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Cellular Basis Of Learning And Memory > Lectures 20, 21, 22, & 23 > Flashcards

Lectures 20, 21, 22, & 23 Flashcards

1
Q

What is an engram?

A

Physical trace of an experience; neural substrate for storing and recalling memories

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2
Q

What are the four properties of the engram?

A

Persistence
Ecphory (essentially retrieval)
Content
Dormancy

I remember being PECD by a bird

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3
Q

An engram has the potential for ecphory, what does this mean?

A

It may be expressed behaviorally through interactions w/ retrieval cues

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4
Q

What are the requirements for concluding that neurons belong to an engram?

A

Cells must be active at time of learning and time of memory test

Activation of cells must correlate w/ the generation of the appropriate memory

Direct activation of these cells generate the appropriate behavior

Inhibiting or ablating the specific cells prevent the occurrence of the appropriate behavior Inhibiting

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5
Q

To accomplish labeling engrams, researchers took advantage of what molecular mechanisms?

A

Immediate early gene activation and protein synthesis

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6
Q

Neuronal depolarization activates the expression of which immediate early genes?

A

C-fos and Arc

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7
Q

How can immediate early genes be used to mark a neuron activated by an experience?

A

Increased expression is a giveaway that a neuron is activated by an experience

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8
Q

What does “TetTag” refer to?

A

Combining tetracycline-controlled transcriptional activation and activity dependent tagging of neurons

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9
Q

What does the Tetracycline-Controlled System allow for?

A

Conditional gene expression based on the presence/absence of a tetracycline antibiotic (ex. Doxycyline)

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10
Q

How can TetTag control temporal expression of the LacZ cell tag?

A

Whenever DOX is present, tTA cannot control LAC promotion, however whenever its absent tTA expression promotes LAC transcription

If DOX is introduced, removed, then returned again, LAC will no longer be expressed but the previously tagged cells stay tagged

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11
Q

How did cells that were exposed to fear conditioning in the absence of DOX show expression of 3 days after fear conditioning? How about during dissection?

A

Immediately early gene ZIF expression was high

Dissection found cells tagged with LAC & IEG marker ZIF were considered the engram cells

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12
Q

How did freezing time and LAC+ZIF cells compare in a fear conditioned group of mice versus a control group of mice?

A

Control had far less freezing and less LAC+ZIF cells

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13
Q

What is a limitation of using IEG markers?

A

They are limited and some last only a few minutes

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14
Q

What did Guzowski et al. Figure out using IEG Arc mRNA?

A

Labeled Arc mRNA at different time points after an experience

immediately: expression seen in the nucleus
Delayed: outside of the nucleus in the nucleus

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15
Q

Describe the optogenetics activating engram cells protocol?

A

ChR2 inserted virally into DG along w/ optic fiber

Mice are habituation to Context A w/ DOX

Mice are then conditioned (shock) in Context B w/ NO DOX

Mice are returned to Context A and tested with blue light to activate engram cells and activate the behavior from the conditioning

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16
Q

What did Opsin-induced inhibition do to freezing?

A

Decreased freezing

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17
Q

What did opsin-induced excitation do to freezing?

A

Increased freezing

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18
Q

What neurons are primed to become engram neurons?

A

Neurons with increased intrinsic excitability

Inhibitory neurons are important to determining engram size

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19
Q

What happened to memory after ablation of random neurons?

A

Nothing

20
Q

What happened to memory after ablation of engram neurons?

A

Decreased memory

21
Q

How do we know synaptic strength was increased in engram cells?

A

Higher AMPA/NMDA ratio after 1 day of training

Greater connectivity between pre and post synaptic engram cells

Increase in the number and size of spines

22
Q

Are engram cells likely in a single area or distributed throughout the brain?

A

Distributed to support different aspects of an experience

23
Q

What is a silent engram?

A

Engrams that cannot be retrieved by natural retrieval cues but can be retrieved w/ experimental

24
Q

What happens if you block protein synthesis immediately after an experience (which leads to amnesia one day later) but reactivate an engram neuron (silent engram) afterwards?

A

You can recover the memory

25
Q

What makes silent engram neurons unique regarding physiological and structural alterations?

A

Weaker physiological and structural alterations

26
Q

What is mimicry?

A

The creation of false memory/formation of false episodic memories

27
Q

How can false memories be formed?

A

When a biologically important event occurs while an animal is retrieving a previously formed memory, the two stimuli can be associated to form a new false episodic memory

28
Q

What aspects of cognition decline with aging?

A

Long term memory
Working memory

29
Q

What happens to the brain with age?

A

Decreased brain weight and enlarged ventricles

30
Q

Significant longitudinal tissue loss for both ___ & ___ ____ even in healthy adults

A

Gray
White matter

31
Q

Do elderly people have widespread neuronal loss?

A

NO! Most areas have minimal neuronal loss

32
Q

What are the structural alterations that occur in both neurons and glia due to aging?

A
  • changes in complexity of dendrites
  • changes in the number of dendritic spines
  • myelin changes on axons
  • changes in the balance of excitatory and inhibitory neurotransmitter systems
33
Q

What happens to dendritic spines density as we age?

A

It decreases

34
Q

What is a longitudinal study?

A

Same people studied over a period of time

35
Q

What is a cross sectional study?

A

People of varying ages studied simultaneously

36
Q

What is a problem with longitudinal studies?

A

They require funding to last the entirely of the study length

37
Q

What is a problem with a cross sectional study?

A

Only shows a screenshot of time of different patients

38
Q

Do cross sectional and longitudinal studies yield the same results?

A

nope

39
Q

What is considered normal aging and cognitive decline?

A

learning at a slower pace, difficulty mastering new things, creativity declines

40
Q

What happened to old mice when they were given a running wheel for 35 days (sweet spot)?

A

Increased spatial learning

41
Q

What are common characteristics of Neurodegenerative Diseases?

A
  • tend to occur during later years of the lifespan
  • time of onset not well defined
  • processes well underway by time of diagnosis
  • accumulation of abnormal protein deposits
42
Q

What aspects of cognitive function does Alzheimer’s Disease affect?

A
  • memory
  • decision making
  • reasoning ability
  • verbal fluency
43
Q

What are the hallmarks of Alzheimer’s Disease?

A

plaques and tangles

44
Q

How are amyloid beta and Tau related to Alzheimer’s disease?

A

aggregation, changes in conformation and buildup of Abeta initiate AD pathogenesis and damage the brain

tau pathology also contributes to AD progression

45
Q

What are the main takeaways of the Oliveira et al. paper?

A

AD brains have increased eIF2alpha-P which leads to protein synthesis dysregulation

System treatment with a compound that increased eIF2alpha prevented memory impairment and decreased plaques in AD models

Cellular Basis Of Learning And Memory (7 decks)

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