Learning and memory -Bi Flashcards

1
Q

What are the 2 types of memory and examples of each?

A
  1. explicit (declarative)=facts and events

2. implicit (nondeclarative). ex: associative learning, habituation, new skills, etc

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2
Q

What did the case of HM (bilateral medial temporal lobe lesions) teach us about memory?

A
  • Medial temporal lobes contribute to declarative memory but NOT non-declarative memory (he could still learn new skills but was unaware of doing so)
  • short term memory does not depend on MTLs
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3
Q

What happened to pt NA after his dorsomedial thalamus was damaged by a fencing foil being stabbed through his right nostril?

A

cannot form declarative long-term memories

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4
Q

Loss of what structures will result in the loss of declarative memory?

A

Medial temporal lobe:
-(para) hippocampal cortex, associate cortex

diencephalon

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5
Q

What does the size of your hippocampus have to do with your memory?

A

the more you use your brain, the more your hippocampus can grow and the better your ability for learning and memory will be

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6
Q

What are some types of non-declarative memory?

A
  • skill learning
  • priming
  • conditioning
  • non-associative memory (habituation/sensitization)
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7
Q

What part of the brain plays an essential role in the classical conditioning of motor responses, such as the eye blink reflex elicited by the air puff?

A

the cerebellum

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8
Q

What brain structure is involved in conditioned fear?

A

amygdala

poor little Albert

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9
Q

What is necessary to convert short term memories to long term? What are the 2 ways to achieve this?

A

rehearsal

  1. maintenance rehearsal: repetition. will not be able to recall after stop the repetition.
  2. elaborative rehearsal: association of new things –> help with tx from short–> long term. Promotes recall after we stop rehearsing
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10
Q

What are the 2 theories for forgetting?

A

decay theory: memory fades with time unless there is rehearsal (Elaborative)

interference theory: memory for other material interferes with information we are trying to remember

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11
Q

What are the 2 broad categories of interference theory? What is the best way to overcome this?

A
  1. retroactive: when what you know now makes it difficult to recall something that occurred previously
  2. proactive: when something that you have already learned interferes with your ability to recall more recent events

**taking more breaks (spaced info) allows for better learning than massed studying

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12
Q

Where are declarative long term memories stored?

A

in the cortex in the same region that was activated during perception

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13
Q

How are episodic (autobiographical) and semantic memories processed differently?

A

Episodic (autobiographical) memories cause greater activation of the right frontal and temporal lobes

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14
Q

What is neuroplasticity?

A

the ability of neurons and neural circuits to be remodeled by experience or environment.

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15
Q

What is long term potentiation?

Where will this be seen?

A

When axons repeatedly excite another cell, there are gross metabolic changes in one or both of the cells that cause more efficient firing after some time.

this is seen in the synapses that the scheaffer collaterals of CA3 neurons make with the dendrites of CA1 neurons in the hippocampus

there will be structural changes (new dendritic spines) that can be visualized an hour after LTP inducing stimulus

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16
Q

What is long-term synaptic depression (LTD)?

A

reduction in synaptic responses from low-frequency stimulation of the synapse

“if you don’t use it, you lose it”

17
Q

How does memory change as we age?

A
  • decline in cognitive function
  • loss of neural connections
  • deterioration of cholinergic pathways (septal complex and nucleus basal is of meynert)
18
Q

How do high functioning older adults compensate for their decrease in cognitive abilities?

A

use of BILATERAL activation of memory areas in the brain

low functioning older adults require more of the same area to be functioning for the same recall as a younger person

19
Q

What is the most common form of dementia?

A

Alzheimer’s disease

20
Q

What are the 2 types of AD?

A
Early onset (30-60 yo)=(Familial AD (FAD))(65 yo) (LOAD) (99%)
-unknown cause
21
Q

What are some risk factors for AD?

A

age, family history, genetic factors (APOE), head injury, cardiovascular disease, environmental

22
Q

What are some treatments for AD?

A

Cholinesterase inhibitors: Donepezil, galantamine, rivastigmine, tacrine

NMDA receptor antagonists: memantine

(want to increase ACh in the brain)

23
Q

What is a major genetic risk in LOAD?

A

APOE epsilon 4 allele

24
Q

What are the 2 major pathologies seen in AD?

A
  1. plaques: alpha beta secretases cause amyloidgenic degradation of APP–> these fragments form plaques
  2. neurofibrillary tangles: aggregated form of the microtubule binding protein tau inside the cells when neurons die
25
Q

How do plaques and tangles spread through the cortex as AD progresses?

A

first affect learning and memory and then to the frontal lobe (planning and functioning)

26
Q

What form of secretase is responsible for the formation of amyloidogenic processes?

A

alpha beta secretase

alpha gamma does not form these segments–> no plaques formed

27
Q

How does cognitive reserve affect cognition?

A

pts with higher cognitive reserve can have greater biomarker abnormalities before a decline in cognitive function than pts with lower cognitive reserve

–>exercising the brain can postpone the onset of disease**

28
Q

What did the test where old mice were physically attached to young mice show?

A

“aging” factors in the systemic environment of old mice (immune related molecules that impair neurogenesis) and “rejuvenating” factors in young mice were able to transfer and cause aging in the young mice and rejuvenation in the old mice

there is some factor in the blood that controls age-related impairments on neurogenesis, synaptic plasticity and cognitive functioning

29
Q

What can help in AD?

A
  • Early diagnosis
  • Developing biomarkers
  • Better imaging tools
  • Exercise
  • Healthy diet
  • Physical exercise (increase protection in brain)
  • Mental exercise: postpone onset of disease