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Psych 002 > Chapter 12: Learning and Memory > Flashcards

Chapter 12: Learning and Memory Flashcards

1
Q

Who is Henry Molaison?

A

A young boy who cracked his skull while riding a bike and experienced frequent seizures. His case allowed for knowing more about how memory worked in the brain.

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2
Q

What was removed in Henry’s surgery?

A

Medial temporal lobe specifically hippocampus and amygdala

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3
Q

What happened after Henry’s surgery?

A

He functioned well and had fewer seizures but could not form new memories. He was only able to remember memories from before his surgery.

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4
Q

What is anterograde amnesia?

A

The inability to form new memories after an injury

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5
Q

What is retrograde amnesia?

A

The inability to recall old memories before the injruy

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6
Q

What is needed to form new declarative memories?

A

hippocampus

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7
Q

What is consolidation?

A

the process where the brain is forming a physical representation of memories

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8
Q

What is retrieval?

A

The accessing of memories

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9
Q

What is needed for consolidation and retrieval?

A

glutamate

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10
Q

What happens when glutamate receptors are blocked?

A

It prevents consolidation and retrieval for memories

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11
Q

Where are memories stored?

A

In the prefrontal cortex and hippocampus for consolidation and retrieval. Other areas in the brain are used to store physical memories.

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12
Q

What are place cells?

A

Cells that fire when in a specific environment. These cells are found in both humans and primates.

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13
Q

What is declarative memory?

A

knowing facts, people, and events

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14
Q

What is non-declarative memory?

A

knowing memories of behaviors, skills, procedures, emotions

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15
Q

What is needed for declarative memory?

A

the hippocampus

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16
Q

What is needed for non-declarative memory?

A

striatum (a part of the basal ganglia)

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17
Q

What memory was intact in Henry Molaison?

A

non-declaritive

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18
Q

What is a working memory?

A

Where memory is temporarily stored. Working memory matches old memory with new memory.

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19
Q

What is used in working memory?

A

the prefrontal cortex

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20
Q

What is Hebb’s rule?

A

When neurons fire together, the synapse strengthen together.

“cells that fire together, wire together”

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21
Q

What is long-term potentiation(LTP)?

A

synapses become stronger over time

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22
Q

What is long-term depression(LDP)?

A

decrease in synaptic strength due to weak pre-synaptic activity towards post-synaptic cell

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23
Q

What is associative LTP?

A

When a weak synapse is present when two strong synapses are together

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24
Q

What stimulates LTP?

A

high frequency

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25
Q

What stimulates LTD?

A

low frequency

26
Q

What is LTP used for?

A

forming and recalling memories

27
Q

What is LTD used for?

A

deleting memories, editing incorrect memories

28
Q

What is associative LTP used for?

A

classical conditioning

29
Q

How is learning measured?

A

theta waves from 4 to 7 Hz

30
Q

What is necessary for LTP?

A

two glutamate synapses which are AMPA and NMDA. AMPA opens sodium channels and causes excitatory postsynaptic potential. As well as NMDA that opens calcium channels

31
Q

What was concluded in the taxi study?

A

Drivers with more experience have large posterior growth in the hippocampus

32
Q

What two enzymes are necessary for consolidation?

A

CaMKII for the establishment of LTP and protein kinase M theta for long-term memory

33
Q

When does consolidation take place?

A

sleep

34
Q

What happens to neurons during learning?

A

hippocampus adds neurons (neurogenesis) as seen in taxi driver study.

35
Q

What is extinction?

A

The deleting of memories through learning requires the activation of NMDA. Similar to Pavlov’s dogs that will stop doing a behavior and is still learning

36
Q

What is forgetting?

A

the active biological process of removing useless information through enzyme PP1 and rac protein

37
Q

What is reconsolidation?

A

during memory retrieval that corrects errors and refines memories. Can create false memories in the process.

38
Q

What was once believed about dementia?

A

Researchers believed that dementia was inevitable and was bound to happen

39
Q

What can memory loss be attributed to?

A

myelin/neuron loss and impaired LTP

40
Q

What can slow down memory loss?

A

enriched activities like crossword puzzles and even exercise

41
Q

What is the reserve hypothesis?

A

an active lifestyle can promote neurogenesis like reading or exercising

42
Q

What did the nun study conclude?

A

More elaborate writing journals can decrease memory loss

43
Q

What is Alzheimer’s disease?

A

the deterioration of the brain that results in memory loss

44
Q

Who is affected by Alzheimer’s disease?

A

10% of people who are over 65 and 50% of those over 85

45
Q

What are the symptoms of Alzheimer’s disease?

A

aggressive, confused about environment and those around them, and loss of reason

46
Q

What are some neural abnormalities?

A

amyloid plaques and neurofibrillary tangles

47
Q

What are amyloid plaques?

A

an interference in neural transmission. Clumps of amyloid protein will cluster around axon terminals and interfere with transmission signals

48
Q

What are neurofibrillary tangles?

A

An abnormal increase of tau protein causes neural death.

49
Q

What happens to the brain when one has Alzheimer’s disease?

A

There is a loss of neurons in the temporal/frontal lobe, enlarged ventricles, and isolated hippocampus

50
Q

How many genes are confirmed for Alzheimer’s?

A

4

51
Q

What is the breakdown of genes for Alzheimer’s?

A

3 early onset for those less than 60 and 1 late on set for those older than 60

52
Q

What gene has the highest risk and is related to neural abnormality?

A

APOE ε4 that causes 3-8x more risk

53
Q

What are the 4 genes in Alzheimer’s?

A

APP, Presenilin 1 &2, and APOE ε4

54
Q

What are some environmental factors that contribute to Alzheimer’s?

A

pesticides, lead exposure, and chronic stress

55
Q

What are some treatments for Alzheimer’s?

A

Memantine for glutamate, drugs that remove tangles and plaques that are somewhat effective but not really. Most of the treatment can slow down but will not cure it

56
Q

How is Alzheimer’s detected?

A

brain scans like PET and MRI

57
Q

What is Korkasoff’s syndrome?

A

brain deterioration that is caused by alcoholism.

58
Q

What is damaged in Korkasoff’s syndrome?

A

mamillary bodies, medial thalamus as well as abnormal frontal lobe

59
Q

What deficiency is found in Korkasoff’s syndrome?

A

Low thiamine (B1) where calories are taken in through alcohol rather than food

60
Q

What are the symptoms found in Korkasoff’s syndrome?

A

anterograde amnesia, confabulation(reality vs. memory), but intact non-declarative memory

61
Q

What is confabulation?

A

the inability to distinguish what is real and a memory due to frontal lobe damage

62
Q

What is some treatment for Korkasoff’s syndrome?

A

High thiamine intake but little treatment as it can’t be reversed

Psych 002 (13 decks)

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