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PSY290: Behavioral Neuroscience > Week 6: Learning and Memory > Flashcards

Week 6: Learning and Memory Flashcards

1
Q

Learning

A

Permanent change in behavior as the result of experience; change in brain structure and/or function

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2
Q

Neuroplasticity

A

Physical change in brain due to experience; required for learning; involved in any event that causes change

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3
Q

Sequence of events in learning

A

Stimulus -> neuronal activity (selective) -> intracellular signaling pathways (events to change) -> gene expression -> protein expression -> structural/functional changes

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4
Q

Types of changes in the brain

A

Neuronal structure, grey or white matter, synapse strength. All can be identified using neuroimaging (usually MRI)

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5
Q

Changes in neurons

A

Structure is changed, not amount. Ex: dendritic arborization (growth of dendrites, thus more synapses)

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6
Q

Grey matter change

A

Dendritic expansion or change to vasculature (supply system to neurons)

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7
Q

Synapse strength change

A

Key to learning; strength of connection between various neurons; improvement of cell communication

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8
Q

Hebb’s Postulate (1950)

A

Activating a synapse repeatedly will change it and strengthen it

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9
Q

Bliss and Lomb synapse activation study

A

Repeatedly activated one axon of one neuron in the hippocampus at a rate of 100 times per second. Found a strengthening of the stimulated neuron. Supported Hebb’s Postulate

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10
Q

Long-term Potentiation (LTP)

A

Long-term increase in ability for cell A to activate cell B; larger excitatory post-synaptic potential (EPSP) in cell B

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11
Q

Measuring LTP

A

Looking at field EPSPs (the response of lots of neurons). After stimulation, there is a spike in PTP (post-tetanic potentiation), and LTP outlasts the PTP spike. Used to measure learning, post-synaptic LTP is the most commonly used

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12
Q

Use of LTP in learning

A

Correlated with learning in many models; fundamental change mechanism across the brain that modifies behavior

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13
Q

Long-term Depression (LTD)

A

Long-term weakening in synaptic strength, induced by prolonged weak stimulus

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14
Q

Use of LTD in learning

A

Tunes the network by eliminating obsolete synapses; acts as a built in reset

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15
Q

Rate remapping

A

Changes in neuron firing rate
Ex: Cell A fires faster than it did before

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16
Q

Population remapping

A

Changes in neuron firing potential
Ex: Cell C fires in response to cell A, where it didn’t before

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17
Q

Use of animals in neuronal learning study

A

Animals are primarily used due to ethical concerns. Studying learning at a neuronal level induces great damage to the brain.

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18
Q

London Taxi Driver Study

A

Argument: learning massive amounts of information should change the brain structure
Method: examining the cortical mass of those who passed the London taxi driver exam and those who did not. To pass you must memorize a massive amount of spatial information
Findings: Larger grey matter amount in those who passed. Increase in posterior hippocampus (spatial info) and decrease in anterior hippocampus (anxiety and stress responses, etc.)
Argument SUPPORTED

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19
Q

Music training age study

A

Argument: long-lasting change should occur, and earlier age of inception should show more change
Method: Correlative observation of musicians who started playing an instrument at various ages. Examining functional differences and cortical response to activity/training
Findings: Those who started at a younger age have a greater response. Changes were specifically seen in the somatosensory cortex
Argument SUPPORTED

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20
Q

Change in gene expression

A

Thousands of genes can be changed during the learning process. Aside from neuronal/structure change, gene expression change is likely the driving factor in learning

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21
Q

Memory

A

Process of information being stored, consolidated, and retrieved. Reconstructive and innacurate

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22
Q

Reconstructive-ness of memory

A

Influenced by current goals, knowledge, expectations and schemas

23
Q

Arousing vs. everyday memories

A

Arousing memories have a higher level of confidence, i.e we believe we remember them better. However, they show the same level of inaccuracy and forgetting as normal memories

24
Q

Intervening events vs. memory

A

Intervening events can alter existing memories or create false memories

25
Q

Memory trace/engram theory

A

Proposes memories are mapped onto small subsets of cells in the brain. When retrieving memories, similar subgroups of cells are activated (not the exact subgroup). Cells within memory subgroups are interconnected with other subgroups (suggests activation of similar memories together)

26
Q

Winner-take-all model

A

Competitive model of cell selection for engram groups. The more excitable calls at the time of the experience will be put into the memory trace.

27
Q

Testing the winner-take-all model

A

Method: Performed in rodents. Manipulated CREB amount in cells to make certain cells more active during learning. After learning phase, these high CREB cells were eliminated.
Findings: after deletion of high CREB cells, the rodents experienced memory loss.
Supports winner-take-all model, suggests active cells (those high in CREB) were made part of the memory trace

28
Q

CREB

A

cyclic AMP-response element binding protein, affects capacity for change during an event; used to test winner-take-all model

29
Q

Forming many memories at once

A

Memories formed close in time are attributed to the same excitable/plastic cells, and are likely to have overlapping cell populations. Changing one memory may affect another that has a similar population.

30
Q

Testing multiple memory formation

A

Method: Studied memories formed close in time vs. not close in time. Conditioned fear response to first memory, but not second.
Findings: fear response transferred/generalized between temporally-linked memories, but not the separate memories
Suggests memories formed close in time share similar cell traces due to the same cells being active during encoding

31
Q

Memory storage

A

Tested by Lashley: no one solid place where memories are stored in the brain. Distributed across all areas. Removal of any brain area affected memory

32
Q

Issues with Lashley study of memory storage

A

Only focused on cortical area, not subcortical structures. Only looked at one type of learning (maze learning), not any other types of learning/memory

33
Q

Role of Hippocampus in memory

A

Acts as the gateway to declarative memory storage AND plays a role in recall of detail rich episodic memory. Not where memories are stored (misconception).

34
Q

Patient HM

A

Hippocampus removed. Saw drastic anterograde amnesia. Could not form new memories, could hold past memories. Suggests hippocampus important in creation of new memories but not storage of old memories.

35
Q

Standard Memory Consolidation Theory

A

Recent memories involve strong connection between the hippocampus and the cortex. As the memory ages the connection weakens and is no longer dependent on the hippocampus

36
Q

Multiple trace theory

A

Argues the hippocampus creates new memory traces with each recall of a memory. What gets put back is not always what was taken out. Suggests hippocampus is involved in memory creation and memory storage specifically for detail-rich episodic memory

37
Q

Issues with Standard Memory Consolidation Theory

A

Case studies other than HM show damage of old/remote memories with hippocampal damage as well as anterograde amnesia. Suggests hippocampus is also involved in memory storage

38
Q

Effect of memory type on storage location

A

Different memory types are stored in different brain areas. Ex: non-declarative memories are stored differently than declarative

39
Q

Brain area associated with recognition

A

Perirhinal cortex (tested in rodents)

40
Q

Can you improve memory?

A

Yes, in theory you could activate the cells upon learning. This has been tested via electrode and TMS, and only subtle results have been found

41
Q

Can you erase memories?

A

Yes, theoretically you should be able to kill the neurons that hold the memory trace.
Issues: you can’t know which neurons hold the memory and they may be involved in other memories or brain functions

42
Q

Can you create false memories?

A

Yes. Tested by activating neurons that are part of a safe memory trace during an unsafe event. Found that fear was present when returned to the context of the first safe memory. Supports that manipulating cells within a trace can change the memory

43
Q

Modifying memory to treat PTSD

A

Aversive memories are recalled while fear responses are blocked using beta-andregernic receptor-blockers. Found that repeated treatments like this can reduce the PTSD responses related to specific memories

44
Q

Benefits of memory modification

A

Removing negative associations with memories can assist processing, can improve quality of life, and can in some cases improve memory

45
Q

Anterograde amnesia

A

Lack of ability to form new memories after the traumatic incident to the brain

46
Q

Retrograde amnesia

A

Inability to remember memories that occurred prior to the traumatic incident/lesion to the brain

47
Q

Declarative memory

A

A fact about the world or yourself that you can objectively tell someone else. Subsets: episodic and semantic

48
Q

Episodic memory

A

Clear memories about yourself or your life; facts about yourself or your life that you can verbally tell someone else. Held in the cortex

49
Q

Semantic memory

A

Facts about the world that you have learned and can verbally express to someone else. Held in the cortex

50
Q

Non-declarative/procedural memory

A

Things you know that you cannot verbally express, but you can show that you know. Subsets: skill-learning, priming, and conditioning

51
Q

Skill-learning

A

Procedural skills that you know how to do, such as movements. Stored in the basal ganglia, cortex, and cerebellum

52
Q

Priming

A

Subconscious preparation of the brain based on seeing or experiencing a stimulus. Stored in the cortex

53
Q

Conditioning

A

The pairing of a memory or learned response with a specific stimulus. Stored in the cerebellum

PSY290: Behavioral Neuroscience (10 decks)

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