memantine - blocks NMDA receptors - prevents Calcification

50
Q

Explain the hypothesis of synaptic plasticity (2)

A

when we learn something, we create specific physical changes in our brain

these changes are modifications of synaptic connections and strength - making synapses more efficient

51
Q

Explain the Hebbian Synapse mechanism (2)

A

neuron A repeatedly excites neuron B - causing a growth process to take place in one/both cells

as a result neuron A is then more able to excite neuron B

52
Q

Define habituation

A

a decrease in response to a stimulus that is presented REPEATEDLY and accompanied by NO CHANGE in other stimuli

53
Q

Describe habituation in an aplysia (2)

A

the aplysia’s siphon is stimulated, causing the sensory neuron to release normal amounts of neurotransmitter

when habituation occurs, the release of neurotransmitter by the sensory neuron decreases

54
Q

Define sensitization

A

an increase in response to a mild stimulus as a result of EXPOSURE to a more INTENSE stimulus

55
Q

Describe sensitization in an aplysia

A

a strong stimulus on an aplysia’s skin intensifies a later withdrawal response to touch

56
Q

What is long term potentiation? (LTP)

What does it depend on? (3)

A

the major cellular mechanism that moves memories into long term storage

changes at synapses

long lasting enhancement of synaptic strength

modification in signal transmission

57
Q

What changes does LTP involve? (2)

A

physical change in neuron structure
strengthening of neural connections

58
Q

How does LTP occur? (2)

A
  1. one or more axons bombard a dendrite with stimulation
  2. the burst of stimulation leaves the synapse potentiated for a period of time - making the neuron more responsive for minutes/days/weeks
59
Q

What are 3 properties of LTP? Explain them.

A

Specificity - only active synapses are strengthened

Cooperativity - simultaneous stimulation by 2 or more axons produces LTP more strongly than repeated stimulation by 1 axon

Associativity - pairing weak input with strong input enhances later responses to weak input

60
Q

What do the biochemical mechanisms of LTP depend on?

A

changes at glutamate synapses - involving AMPA and NMDA receptors

61
Q

What type of receptors are AMPA and NMDA?

A

Ionotropic - allows ions into postsynaptic neuron when stimulated

62
Q

Describe the process of LTP (4)

A
  1. repeated glutamate excitation of AMPA receptors strongly depolarizes the membrane
  2. depolarization removes Mg ions blocking NMDA receptors - allowing glutamate to excite them
  3. Ca ions enter the neuron, triggering the activation of the protein CaMK2
  4. More AMPA receptors are built and dendritic branching increases - resulting in increased responsiveness to glutamate
63
Q

What occurs when CaMK2 is activated? (3)

A
  1. CaMK2 sets in motion a series of reactions resulting in the release of another protein: CREB
  2. CREB goes to the nucleus of cell regulating gene expression
  3. CaMK2 and CREB propagate into the dendrites, triggering the release of BDNF
64
Q

What are the functions of BDNF (3)?

A

prevents cell death
induces neurogenesis
maintains neurons’ survival

65
Q

What changes occur in the presynaptic neuron after LTP? (2)

A
  1. postsynaptic neuron releases retrograde neurotransmitter - which gets absorbed by the presynaptic neuron
  2. retrograde neurotransmitter modifies and regulates neurotransmission - creating a stronger link between neurons
66
Q

What is long term depression? (LTD)

A

processes selectively weaken specific sets of synapses in order to make synaptic strengthening useful - occurs after LTP