Chapter 12: Memory Phases - Consolidation Flashcards

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1
Q

In what way is ultra long term memory the “final repository” for memory?

A

to achieve permanence, memories must be consolidated into ultra-long term memory

does this imply that memory traces must be moved/changed

retrieval to STM can also occur from this store; return to lability and reconsolidation (through LTM)

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2
Q

What is the adaptive power of having a “consolidation” process for long-lasting memories?

A

ability to modulate strength of memory trace; have the ability to “lock in” info, choose what we want to lock in or let go

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3
Q

What are “Flash Bulb” memories?

A

memories that are encoded extremely well do to emotional salience

last a long time, associated with a very intense emotion

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4
Q

Could activation of the sympathetic nervous system modulate consolidation?

A

emotional sequences can aid in memory, regardless of what type of memory it is

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5
Q

What is the nature of a “consolidated” memory trace?

A

is a “remote” engram identical to its more “recent” form?; for procedural it’s identical, for explicit memory it is highly unlikely to be identical

what is the nature of change, if any, to the physical substrate of the memory?

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6
Q

What is fixation?

A

a.k.a. cellular consolidation

the idea that activity-dependent plastic changes need to be “fixed” or made more permanent through some cellular/molecular processes

e.g. protein synthesis (translation), gene activation (transcription)

original cellular changes in learning have to be fixed in some way

relevant for both explicit and implicit memory

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7
Q

What is reorganization?

A

a.k.a. systems reconsolidation

the idea that the memory trace (engram) is changed (moved?) and becomes differentially dependent on brain structures other than the one responsible for encoding it

hippocampus to neocortex

only relevant to explicit forms of memory, particularly episodic, maybe also semantic

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8
Q

What is the behavioral evidence for memory consolidation?

A

spaced versus massed learning paradigms: by extending learning period there was less forgetting

interference (learning new material): people had a hard time not thinking of things after learning (spontaneous rehearsal), prevent this rehearsal, more forgetting, time after learning is important

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9
Q

What is the clinical evidence for memory consolidation?

A

loss of consciousness (concussion - surgery): don’t remember the sequence of events before the concussion

disrupted activity (epilepsy - ECT): cannot recall events that lead up to episode, particularly MTL, wake up confused, ECT shows temporally graded retrograde amnesia

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10
Q

What is the experimental evidence for memory consolidation?

A

post-learning manipulations of hormones or neuromodulators: can either enhance or hinder ability to remember when make manipulations in the period right after learning

post-learning influence of “offline” states (e.g. sleep): important for procedural and declarative

disruption of protein synthesis: also occurs in disrupting activity, pain synthesis dependent phase

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11
Q

What does all of the evidence for memory consolidation suggest?

A

that recent memories are labile (easily disrupted) while remote memories are stable (immutable)

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12
Q

What was the experiment that tested the timing dependencies for amnestic effects of protein synthesis inhibition?

A

train animals then give protein synthesis inhibition

give short-term test and long-term test

does inhibition interfere with STM, LTM, or both?

is timing of the manipulation (inhibition) important?

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13
Q

What were the results on STM and LTM of administering a drug to block consolidation at immediate time intervals?

A

no difference between experiment and control at STM

severe impairment of LTM function in experimental group

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14
Q

What were the results on LTM of administering a drug to block consolidation at immediate and delayed time intervals?

A

after a delay of 6 hours between test and inhibition perform like control

inhibition of consolidation needs to be delivered at a certain time after memory training

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15
Q

What is the post training brain region neuromodulation paradigm?

A

manipulation occur following training

no interference with motor, cognitive abilities in task itself during training/testing

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16
Q

What was the Morris water maze and intracranial infusion of amphetamine experiment of post-learning memory-modulating manipulations?

A

spatial version: dropping rat at random spot, fixed platform below surface, need to use spatial cues to figure out its location and path to platform, only get one training session

cued version: learn that a cue signals the platform, then escape

17
Q

What were the results of the Morris water maze and intracranial infusion of amphetamine experiment of post-learning memory-modulating manipulations?

A

spatial version: enhancement with HPC and amygdala infusions of amphetamine

cued version: enhancement with striatal and amygdala infusions of amphetamine

suggests that activating amygdala is important for solidifying either type of memory

18
Q

How do stress hormones modulate consolidation?

A

stress hormones (adrenaline & cortisol) modulate consolidation by direct brain (& amygdala) activation

amygdala lesions or infusions of adrenergic antagonists block these effects

amygdala infusions of adrenergic agonists mimic these effects of amygdala activation, memory enhancement in post learning environment

19
Q

How do emotions and drugs that mimic endogenous responses to emotion enhance memory consolidation?

A

protein synthesis?

blockers of protein synthesis inhibit memory consolidation when applied in the post-training period as well

de novo protein synthesis hypothesis of long-term memory: need new proteins to be expressed

enhanced neural activity: replay and reactivation of ensembles in post-training period

20
Q

What makes an old memory different from a new one?

A

time: longer the time, more able to retain

recall frequency/probability: recollecting, older memories have been rehearsed longer

intervening experiences

21
Q

Is the HPC the location of the consolidated engram?

A

experimentally, HPC damage has been suggested to affect newly learned material more than material learned in the distant past

implication: HPC is needed only to lay down and recall recent memories, but is not needed to recall remote memories

longer delay between learning and lesion –> less impaired

when you lesion HPC you get impairments in HPC dependent memories

where are these remote memories located? what structure are they dependent on?

22
Q

What is the controversy regarding temporal retrograde gradients?

A

previous studies didn’t have lesions of the full HPC in rats, a quarter was still left

gradient may not exist if only lesioning a small part

systematically lesioned the entire hippocampus

if you damage HPC (no matter the delay) can’t access info

not sure if you have the memory of your childhood, or the memory of a picture, video, or your parents saying it

are remote memories of the HPC dependent on the HPC, or do they become something else, a story?

23
Q

What is the hippocampal involvement in both recent and remote memories?

A

precise temporal control of hippocampal activity during recall

recent and remote memories depend on the immediate activity of the HPC

interaction between hippocampus and prefrontal region to retain info in the absence of HPC

24
Q

What was the optogenetics experiment to test the hippocampal involvement in both recent and remote memories?

A

infect neurons with viral vector for opsin, imbedded in membrane, allow them to get excited by light (movement of cations)

pumps Cl- into cell, inhibits firing

inhibit activity of CA1: stop expressing fear

after a week: CA1 inhibition showed no fear

prolonged CA1 inhibition: gradually express fear, reactivate memory, looked at anterior cingulate cortex

25
Q

What is the location of the consolidated engram?

A

neocortex?

hippocampus computes inputs and sends them back, return loop; encodes so it can be accessed in a different way

cortical modifications of sensory maps

specific cortical lesions produce specific sensory memory (perceptual) deficits

stimulation of certain (MTL) cortical sites can produce mnemonic sensations (evocation of memories)

26
Q

What is the mechanism for “transferring” location of memories?

A

activity in cortico-hippocampo-cortical loop

differential learning/dependence of hippocampus versus neocortex

train animals a lot to show plasticity in the cortex, hippocampal changes happen almost instantly

27
Q

What is the cortico-hippocampo-cortical loop?

A

damage causes anterograde amnesia and recent retrograde amnesia

return circuit important for systems consolidation?

return outputs from HPC to parahippocampal back to sensory encoding areas

28
Q

How is the cortical-hippocampal system set up to produce ITM, LTM and to permanently consolidate memories?

A

HPC: labile trace storage; synaptic weights are easily and quickly modifiable; finite capacity, not permanent

NCTX: permanent trace storage; synaptic weights require more stimulation and greater time to modify; infinite capacity and longer lasting

29
Q

What kind of activity might be important in the cortical-hippocampal system in order to set up a systems-level transfer of memory traces?

A

need to have activity in the circuit in the first place

recall frequency is biased to old memory, build further connections downstream

30
Q

What are the different sleep stages?

A

awake: alpha activity when eyes are closed

stage 1: theta activity; generate theta activity when you’re upset as well; going from fast activity to a little slower

stage 2: K complexes, spindling

stage 3: high amplitude, delta activity

stage 4: delta activity

REM sleep: low voltage, high frequency, similar to waking, theta and beta activity

31
Q

What is the relationship between sleep stages and memory consolidation?

A

sleep is an intervening state between training and testing important for memory; sleep deprivation impairs while sleep enhances subsequent recall

differential effects of sleep stages on declarative versus procedural memory; REM - procedural, SWS - declarative

hippocampal neuronal replay during SWS

slow oscillation density and coherence correlates with declarative improvement

boosting slow oscillation improves memory

32
Q

What was the procedure for the experiment testing conditioned fear response and protein synthesis in the amygdala?

A

cued fear conditioning, auditory cue paired with shock; put rat in different environment and play the cue; induce the control and doses of drugs; retest on same cue

results: low dose performed same as control, high dose wiped out the memory

no reminder trial: no difference between the groups

conclusion: when you reactivate memory it puts it into a labile state where it needs to be consolidated again

33
Q

What was the procedure for the experiment testing conditioned fear response and protein synthesis in the amygdala on if reconsolidation has a critical window?

A

experiment: training; cue in new environment; delay timing of infusion; test again

result: slight lowering of fear response, little bit of an effect but closer to control

reconsolidation occurs at a critical window, just like consolidation

34
Q

What was the procedure for the experiment testing conditioned fear response and protein synthesis in the amygdala on if long term memories can be reconsolidated?

A

experiment: train; leave for 2 weeks; test in new environment, infuse, test again after 24 hours

change in ability to recall after drug infusion

even a long-term memory can be reconsolidated

35
Q

What was the procedure for the experiment testing conditioned fear response and protein synthesis in the amygdala on if reconsolidation is a form of LTM dependent on the production of proteins?

A

experiment: infuse drugs after test 1; test 4 hours later (STM); test 24 hours later (LTM)

STM should be unaffected; LTM affected because it is protein synthesis dependent

no difference in STM; LTM was severely impaired

specific for LTM; not STM

36
Q

Does memory reconsolidation exist?

A

following reactivation, memories are reconsolidated

thus, retrieval involves a repeated episode of lability and likely changes the memory itself

this requires protein synthesis